Failing Up

It as a given that we will fail.  All of us.  Medical or not.  We are all human, which means we make mistakes. So once we accept this as fact, we can then move towards failing better.

When we make a medical error we have a few choices:

 

1. Live in perpetual doubt

Blame yourself and practice defensive medicine

 

2. Ignore the error and do nothing, stop caring

 

3. Failing up – learn from the fail

-       Learning from your medical error takes effort, consideration and time -makes one even more accountable, compassionate and competent.

-       We are all going to fail.

-       When one sweep failures under the carpet, one cannot learn from them effectively and neither can one heal from them effectively

-       Learning to accept this eventuality and incorporating it into our daily life, will allow us to grow as individuals, to more effectively teach others and to take better care of our patients.

-       Strive for post traumatic growth and thriving after failure instead of feelings of shame and isolation.

 

 

Failing up strategies:

-       Find a Failure Friend: An empathetic work friend who understands the context; someone who is your safety net and in return you can be their safety net.

-       Be a good Failure Friend to a colleague: Listen/hear them out and empathize/provide affirmation rather than giving advice or solutions. Use reflective listening like you would with a patient and then come up with a joint plan.

-       Teach from your mistakes: Give talks around your difficult cases that incorporate personal strategies on how to cope after the fact, rather than only concentrating on the medical aspects of the case. Talk with peers, residents and medstudents

 

Watch this excellent FeminEM talk by Dr Sara Gray: https://www.youtube.com/watch?v=aGS6O98p4Q8

 

References:

https://emergencymedicinecases.com/preventing-burnout-promoting-wellness-emergency-medicine/

https://www.entrepreneur.com/article/331332

https://saragray.org/2017/03/07/failure-friends/

 · 

Pressors in cardiogenic shock

“Pressors” in Cardiogenic Shock in adults

 

  • Vasopressors- Pure vasoconstriction without any inotropy eg Phenylephrine and Vasopressin

  • Inotrope- Increase cardiac contractility à improving SV and cardiac output without any vasoconstriction eg Milrinone

  • Inopressors - a combination of vasopressors and inotropes, because they lead to both increased cardiac contractility and increased peripheral vasoconstriction eg Norepinephrine, Epinephrine and Dopamine

 

Norepinephrine- Inopressor

  • Considered the safest Inopressor

  • Less arrhythmogenic than Epinephrine and Dopamine


Mechanism of action

  • Stimulates alpha-1 and alpha-2 receptors

  • Small amount of beta-1 agonist- modest inotropic effect

  • Increased coronary blood flow and afterload

  • Increases venous tone and return with resultant increased preload

Adverse effects

  • Norepinephrine is considered safer than both epinephrine and dopamine.

  • Still carries risk of toxicity to cardiac myocytes, cardiac arrhythmias, and peripheral vasoconstriction leading to tissue ischemia

Indications

  • Norepinephrine is considered first-line in cardiogenic shock with profound hypotension (SBP < 70 mm Hg)

  • Should be used in conjunction with dobutamine in patients with cardiogenic shock and blood pressure higher than 70 mm Hg who fail to respond to dobutamine.

Dosing

  • Use weight-based dosing to avoid the adverse effects associated with norepinephrine use

  • Weight-based dosing is based on GFR

  • Norepinephrine has a rapid onset of action (minutes) and can be titrated every 2-5 minutes

 

Dobutamine- Inopressor

Mechanism of action

  • Stimulates beta-1 and beta-2 receptors at approximately a 3:1 ratio

  • At high doses (greater than 15 ug/kg/min), dobutamine also becomes a mild alpha-1 agonist.

  • Because it mainly stimulates beta-1 receptors, dobutamine is mostly an inotrope

  • Dobutamine’s stimulation of beta-2 receptors can result in peripheral vasodilation, though the magnitude of this effect is variable à blood pressure in some (but not all) patients.

  • Due to its vasodilatory effects, dobutamine has been shown to improve capillary perfusion independent of changes in blood pressure and cardiac index.

Adverse Effects

  • Studies have demonstrated increased myocardial oxygen demand and malignant arrhythmias typically occuring at doses higher than 15 ug/kg/min

  • Many patients experience hypotension associated with dobutamine use and should be used with caution in patients with systolic blood pressure less than 90 mmHg

  • Dobutamine should only be used in patients with adequate fluid resuscitation


Indications

  • Current ACC/AHA guidelines à first-line agent in management of hypotension associated with acute myocardial infarction

  • But because dobutamine can lower BP, it should only be used if SBP is between 70-100 mmHg, with norepinephrine ready (or already infusing) as well.

  • Dobutamine is typically recommended as the first line agent in cardiogenic shock , but this is not a strong recommendation because several studies have demonstrated benefits to norepinephrine in this setting.

  • If dobutamine is used as a first-line agent, then norepinephrine should be second-line or already infusing, followed by milrinone.


Dosing

  • Dobutamine can be started at 2 mcg/kg/min and titrated to effect, with a maximum dose of 20 mcg/kg/min.

  • Onset of action is 1-2 minutes and the half-life is also approximately 2 minutes à rapidly reversible.


Milrinone- Inodilator

Mechanism of action

  • Milrinone is a phosphodiesterase-3 (PDE3) inhibitor à leads to cardiac smooth muscle relaxation and peripheral vasoconstriction

  • Potent inotropy + diastolic relaxation and vasodilation à to reduced preload, afterload, and systemic vascular resistance (SVR)

  • Milrinone has no beta-adrenergic activity à minimal chronotropic effects.


Adverse Effects

  • Because milrinone decreases preload (and therefore often leads to hypotension), it should only be used in patients who have undergone appropriate fluid resuscitation

  • Use of milrinone often necessitates concurrent vasopressor administration.

  • Because milrinone is metabolized in the kidneys, it should be avoided in patients with renal disease


Indications

  • Recommended for use in patients with daily beta-blocker use and in patients with long-standing heart failure who have developed resistance to catecholamine derivatives

  • Due to PDE’s vasodilatory effect on pulmonary vasculature à theoretical benefit in patients with pulmonary hypertension

Dosing

  • The starting dose of milrinone should ideally be chosen based on that patient’s renal function. The general range is 0.25-0.75 mcg/kg/min.

  • Avoid its use in patients with creatinine clearance less than 50 mL/min.

  • Because of its long onset of action and half-life, milrinone should be titrated every 2 hours (or slower, in the presence of renal disease).


Vasopressin- Pressor

Mechanism of action

  • Vasopressin is an endogenously released hormone (also known as anti-diuretic hormone) à vasopressin receptors in the kidneys à improve GFR

  • Vasopressin receptors on the peripheral vasculature à vasoconstriction.

  • Also causes coronary and cerebral vasodilation


Adverse Effects

  • Vasopressin increases the risk of digital ischemia more significantly than the catecholamine derivatives.

  • No evidence to support the use of vasopressin through a peripheral intravenous line

  • Vasopressin does not have an antidote if extravasation does occur.

Indications

  • Due to its increased risk for digital ischemia à avoid vasopressin in patients with known PVD

  • It has been proposed that because vasopressin leads to coronary vasodilation, it may be a preferable agent in cardiogenic shock but few RCTs investigating vasopressin use in cardiogenic shock.

  • Vasopressin may not lead to pulmonary vasoconstriction à ideal pressor choice in hypotension secondary to pulmonary hypertension à but not enough literature to support routine use in this setting


Dosing


Vasopressin is an endogenous à no utility to titrating vasopressin à used at a set dose of 0.04 U/min, regardless of weight.

 

Epinephrine- Inopressor

 

Mechanism of action

  • Beta-1 and beta-2 receptors agonism à more inotropic effects than norepinephrine

  • Epinephrine greatly increases chronotropy (heart rate) and thus stroke volume

  • Some stimulatory effect on alpha-1 receptors

  • Lower doses (1-10 mcg/min) à a beta-1 agonist

  • Higher doses (greater than 10 mcg/min) à an alpha-1 agonist

 

Adverse effects

  • Associated with an increased risk of tachycardia and lactic acidosis

  • Hyperglycemia

  • Increased incidence of arrhythmogenic events associated with epinephrine

  • More difficult use lactate as a marker of the patient’s response to treatment

 

Indications

Should be used with extreme caution in cases of cardiogenic shock:

  • RCT of 219 patients with cardiogenic shock found epinephrine to be independently associated with increased 90-day mortality and worsened renal function compared to dobutamine and norepinephrine (not validated).

  • Known increased incidence of arrhythmogenic events associated with epinephrine

 

Dosing


  • doses of 1-10 mcg/min predominantly activate beta-1 receptors, while doses greater than 10 mcg/min begin to primarily affect alpha-1-mediated vasoconstriction.

 

 

Phenylephrine: Not recommended in Cardiogenic shock

 

 

Resource: Awesome chart summarizing plessors

 http://www.emdocs.net/wp-content/uploads/2018/02/Inopressor-Summary_chart.pdf

 

References:

http://www.emdocs.net/evidence-based-approach-pressors-shock-part/

emDOCs.net – Emergency Medicine EducationAn Evidence-Based Approach to Pressors in Shock: Part I - emDOCs.net - Emergency Medicine Education

www.emdocs.net


 

http://www.emdocs.net/evidence-based-approach-pressors-shock-part-ii/

emDOCs.net – Emergency Medicine EducationAn Evidence-Based Approach to Pressors in Shock: Part II - emDOCs.net - Emergency Medicine Education

www.emdocs.net


 

Tarvasmäki T, Lassus J, Varpula M, Sionis A, Sund R, Køber L, et al. Current real-life use of vasopressors and inotropes in cardiogenic shock-adrenaline use is associated with excess organ injury and mortality. Critical Care. 2016;20(1):208.

 · 

Trauma in Pregnancy

Resuscitation of the Pregnant Trauma patient

 

General principles

·      Trauma is the most common cause of non-obstetrical maternal death in the United States

·      Best fetal resuscitation is good maternal resuscitation.

·      Stabilization of the pregnant women is the first priority; then, if the fetus is viable (≥ 23 weeks), fetal heart rate auscultation and fetal monitoring can be initiated and an obstetrical consultation obtained as soon as feasible

·      In Rh-negative pregnant trauma patients, quantification of maternal–fetal hemorrhage by tests such as Kleihauer-Betke should be done to determine the need for additional doses of anti-D immunoglobulin.

·      Tetanus vaccination is safe in pregnancy and should be given when indicated.

 

 

Airway

·      Greater risk for difficult intubation than non-pregnant patient

·      Pregnancy related changes à decreased functional residual capacity, reduced respiratory system compliance, increased airway resistance, and increased oxygen requirements

·      Gastric emptying is delayed in pregnancy à greater risk for aspiration

·      Respiratory tract mucosal edema à A smaller size of endotracheal tube is recommended

·      Choice of RSI medications NOT affected by pregnancy status

 

Breathing

·      Place chest tube one to 2 intercostal spaces higher than usual to account for displacement of the diaphragm during pregnancy

·      Marked increases in basal oxygen consumption à lower threshold for supplemental oxygen

 

Circulation

·      Fluid and Colloid resuscitation like standard trauma protocol

·      Uteroplacental vasculature is highly responsive to vasopressors, and their administration may decrease placental perfusion à vasopressors should be avoided unless refractory

·      Avoid supine hypotension: Compression of IVC by the uterus can cause up to 30% reduction in cardiac output à Place in left lateral position or by manual displacement of the uterus while the injured patient is secured in the supine position

·      O-negative blood should be transfused in order to avoid Rh sensitization in Rh-negative women

·      Vital signs: heart rate increases by 15% during pregnancy. Tachycardia and hypotension, typical of hypovolemic shock, may appear late in the pregnant trauma patient because of her increased blood volume.

·      Maternal vital signs and perfusion may be preserved at the expense of uteroplacental perfusion, delaying the occurrence of signs of hypovolemic shock

·      Attempt to obtain supra-diaphragmatic intravenous or intraosseous access for volume resuscitation and medication administration.

 

 

FAST

·      The FAST is less sensitive for free fluid in the pregnant patient than in non-pregnant patients.  Sensitivity decreases with increasing gestational age, likely due to altered fluid flow within the abdomen.

·      Management of suspected placental abruption should not be delayed pending confirmation by ultrasonography as ultrasound is not a sensitive tool for its diagnosis.

 

 

Secondary survey

·      In cases of vaginal bleeding at or after 23 weeks, speculum or digital vaginal examination should be deferred until placenta previa is excluded by a prior or current ultrasound scan.

 

Imaging

·      Radiographic studies indicated for maternal evaluation including abdominal computed tomography should not be deferred or delayed due to concerns regarding fetal exposure to radiation.

·      Ionizing radiation has the highest teratogenic potential during the period of organogenesis (5–10 weeks), with an increased risk of miscarriage before this period.

·      With abdominal CT during the third trimester the fetal exposure is around 3.5 rads, which is still under the threshold for fetal damage

·      Contrast agents should be used if indicated.

 

 

Resuscitative Hysterotomy in Cardiac Arrest

·      Should begin within 4 minutes and completed within 5 minutes of cardiac arrest

·      Both maternal and fetal survival decrease significantly after 5 minutes

·      Do NOT delay the procedure for the arrival of an obstetrician or neonatologist.

·      Do NOT evaluate for fetal cardiac activity or tocometry.

·      Do NOT prepare a sterile field (but be as clean as possible).

·      Do NOT transport to an alternative location.

·      Performing RH increases maternal cardiac output by 30%.

 

RH Algorithm.png


 

References:

 

Tamingthesru.com

EmDocs

Jain, Venu, et al. "Guidelines for the management of a pregnant trauma patient." Journal of Obstetrics and Gynaecology Canada 37.6 (2015): 553-571.

Smith, Kurt A., and Suzanne Bryce. "Trauma in the pregnant patient: an evidence-based approach to management." Emergency medicine practice 15.4 (2013): 1-18.

 

 · 

Resuscitative TEE

Important: Please complete the Sexual Harassment Online Module ASAP!




Resuscitative Transesophageal echocardiography (TEE)

  • TEE allows the emergency physician to maintain the standard of an ultrasound-informed resuscitation in the scenario of cardiac arrest, where TTE is significantly limited.

  • Focused or resuscitative TEE (4 views) differ from comprehensive TEE (>20 views) that cardiology performs in that it is employed to identify specific questions.

  • TEE allows for potentially shorter chest compression pauses

  • TEE allows for evaluation for the quality of chest compressions

  • TEE allows for visualization of fine V-fib not seen on the monitor

 

Indications: Cardiac arrest (ACEP)

Contraindications: Esophageal injury or stricture and lack of a definitive airway

How to manipulate a TEE Probe:

5 different ways you can physically manipulate the TEE probe

1. Withdraw or Advance up or down patient’s esophagus

2. Turn probe to right or left

3. Turn tip of flip in anterior- ante-flexing or in the posterior direction called retro-flexing --> large wheel

4. Turn tip to Left or right -->  small wheel (not typically used for our purposes)

5. In addition, you can rotate the transducer housed within the probe itself (AKA omniplane or multiplane)-->  adjusts the beam angle anywhere between 0° and 180° -->  two smaller buttons ( crystal rotation)

TEE manipulation.jpg

 

TEE-controls- wheels.png

 

 

The views are obtained in the following order: : 

The midesophageal 4-chamber view (ME 4C) is obtained by advancing the TEE probe to the thoracic esophagus and orienting the multiplane at 0-20° in neutral flexion. You may need to retroflex slightly to see all four chambers.

-   The midesophageal long-axis view (ME LAX) is obtained by leaving the probe in the same location as the midesophageal 4-chamber, but increasing the multiplane to between 110° and 160° while in neutral flexion. 

-   The transgastric short axis view (TG- SAX) is obtained by first moving the multiplane to 0°, then advancing the probe into the stomach and ante-flexing the probe

-   The bicaval view (ME bicaval) is obtained by turning the entire probe to the patient’s right towards the superior vena cava (SVC) and inferior vena cava (IVC) while in the mid-esophagus, keeping the multiplane at 90-100° with neutral flexion

 ( The first 3 views are recommended by ACEP. Bicaval not recommended by ACEP) 







TEE views and their analogous TTE views



TTE-and-TEE.gif

Midesophageal four chamber view (ME 4C)

-  Apical four chamber view

-  Great visualization of all chambers as well as the tricuspid and mitral valves in one plane.

-   Evaluation of right and left ventricular systolic function and size

-   Preferred view to evaluate for the presence or absence of a perfusing rhythm during a pulse check.

ME4C.png

 

Midesophageal Aortic Long Axis view (ME LAX)

-  Midesophageal analogous to the parasternal long axis view in TTE

-   View includes the mitral and aortic valves, as well as the left atrium, left ventricle, and left ventricular outflow tract of the right ventricle.

-   Evaluate left ventricular systolic function, and provides feedback on compression adequacy and location. High-quality compressions cause maximal compression of the left ventricle and visualization of the aortic valve opening and closing indicating forward flow of blood.  Poor quality compressions are seen over the aortic root and there is no valvular indication of forward flow. 

ME- LAX.png

 

Transgastric Short Axis view (TG- SAX)

- Analogous to the parasternal short axis TTE view

- Evaluate left ventricular systolic function, including any regional wall motion abnormalities

- Can evaluate for acute MI and the presence of septal flattening in this view

TGSAX.png

Mid Esophageal Bicaval View (ME bicaval)

-   Analogous to the inferior vena cava view of TTE

-   Transducer plane cuts through the left atrium (LA), right atrium (RA), IVC and SVC.

This view allows the operator to evaluate for hypovolemia, atrial size, and interatrial septum bowing.

-   Aids in the placement of central venous catheters, transvenous pacemakers, or extracorporeal life support (ECMO) vascular cannulas by observing the initial wire placement in the vasculature

- Can aid inevaluation of fluid status to guide fluid resuscitation (looking at respiratory variation in SVC)

bicaval.png

 

Pitfalls

-  Compressions do not need to be stopped for TEE insertion. Additionally, the TEE can be left in the esophagus during defibrillation. The probe should be inserted or withdrawn while the tip is in neutral position, and not while the tip is flexed to avoid esophageal injury. 

-  Images should be optimized to avoid foreshortening of the ventricles and to include the appropriate structures for each view.

-  Pericardial effusions must be taken into clinical context, as small effusions can cause tamponade if accumulated rapidly, while large effusions can be well tolerated if they accumulate slowly.

-   Clotted hemopericardium may be isoechoic with the myocardium, making it difficult to identify.

-  Right ventricular failure is not specific to pulmonary embolism, and can be due to pulmonary hypertension or other etiologies such as right sided myocardial infarction, or even cardiac arrest itself.

-  Pleural effusions can be mistaken for pericardial effusions. Multiple views should be used to corroborate findings.

-  Fat pads can be mistaken for pericardial effusions, but these are hypoechoic rather than anechoic and limited to the anterior and apical regions of the heart, not circumferential.

 

 Resource: 

Check out this 3D module that you can practice on 

https://pie.med.utoronto.ca/TEE/TEE_content/TEE_standardViews_intro.html

References:

Drs Lawrence Haines, Judy Lin and Alyssa Phuoc-Ngyuyen

Images: Adapted from Arntfield R, Pace J, McLeod S, et al. Focused transesophageal echocardiography for emergency physicians-description and results from simulation training of a structured four-view examination. Crit Ultrasound J. 2015;7(1):27.

Teran, Felipe, et al. "Evaluation of out-of-hospital cardiac arrest using transesophageal echocardiography in the emergency department." Resuscitation 137 (2019): 140-147.

EmDocs

ACEP policy statement

https://www.acep.org/patient-care/policy-statements/guidelines-for-the-use-of-transesophageal-echocardiography-tee-in-the-ed-for-cardiac-arrest/

 · 

Non Invasive Ventilation

Non Invasive Ventilation

 

Definitions:

  • CPAP: applies constant pressure throughout the breathing cycle to increase functional residual capacity (FRC) by recruiting alveoli, decreasing work of breathing, and improving oxygenation.

  • PEEP/EPAP: alveolar pressure before inspiratory flow begins. PEEP à decrease the amount of work required to initiate a breath and decrease atelectasis

  • Bi-level: Cycled ventilation between Inspiratory Positive Airway Pressure (IPAP) and Expiratory Positive Airway Pressure/PEEP. BiPAP supports ventilation and increases oxygenation.

  • Pressure Support: The difference between EPAP and IPAP is referred to as pressure support. Pressure support makes it easier to draw larger tidal volumes

 

BiPAP/ NIPPV/ Bi-level vs HFNC

·       Oxygenation:  Both devices can almost à  100% FiO2.  HFNC à small PEEP ~5cm, max vs much higher PEEP on NPPV

·       Work of Breathing:  HFNC may wash out the anatomic deadspace à  reduces the work of breathing.  BiPAP can higher pressures and support majority of the work of breathing.

·       Secretion clearance: Important in pneumonia to prevent mucus plugging improve clearance.  BiPAP impairs secretion clearance, whereas HFNC does not seem to.

·       Monitoring: Unable to communicate with patient effectively on BIPAP. BiPAP anxiety provoking and makes it difficult to differentiate between worsening clinical resp status vs anxiety. HFNC facilitates communication  

 

 

NIPPV/Bi-level/ BiPAP

COPD

·      Bi-level ventilation à decreases the risk of death (relative risk reduction 48%) and intubation rates (RRR 60%)

·      Number Needed to Treat (NNT) for mortality benefit = 10

·      NNT to prevent intubation = 4

·      Furthermore, when comparing patients with moderate and severe acidosis, bi-level ventilation decreased mortality, rates of intubation, and lengths of stay.

·      ** Ensure patient does not have a PTX that could tension once placed in PPV

Initial Settings:

-       IPAP 8-20 cm H2O (up to 30 cm H20)

-       EPAP 2-6 cm H2O to overcome intrinsic airway collapse

-       Begin with either high IPAP and then titrate down, or low and titrate high.

 

SCAPE/ CHF exacerbation

·      IPAP assists ventilation à  decreases the WOB

·      EPAP/PEEP increases the FRC by recruiting collapsed alveoli, improving oxygenation, and helping to force interstitial fluid back into the pulmonary vasculature

·      Also, increases intrathoracic pressure à decreased left ventricular (LV) end diastolic volume à decreased afterload and increased LV ejection fraction/stroke volume.

·      Common Initial Settings:

·              IPAP: 10 to 20 cm H20

·              EPAP: 5 to 10 cm H20

·              I:E ratio of IT to ET and is usually set at 1:3 or 1:4 (Inspiratory to Expiratory ratio)

·      Evidence for Bi-level ventilation in CHF exacerbations is unfortunately mostly supportive of CPAP with few trials comparing CPAP and BiPAP

·      Cochrane review looking at NIPPV in CHF exacerbations à CPAP alone has been proven to decrease intubation rates and to decrease in-hospital mortality, without the same benefit seen using bi-level ventilation

·      Lack of evidence does not mean lack of efficacy

BIPAP titration.gif

 

How to assess your patients on NIV

·       Oxygenation:   good pulse oximetry waveform. ABG is rarely needed to measure oxygenation

·       Work of breathing:  The best metric is the respiratory rate.  Worsening retractions, diaphoresis, tripoding, shallow breathing, and an abdominal paradoxical breathing pattern. 

·       Mentation:  A patient who is easily arousible and mentating adequately doesn't have life-threatening hypercapnia

·       BiPAP screen:  Low tidal volumes and/or low minute ventilation àhypoventilation. But  adequate tidal volumes and minute ventilation suggest a adequate response to NIV

·       Treat the patient, not the ABG- Proven by Brochard 1995 (RCT) investigating the use of BiPAP in COPD:  BiPAP improved mortality despite having no effect on ABG parameters after one hour à  BiPAP can be successful without any immediate effect on the ABG.

 

 

High Flow Nasal Cannula

HI-FLOW.png



·       Low flow: NC ~ 1-5 L/min vs NRB ~15 L/min

·       High Flow- 20-60 L/min

·       Normal Resting breathing flow ~15-30 L/min

·       Respiratory distress 60-180 L/min 

  • Adult devices max out at 50-60 L/Min (max it out to start) and the dose for pediatric patient’s (based on trials) is 2L/Kg/Min

  • Maximize your devices flow rate initially then wean the fi02 to maintain your oxygen saturation goal

 

Adult Indications: Hypoxemic Respiratory failure (mostly Pneumonia) FLORALI Trial, DNR/DNI patients , Pre-oxygenation prior to Intubation

 

Pediatric Indications: Bronchiolitis, Asthma, Pneumonia, Croup

 

Take Home Points:

·      Rule out pneumothorax (auscultation, US) prior to placing patients on NIPPV

·      Do not base clinical management solely based off of an ABG esp if patient clinically improving

·      Choose Bi-level vs HFNC based on patient’s diagnosis

·      Best Metric to assess NIV success is respiratory rate

 

 

References:

 

Vital, F. M. R., Ladeira, M. T. & Atallah, A. N. Non-invasive positive pressure ventilation (CPAP or bilevel NPPV) for cardiogenic pulmonary oedema. Cochrane Database Syst. Rev. CD005351 (2013). doi:10.1002/14651858.CD005351.pub3

 

Frank Lodeserto MD, "High Flow Nasal Cannula (HFNC) – Part 1: How It Works", REBEL EM blog, August 20, 2018. Available at: https://rebelem.com/high-flow-nasal-cannula-hfnc-part-1-how-it-works/.

 

Frank Lodeserto MD, "High Flow Nasal Cannula (HFNC) – Part 2: Adult & Pediatric Indications", REBEL EM blog, August 23, 2018. Available at: https://rebelem.com/high-flow-nasal-cannula-hfnc-part-2-adult-pediatric-indications/.

 

EmDocs

EMCrit

 · 

Heparin Anticoagulation in Acute Coronary Syndrome

Heparin Anticoagulation in Acute Coronary Syndrome

 

STEMI:

·      Anticoagulation for primary PCI addresses 2 pathophysiologic processes: initial thrombin generation caused by spontaneous coronary plaque rupture and secondary thrombin generation caused by iatrogenic introduction of foreign bodies (stents) and arterial dissection (balloon angioplasty)

·      The thrombotic process does not cease on successful implantation of a coronary stent: platelet activation in the setting of endothelial disruption continues and peak ≈2 hours after coronary intervention

·      AHA 2013 Latest Guidelines:

Screen Shot 2019-10-10 at 11.12.57 AM.png



·      European Society of Cardiology guidelines 2017:

Screen Shot 2019-10-10 at 11.12.04 AM.png



·      Both AHA/ ACC and European Society for Cardiology rate LOE as C for UFH but have Class I recommendation

·      Stronger evidence for Bivalirudin and Enoxaparin with either the same Class recommendation or lower

·      No RCTs have been performed since this has been standard of care in the PCI era

 

 

 

Undifferentiated NSTEMI and Unstable Angina:

This is more controversial in terms of choice of agent as well as the therapy but continues to be standard of care with guidelines supporting use of heparin

 

2014 AHA guidelines for the management of NSTEMI

-       Recommend unfractionated heparin continued for 48 hours or until PCI is performed (LOE B)  

-       With even a higher level of evidence the same guidelines also recommend enoxaparin 1mg/kg subcutaneously every 12 hours with reduced dosing to 1mg/kg subcutaneously in patients with a creatinine clearance <30mL/min) (LOE A)

-       The guidelines recognize that studies supporting this therapy were performed primarily on patients with a diagnosis of unstable angina and in the era before dual anti platelet therapy and early catheterization/revascularization. 

·      Recent retrospective Chinese review published in 2018 concluded that parenteral anticoagulation therapy did not decrease mortality in patients with NSTEMI undergoing PCI but did have more bleeding events compared to non-parenteral anticoagulation therapy

·      Cochrane review à patients treated with heparins had a similar risk of mortality, revascularization and recurrent angina. However, those treated with heparins had a decreased risk of myocardial infarction (driven by the largest study (FRISC), and they used the 6 day outcome of that trial, rather than the 40 or 150 day outcomes that we know were negative) this was based on a higher incidence of minor bleeding. 

·      Shared decision making can be employed in this setting

·      The risk versus benefit profile might be different for patient who have a history of GIB, known brain aneurysm, high fall risk patients etc

 

NSTEMI with noninvasive management

 

 

·      Rebound effect- Heparin causes a transient reduction in MI rates, with a rebound in infarction after anticoagulation is withdrawn.   There is no long-term sustained mortality benefit in literature

·      Anticoagulation with heparin exposes the patient to a risk of hemorrhage without any known long-term benefit evidenced in literature.  

·      Furthermore, heparin delays the occurrence of ischemic events to a later time-point in their hospital course, when the patient may be less closely monitored.

·      The potential benefit heparin “bridging” to definitive therapy is not realized when patients’ are managed medically and don’t receive an intervention (PCI or CABG)

·      Decision to anticoagulated can be deferred to the consultants managing the patient as they would be more aware of the likely management of the patient with an intervention.

 

 

 

 

Special considerations:

 

Instent thrombosis- Benefit anticoagulation as secondary thrombin generation caused by iatrogenic introduction of foreign bodies

Effect of Hemodialysis on troponin levels in ESRD patients - “Troponinemia” could reflect chronic microinfarctions or correlate with left ventricular hypertrophy. HD process itself might cause undesirable myocardial injury and enhance post HD TnI levels. The effect of HD on TnI levels are unestablished, reporting either increasing, unchanged or decreasing of post-dialysis hsTnI levels 

Rhabdomyolysis- The prevalence of false positive cTnI in the ED patients with rhabdomylolyiss was 17% in one study although there is significant paucity of evidence.

 

Reference:

REBELEM

PulmCrit

First10EM

 

Amsterdam, Ezra A., et al. "2014 AHA/ACC guideline for the management of patients with non–ST-elevation acute coronary syndromes: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines." Journal of the American College of Cardiology 64.24 (2014): e139-e228.

 

Ibanez, Borja, et al. "2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: The Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC)." European heart journal 39.2 (2017): 119-177.

 

Dauerman, Harold L. "Anticoagulation Strategies for Primary Percutaneous Coronary Intervention." (2015).

 

Li, Siu Fai, Jennifer Zapata, and Elizabeth Tillem. "The prevalence of false-positive cardiac troponin I in ED patients with rhabdomyolysis." The American journal of emergency medicine 23.7 (2005): 860-863.

 

Tarapan, Tanawat, et al. "High sensitivity Troponin-I levels in asymptomatic hemodialysis patients." Renal failure 41.1 (2019): 393-400.

 

Chen, JY et al. Association of Parenteral Anticoagulation Therapy With Outcomes in Chinese Patients Undergoing Percutaneous Coronary Intervention for Non-ST-Segment Elevation Acute Coronary Syndrome. JAMA Intern Med 2018. PMID: 30592483

 

 

 

 

 · 

Indications for use of Tranexamic Acid (TXA)

Indications for use of Tranexamic Acid (TXA)

Trauma

 

Trial Name: CRASH 2 (Positive trial)

Trial Type: Multicenter, double-blind RCT

Sample size: 20,211

Dose/Route of TXA: Loading dose 1g over 10 min, then infusion of 1g over 8hr

Primary outcome: All-cause mortality within 4 weeks of injury

Secondary outcome: Vascular occlusive events (AMI, stroke, PE, and DVT), surgical intervention, receipt of blood transfusion, and units of blood products transfused

Results:  Reduced All-cause mortality p 0.0035, death due to hemorrhage p 0.0077, no significant vascular occlusion p 0.96

Risk of thrombotic events: No increase in risk

Take home point: The use of TXA in trauma patients with “significant bleeding” reduces all-cause mortality without an increase in thromboembolic events.  This effect seems to be greatest in the subset of patients with severe shock (SBP ≤70mmHg) and when given ≤3 hours from time of injury 

 

Shakur H et al. Effects of Tranexamic Acid on Death, Vascular Occlusive Events, and Blood Transfusion in Trauma Patients with Significant Haemorrhage. Lancet 2010. PMID: 20554319

 

Trial Name: MATTERs (Positive trial)

Trial Type: Single center, retrospective, observational study

Sample size: 896

Dose/ route of TXA: 1 g initially, 2nd dose per MD discretion

Primary outcome: 24hr mortality, 48hr mortality, and 30-day mortality

Secondary outcome: Transfusion requirements and rate of thromboembolic complications.

Results: Not significantly decreased 24 hr p >0.05, Significantly decreased 48hrs p 0.004 and 30 day mortality p 0.03

Risk of thrombotic events: Increased overall VTE p 0.001 but patients who had a VTE also had higher burden of injury

Take home point:  Patients with penetrating injuries, requiring blood transfusions within 1hr of presentation the use of TXA reduced overall mortality

 

Morrison JJ et al. Military Application of Tranexamic Acid in Trauma Emergency Resuscitation (MATTERs) Study. Arch Surg 2012. PMID: 22006852

 

 

ICH

 

Trial Name: Meta-Analysis of TXA for Traumatic Brain Injury- negative trial

Trial Type: Meta-analysis and systematic review of RCTs or quasi-RCTs 

Sample size:  510

Outcome: Mortality, neurological function, hematoma expansion

Results: statistically significant reduction in ICH progression with TXA non-statistically significant improvement of clinical outcomes in ED patients with TBI.

Risk of thrombotic events: No adverse effects reported

Take home point: Did not lead to a statistically significant mortality benefit or improved neurological functional status. Further evidence is required to support its routine use in patients with TBI.

 

Zehtabchi S et al. Tranexamic Acid for Traumatic Brain Injury: A Systematic Review and Meta-Analysis. Am J Emerg Med 2014. PMID: 25447601

 

 

Trial Name: Tranexamic Acid for Hyperacute Primary IntraCerebral Haemorrhage (TICH-2)- Negative

Trial Type: International, randomized, double-blind, placebo-controlled, parallel group

Sample size:  2325

Dose of TXA used: 1g IV TXA bolus followed by an 8hr infusion of 1g of TXA 

Outcome:  Functional Status at Day 90, Hematoma Expansion at Day 2, Mean Hematoma Volume Expansion from Baseline to 24hr, Death by Day 7, Death by Day 90

Results: No difference in neurological impairment (mean NIHSS score at day 7), 90-day functional outcomes, length of hospital stay, discharge disposition, venous thromboembolic events, or arterial occlusions

Risk of thrombotic events: None

Take home point: TXA was given >3hrs after stroke onset, patients had more severe strokes, and larger hematoma volumes (>60mLs) than prior studies. Possible benefit if given to a subset of patient within 3 hours with smaller strokes but cannot be recommended at this time in clinical practice for spontaneous ICH based on the results of these trials

 

Sprigg N et al. Tranexamic Acid for Hyperacute Primary IntraCerebral Haemorrhage (TICH-2): An International Randomised, Placebo-Controlled, Phase 3 Superiority Trial. Lancet 2018. PMID: 29778325

 

 

Post Partum Hemorrhage

 

Trial Name: WOMAN trial – Negative trial

Trial Type: Randomized, double-blind, placebo-controlled trial,

Sample size:  20,060 ≥16 years of age with post-partum hemorrhage after vaginal delivery or caesarean section 

Dose of TXA used: 1 g IV vs matching placebo, If bleeding continued after 30 minutes or stopped and restarted within 24hrs, a second dose of 1g of TXA or placebo was given

Outcome: Initial outcome of all-cause mortality and/or hysterectomy within 42 days of giving birth

Final Primary Outcome: Death from PPH

Results: No difference in all cause mortality or hysterctomy

Risk of thrombotic events:

Take home point: It is difficult to draw definitive conclusions from this trial as the NNT was still large (i.e. ≈250) and the study had a fragility index of 0. Data showed a consistent association of delayed administration of TXA with no benefit

WOMAN Trial Collaborators. Effect of Early Tranexamic Acid Administration on Mortality, Hysterectomy, and Other Morbidities in Women with Post-Partum Haemorrhage (WOMAN): An International, Randomised, Double-Blind, Placebo-Controlled Trial. Lancet 2017. PMID: 28456509

 

UGIB

 

Trial Name: Cochrane review

Trial Type: Systematic review and meta-analysis of 8 RCTs

Sample size:  1700

Dose of TXA used: Total daily dose of TXA ranged from 4 – 8g and ranged from 2 – 7 days with both PO and IV adminsteration

Outcome: Primary: all-cause mortality and adverse events

Secondary: Rebleeding and surgery

Results: All-Cause Mortality p 0.007, rebleeding P = 0.07

Risk of thrombotic events: No difference in thromboembolic events (only evaluated in 4 trials)

Take home point: May benefit in higher risk patients but better RCTs required to confirm or refute evidence. HALT IT trial underway currently with N of 12000

 

Bennett C et al. Tranexamic Acid for Upper Gastrointestinal Bleeding (Review). Cochrane Database Syst Rev 2014. PMID: 25414987

 

 

Epistaxis

 

Trial Name: Zahed et al 2017 – Positive study

Trial Type: Randomized, parallel group clinical trial

Sample size:  124 on antiplatelets

Dose of TXA used: topical TXA (500mg in 5mL) or anterior nasal packing.

Outcome: Primary outcome resolution at 10 minutes. Secondary outcomes were re-bleeding rate at 24hours and one week, ED length of stay, and patient satisfaction

Results: epistaxis treatment with topical application of TXA resulted in faster bleeding cessation (NNT 2) , less re-bleeding at 1-week, shorter ED LOS, and higher patient satisfaction as compared with anterior nasal packing.

Risk of thrombotic events: not evaluated

Take home point: Do it!

Zahed R et al. Topical Tranexamic Acid Compared With Anterior Nasal Packing or Treatment of Epistaxis in Patients Taking Antiplatelet Drugs: Randomized Controlled Trial. Acad Emerg Med 2017. PMID: 29125679

 

Post-Tonsillectomy Bleeding

 

Trial Name: Meta-Analysis 2012

Trial Type: Systematic review and meta-analysis

Sample size:  7 studies with 2,444 patients

Dose of TXA used: 250mg for children <25kg, 500mg for children >25kg

Outcome: mean volume of blood loss

Results: TXA led to a significant reduction of tonsillectomy blood loss volume but had no impact on the rate of patients with post-tonsillectomy hemorrhage.

Risk of thrombotic events: Not evaluated

Take home point:  In patients with minor post-tonsillectomy bleeding consider using nebulized TXA to reduce or stop bleeding.  

Chan CC et al. Systematic Review and Meta-Analysis of the Use of Tranexamic Acid in Tonsillectomy. Eur Arch Otorhinolaryngol 2013. PMID: 22996082

 

Heavy Menstrual Bleeding

 

Trial Name: Cochrane Review

Trial Type: Systematic review and metanalysis

Sample size:  1312 in 13 RCTs

Dose of TXA used: majority of studies used regular dose TXA (ranging from 3 g/day to 4 g/day), Four other studies used low‐dose TXA (ranging from 2 g/day to 2.4 g/day) 

Outcome: Volume of blood loss, Quality of life

Results:  Appears effective for treating HMB compared to placebo, NSAIDs, Oral luteal progestogens, ethamsylate or herbal remedies but less effective than levonorgestrel intrauterine system

Risk of thrombotic events: Not studied in most RCTs

Take Home point: Antifibrinolytic treatment (such as TXA) appears effective for treating HMB compared to placebo, NSAIDs, oral luteal progestogens, ethamsylate, or herbal remedies. There were too few data for most comparisons to determine whether antifibrinolytics were associated with increased risk of adverse events, and most studies did not specifically include thromboembolism as an outcome.

 

Bryant-Smith AC, Lethaby A, Farquhar C, Hickey M. Antifibrinolytics for heavy menstrual bleeding. Cochrane Database of Systematic Reviews 2018, Issue 4. Art. No.: CD000249. DOI: 10.1002/14651858.CD000249.pub2

 

Hemoptysis

Trial Name: Inhaled TXA RCT 2018

Trial Type: Prospective, double-blind, placebo-controlled randomized controlled trial 

Sample size:  47

Dose of TXA used: nebulized TXA (500mg/5mL

Primary outcome: rate of complete resolution of hemoptysis during first 5 days from admission, difference in daily volume of expectorated blood

Secondary outcome: rate of interventional bronchoscopy, rate of angiographic embolization, rate of surgery, mean hospital LOS

Results: Resolution of hemoptysis within 5 days of admission, NNT = 2, P<0.0005. Statistically shorter LOS, less invasive procedures

Risk of thrombotic events: not studied

Take home point: Although this was a small study, the advantages of inhaled TXA vs placebo in patients with non-massive hemoptysis included faster resolution of hemoptysis, shorter hospital LOS, fewer invasive procedures, and although not statistically significant, a trend toward improved 30d mortality.

 

Wand O et al. Inhaled Tranexamic Acid for Hemoptysis Treatment: A Randomized Controlled Trial. Chest 2018. PMID: 30321510

 

References:

See above

RebelEM

 

 · 

Box Breathing Technique   

Box Breathing Technique   

Next time you’re on shift and get a notification for a baby in arrest or have to prep the neck for a cric take a minute to do some Box Breathing to get you prepped and mentally ready

·      Easy, Quick and Navy SEAL approved

·      Effective in anxiety, insomnia, pain management and even labor!

·      Box breathing with this 4-4-4- ratio has a net neutral energetic effect

·      It’s not going to charge you up or put you into a sleepy relaxed state. But it will, as mentioned, make you very alert and grounded, ready for action.


Box breathing.gif

 

·      To begin, expel all of the air from your chest.

·      Keep your lungs empty for a four-count hold.

·      Then, inhale through the nose for four counts.

·      Hold the air in your lungs for a four-count hold.

·      When you hold your breath, do not clamp down and create back pressure. Rather, maintain an open, neutral feeling even though you are not inhaling.

·      When ready, release the hold and exhale smoothly through your nose for four counts. This is one circuit of the box-breathing practice.

·      Repeat this cycle for at least five minutes to get the full effect.  

 

References

 

Dr Arlene Chung

TIME

https://www.mindfulwellnessrochester.com/single-post/2017/06/02/Box-Breathing-for-Anxiety-Stress-Reduction

 · 

“Pressors” in Distributive Shock in Adults

“Pressors” in Distributive Shock in Adults

Thank you, Dr Dastmalchi, for requesting this POTD. I will review “pressors” for cardiogenic shock separately

  • Vasopressors- Pure vasoconstriction without any inotropy eg Phenylephrine and Vasopressin

  • Inotrope- Increase cardiac contractility à improving SV and cardiac output without any vasoconstriction eg Milrinone

  • Inopressors - a combination of vasopressors and inotropes, because they lead to both increased cardiac contractility and increased peripheral vasoconstriction eg Norepinephrine, Epinephrine and Dopamine

Norepinephrine- Inopressor

  • First line vasopressor in septic shock per Surviving Sepsis Guidelines

  • Less arrhythmogenic than Epinephrine and Dopamine


Mechanism of action

  • Stimulates alpha-1 and alpha-2 receptors

  • Small amount of beta-1 agonist- modest inotropic effect

  • Increased coronary blood flow and afterload

  • Increases venous tone and return with resultant increased preload

Adverse effects

  • Norepinephrine is considered safer than both Epinephrine and Dopamine.

  • ARR of 11% compared to dopamine with NNT 9

  • NE superior in improving CVP, urinary output, and arterial lactate levels compared to Epinephrine, Phenylephrine, and Vasopressin.

Indications

  • First-line pressor choice in distributive shock, including both neurogenic and septic shock

  • Norepinephrine as the only first-line pressor per SSC guidelines

Dosing

  • Use weight-based dosing to avoid the adverse effects associated with norepinephrine use

  • Weight-based dosing is based on GFR

  • Norepinephrine has a rapid onset of action (minutes) and can be titrated every 2-5 minutes

Epinephrine- Inopressor

Mechanism of action

  • Beta-1 and beta-2 receptors agonism à more inotropic effects than norepinephrine

  • Epinephrine greatly increases chronotropy (heart rate) and thus stroke volume

  • Some stimulatory effect on alpha-1 receptors

  • Lower doses (1-10 mcg/min) à a beta-1 agonist

  • Higher doses (greater than 10 mcg/min) à an alpha-1 agonist

Adverse effects

  • Associated with an increased risk of tachycardia and lactic acidosis

  • Hyperglycemia

  • Increased incidence of arrhythmogenic events associated with epinephrine

  • More difficult use lactate as a marker of the patient’s response to treatment

Indications

  • SSC guidelines recommend epinephrine as a second-line agent, after norepinephrine

  • “push-dose pressor”

  • Due to beta-2 receptors agonism causing bronchodilation, epinephrine is first-line agent for anaphylactic shock

Dosing

  • Guidelines for anaphylactic shock recommend an initial bolus of 0.1 mg (1:10,000) over 5 minutes, followed by an infusion of 2-15 mcg/min however associated with adverse cardiovascular events

  • For septic shock start epinephrine at 0.05 mcg/kg/min (generally 3-5 mcg/min) and titrate by 0.05 to 0.2 mcg/kg/min every 10 minutes. maximum drip rate is 2 mcg/kg/min

Dopamine- Inopressor

  • Fallen out of favor

  • Associated with higher arrhythmogenic events

Mechanism of action

  • Effects are dose-dependent

  • Low doses à dopaminergic receptors à leads to renal vasodilation à increased renal blood flow and GFR although studies failed to demonstrate improved renal function with dopamine use clinically

  • Moderate doses à beta-1 agonism à increased cardiac contractility and heart rate

  • High doses à alpha-1 adrenergic effects à arterial vasoconstriction and increased blood pressure

Adverse Effects

  • Several large, multi-center studies that demonstrate increased morbidity associated with its use

  • Significantly higher rates of dysrhythmias à NNH 9

Indications

  • Rescue medication when shock is refractory to other medications

Dosing

  • Start at 2 mcg/kg/min and titrate to a maximum dose of 20 mcg/kg/min.

  • Less than < 5 mcg/kg/min à vasodilation in the renal vasculature

  • 5-10mcg/kg/min à beta-1 agonism

  • 10 mcg/kg/min à alpha-1 adrenergic

Vasopressin- Vasopressor

  • Add vasopressin (doses up to 0.04 units/min) to norepinephrine to help achieve MAP target or decrease norepinephrine dosage

  • Restore catecholamine receptor responsiveness, particularly in cases of severe metabolic acidosis.

  • pH independent

  • Pure pressor à increase vasoconstriction with minimal effects on chronotropy or ionotropy

Mechanism of action

  • At low doses (< 0.04 units/min) à increases vascular resistance (V1)

  • No effect on heart rate and cardiac contractility

Adverse Effects

  • Vasopressin has been shown to be as safe as norepinephrine at lower doses

  • Increases SVR and afterload and decreases cardiac output although unclear if effect significant at lower doses

Indications

  • Second line vasopressors per SSC guidelines for septic shock

  • pH independent- Vasopressin in combination with epinephrine demonstrated improved ROSC in cardiac arrest patients with initial arterial pH <7.2 compared with epinephrine alone

Dosing

  • Steady dose at 0.03-0.04 units/min

  • Vasopressin is not titrated to clinical effect as are other vasopressors

  • Think about it more as a replacement therapy and treatment of relative vasopressin deficiency

Phenylephrine- Vasopressor

  • Pure pressor à increase vasoconstriction with minimal effects on chronotropy or ionotropy

  • SSC guidelines does not make rated recommendations on Phenylephrine

  • Limited clinical trial data

Mechanism of action

α1 agonism with peripheral vasoconstriction

Adverse Effects

  • Bradycardia - decrease in heart rate mediated by the carotid baroreceptor reflex 2/2 increase in SVR

  • Increases SVR and afterload and decreases cardiac output

Indications

  • Patients that are susceptible to beta-adrenergic generated arrhythmia

  • Push dose formulation

  • Refractory shock

Dosing

0.1-2mcg/kg/min (onset: minutes, duration: up to ~20 minutes)

References:

Emdocs

LITFL

Pollard, Sacha, Stephanie B. Edwin, and Cesar Alaniz. "Vasopressor and inotropic management of patients with septic shock." Pharmacy and Therapeutics 40.7 (2015): 438.

Amlal, Hassane, Sulaiman Sheriff, and Manoocher Soleimani. "Upregulation of collecting duct aquaporin-2 by metabolic acidosis: role of vasopressin." American Journal of Physiology-Cell Physiology 286.5 (2004): C1019-C1030.

Khanna, Ashish, and Nicholas A. Peters. "The Vasopressor Toolbox for Defending Blood Pressure."

Turner, DeAnna W., Rebecca L. Attridge, and Darrel W. Hughes. "Vasopressin associated with an increase in return of spontaneous circulation in acidotic cardiopulmonary arrest patients." Annals of Pharmacotherapy 48.8 (2014): 986-991.

 · 

HiNTS exam

What

Series of three quick, bedside, physical exam maneuvers that can potentially rule out a central cause of vertigo

 

Hi for head impulse testing, or head thrust testing.
N for nystagmus to remind you to look for direction-changing or vertical nystagmus
TS for test of skew.

 

HINTS1.png




 

Why

  • Nearly two-thirds of patients with stroke lack focal neurologic signs that would be readily apparent to a nonneurologist

  • Presence of all three “reassuring” exam findings suggests it can be ruled out with a 100% sensitivity for ischemic stroke in AVS while an initial MRI with diffusion-weighted imaging (DWI) had a 88% sensitivity





 

Who

Maneuvers used to help distinguish between central and peripheral vertigo in patients experiencing an acute vestibular syndrome (AVS) which is best defined as: rapid-onset vertigo, nausea and/or vomiting, gait unsteadiness, head motion intolerance, and nystagmus.

 

When

The patient must be experiencing continuous vertigo for the results to be reliably interpreted.

How

Head Impulse Test

HINTS2.png







  • Ask the patient to relax his/her head and maintain his/her gaze on your nose. Gently move the patient’s head to one side, then rapidly move it back to the neutral position. The patient may have a small corrective saccade. The head impulse test is positive (consistent with peripheral vertigo) if there is a significant lag with corrective saccades. If you can see the correction, it is abnormal. Compare this to the contralateral side; a difference in the speed of correction should be noted.

  • In acute vestibular syndrome, an abnormal result of a head impulse test usually indicates a peripheral vestibular lesion, whereas a normal response virtually confirms a stroke.

  • Abnormal exam rules in peripheral vertigo and thus rules out central vertigo if only unilateral

  • Video- https://www.youtube.com/watch?v=XpghlvnrREI&feature=youtu.be&t=665

 

Nystamus

  • Note if it is present in primary gaze (i.e. looking straight ahead) and or in lateral gaze. Unidirectional, horizontal nystagmus is reassuring for peripheral vertigo where as purely bidirectional, vertical or torsional can be consistent with central cause

  • The most common peripheral nystagmus, BPPV, in the posterior semicircular canal consists of a unidirectional horizontal nystagmus with a torsional component.

 

Test of Skew

  • Have the patient maintain his/her gaze on your nose. Alternate covering each of the patient’s eyes

  • Positive result will be the deviation of one eye while it is being covered, followed by correction after uncovering it.

https://www.youtube.com/watch?v=WAPaIMMsV_A

 

Summary

  • If the HiNTs exam is entirely consistent with peripheral vertigo (positive head impulse test, unidirectional and horizontal nystagmus, negative test of skew), then, according to the derivation paper, it is 100% sensitive and 96% specific for a peripheral cause of vertigo.

  • Use of HiNTs exam in the ED is currently controversial as the primary study was performed by neurologists in a partially differentiated patient population

  • likely has higher utility in the patient population in whom the clinician suspects a peripheral cause of their vertigo to rule out central cause and limit needless imaging

 

 

Limitations

  • Do not perform on any patient that has head trauma, neck trauma, an unstable spine, or neck pain concerning for arterial dissection.

  • Do not perform in patients with known severe carotid stenosis as it may embolize unstable plaque

  • Challenging to differentiate between catch up saccade and nystagmus

  • Patients with acute active AVS likely to not tolerate the testing

  • Patient must be awake and cooperative.

  • Essentially an awake “doll’s eye” that requires conscious fixation on an object. Cannot perform on mentally impaired or sedated patients

  • Not yet been validated by a large external group, let alone a large external group of emergency medicine providers.

  • In the study, exam performed by ophtho neurologists

 

References

 

NUEMBlog

Tamingthesru

Nelson, James A., and Erik Viirre. "The clinical differentiation of cerebellar infarction from common vertigo syndromes." Western Journal of Emergency Medicine 10.4 (2009): 273.

Kattah, Jorge C., et al. "HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging." Stroke 40.11 (2009): 3504-3510.

Tarnutzer, Alexander A., et al. "Does my dizzy patient have a stroke? A systematic review of bedside diagnosis in acute vestibular syndrome." CmAJ 183.9 (2011): E571-E592.




 · 

Metformin Associated Lactic Acidosis 


Metformin Associated Lactic Acidosis 

"The dose makes the poison"

Metformin a common medication used to treat DM II can cause metformin-associated lactic acidosis and Metformin toxicity with a mortality rate between 45-48%. Neither arterial lactate levels nor plasma metformin concentrations predicted mortality.

met cycle.jpg









  • · The main effect of metformin is inhibition of the mitochondrial transport chain complex-I, which essentially poisons the mitochondria.

  • · If the mitochondrial transport chain stops working: NADH builds up, Krebs cycle eventually gets backed up, Pyruvate gets converted into lactate which builds up.


 

Best described a spectrum depending on cause of lactic acidosis








Metformin-induced lactic acidosis (MILA)


  • · High levels of metformin are the primary cause of illness.


Acute metformin overdose


    • · Acute poisoning may lead to MILA in the absence of renal dysfunction.

    • · Precise amount of metformin required to do this is unclear, but seems to be high (e.g. >20 grams).

    • · Patients with acute ingestion look fine initially, but deteriorate subsequently (“toxin bomb”).

Subacute accumulation of metformin due to renal failure



    • · Metformin is renally cleared

    • · Progressive renal failure (with GFR << 30 ml/min) eventually leads to metformin accumulation and toxicity.

    • · These patients may present with marked lactic acidosis, yet have fairly preserved hemodynamics and look OK.




Metformin-associated lactic acidosis (MALA)

Patient on metformin develops an acute life-threatening illness (e.g. septic shock, cardiogenic shock). Metformin amplifies the degree of lactic acidosis, but it's not the sole cause of the illness. Risk factors include renal insufficiency, higher doses of metformin, and alcoholism.

 

Metformin-unrelated lactic acidosis (MULA)


  • · Metformin levels are low; metformin is an innocent bystander.

  • · Clinically it will be impossible to differentiate this from MALA. Differentiation of MULA from MALA requires measurement of metformin levels, which isn't available at most hospitals.




Signs & symptoms


  • · Vitals: The following abnormalities may be seen: Hypothermia, Hypotension progressing to vasopressor-refractory shock can occur.

  • · GI symptoms often predominate: Nausea, vomiting, diarrhea, epigastric pain.

  • · Delirium, decreased consciousness


 

Management


  • · Fingerstick glucose (hypoglycemia may occur)

  • · VBG with lactate

  • · Complete set of chemistries (including Ca/Mg/Phos), Coags

  • · Beta-hydroxybutyrate level (frequently elevated)

  • · Liver function tests

  • · Blood cultures, urinalysis, chest X-ray, procalcitonin.

  • · Administer Broad-spectrum empiric antibiotics

  • · Additional toxicologic evaluation (e.g. acetaminophen, salicylate levels, toxic alcohols, carboxyhemoglobin).

  • · Obtaining a serum metformin concentration is unhelpful in most cases because few hospitals perform the test and thus timely results are rarely available, and because the serum concentration often does not correlate with the severity of the poisoning or patient outcome

  • · Obtain early consultation with a medical toxicologist and a nephrologist


 

Metformin-induced lactic acidosis vs. DKA


  • · Compared to isolated DKA, patients with metformin-induced lactic acidosis have greater degree of hyperlactatemia, with less extensive ketoacidosis.

  • · Difficult to sort this out in some situations- treat both conditions (the treatment for DKA may actually improve MILA/MALA).

  • · Activated charcoal may be considered for patients who present very shortly following acute ingestion, without contraindications (e.g. normal mental status without risk of aspiration)

  • · Evaluate for alternative causes of illness, especially septic shock.

  • · Insulin therapy may be beneficial for metformin poisoning (aside from any question of DKA) by reducing generation of lactate and ketosis thereby improving acidosis



 

Bicarbonate?


  • · Undesirable for a few reasons: Might increase cellular permeability to metformin, Bicarbonate has never been shown to be a useful therapy for lactic acidosis, Raising the pH with bicarbonate may actually stimulate glycolysis and thereby increase lactate generation

  • · Normal saline is an acidotic fluid that will exacerbate the acidosis.

  • · Lactated Ringers and Plasmalyte not good choice, as these patients cannot metabolize lactate or acetate respectively


 

Other options?


  • · D5W with 1/2 normal saline, plus one ampule (50 mEq) of bicarbonate added per liter.

  • · Simultaneous infusions of normal saline and isotonic bicarbonate

  • · High-flow nasal cannula may be used to improve ventilatory efficiency and reduce the work of breathing



 

Indications for dialysis


  • · Main indications

    • · Lactate >15-20 mM

    • · pH <7.0-7.1

    • · Failure to improve despite standard supportive measures

  • · Comorbid conditions which may lower the threshold for dialysis

  • · If the patient is hemodynamically unstable, CVVH or CVVHD should be considered. The clearance of drug by CVVH was less than that generally reported to occur with conventional hemodialysis and should only be considered in patients who are too hemodynamically unstable to tolerate hemodialysis.


 

Methylene Blue


  • Methylene blue is capable of accepting electrons from NADH could function as a bridge to re-establish the flow of electrons through the mitochondria and can theoretically re-starts the stalled Krebs cycle and re-establishes normal metabolism

  • Vasoconstriction: Methylene blue can also function as a vasoconstrictor (by scavenging nitric oxide). It's possible that its efficacy in some cases of refractory shock with metformin toxicity is due purely to its efficacy as a vasoconstrictor.



 

References:

UptoDate

EMCrit

 · 

EKG in Tox

EKG#1

80 year old demented female, unresponsive, BP 55/20, blood glucose 24

1. What’s the rhythm?  2. What’s the differential for bradycardia?  3. Think tox – now narrow your differential. What do the vitals suggest?  4. How do you want to treat this patient?

1. What’s the rhythm?

2. What’s the differential for bradycardia?

3. Think tox – now narrow your differential. What do the vitals suggest?

4. How do you want to treat this patient?

EKG#2

21 year old male, suicidal, intentional overdose

1. Rate, rhythm, axis, intervals – you can glean a lot of information from these pieces alone  2. What’s the suspected overdose?  3. Treatment?

1. Rate, rhythm, axis, intervals – you can glean a lot of information from these pieces alone

2. What’s the suspected overdose?

3. Treatment?

EKG#3

41 year old female, sent from methadone clinic for nausea. Given Zofran at the clinic. Was acting belligerent at triage and required Haldol. Records show she is currently on azithromycin outpt for recent pneumonia.

You get this EKG right before she goes into cardiac arrest.

1. What the hell happened?  2. How you gonna treat?

1. What the hell happened?

2. How you gonna treat?

EKG#4

92 year old demented man, wife found him unresponsive near an open medicine cabinet

1. This is a classic dysrhythmia secondary to  which  toxicity?  2. What is a classic, more subtle finding you can see when the patient in normal sinus rhythm?

1. This is a classic dysrhythmia secondary to which toxicity?

2. What is a classic, more subtle finding you can see when the patient in normal sinus rhythm?

ANSWERS

EKGotW #4 – Tox Edition

 

Brown and University of Cincinnati have amazing reference websites for this topic!

 

Here are some reference tables from their sites with links that you should totes check out!

EKG#1

Beta Blocker Overdose

1.     What’s the rhythm?

a. Junctional bradycardia.

These are QRS complexes without P waves – no P waves means the ventricles are either being triggered from the AV node or more distally (in the actual ventricles).

The complexes are narrow, which means the AV node is likely triggering the impulses, conducting electricity down the bundle of his through the normal conduction pathway.

If the complexes were wide, these might be ventricular escape rhythms – not only do the SA and AV node have their own automaticity, but the actual myocytes themselves may trigger impulses as well.

1.     What’s the differential for bradycardia?

a.     H.I.D.E.

                                               i.     Hypothyroid/Hypothermia

                                             ii.     Ischemia/Increased ICP

                                           iii.     Drugs

                                            iv.     Electrolytes (K, Ca, Mag)

2.     Think tox – now narrow your differential. What do the vitals suggest?

a.     Several toxidromes may cause severe bradycardia. Commonly we talk about calcium channel blockers and beta blockers. (Don’t forget digoxin from David Elkin’s M&M a few weeks ago!)

Classically, hypoglycemia + bradycardia = beta blocker overdose.

Beware of bronchospasm as a clue as well.

3.     How do you want to treat this patient?

a. Glucagon – increases intracellular cAMP and calcium

                      i.   Give with Zofran!

b. Calcium – increase inotropy

c. Epi Drip – for cardiogenic shock

d. High Dose Insulin – 1u/kg/hr, 30-60 min to take effect

e. Lipid Emulsion Therapy – uncertain mechanism

f. Atropine / Pacing can be considered – atropine often ineffective. (Remember, atropine counteracts excessive vagal stimulation, but this is not the etiology of bradycardia in BB OD patients!)
My fave article on this:
https://emcrit.org/pulmcrit/epinephrine-atropine-bradycardia/

EKG#2

TCA Overdose

1.     Rate, rhythm, axis, intervals

a.      Rate = QRS x 6 = 21 x 6 = 126

b.     Rhythm – You can see P waves hiding in I, V5/V6, and maybe small irregularities in the T waves of V3/V4 that hint at presence of P waves. This is sinus.

c.      Axis - Downward deflection in I, upward in aVF = RIGHT AXIS

d.     Intervals

                                               i.     PR < 200msec

                                              ii.     QRS > 120msec

                                            iii.     QTc = QT/Ö(RàR’) = 0.312 / Ö0.48 = 450msec

^^^(I used V2 for this)

Sinus tachycardia with RIGHT AXIS deviation and WIDE QRS complex

2.     What’s the suspected overdose?

a. Hallmarks of TCA Overdose EKG

                 i.  Widened QRS

                ii.  Big-ass R wave in aVR

              iii.  New right axis

iv. Deep slurred S waves, I & aVL

3.     Treatment?

a. Sodium Bicarb pushes

                      i.   Until the QRS narrows

b. Lidocaine for refractory arrythmia

Read about TCA -- http://www.emdocs.net/ecg-pointers-tca-overdose/

Video about TCA -- https://emin5.com/2015/12/22/tca-toxicity/

EKG#3

Long QT

1.     What the hell happened?

a. Haldol, azithromycin, methadone are all QT prolonging agents, which predispose to Torsades de Pointes, or Polymorphic Ventricular Tachycardia

b.     Using V5…
QTc = QT / (Square root of R->R’) = 0.74 / (SqRt(1.08) = 711msec

2.     How you gonna treat?

a. Defibrillate if in arrest

b. 2g Mag Sulfate slow IV push

c. Isoproterenol +/- pacer if super brady

This case: http://hqmeded-ecg.blogspot.com/2014/06/acquired-long-qt-do-not-trust.html

Torsades overview: https://wikem.org/wiki/Torsades_de_pointes

EKG#4

Digoxin Toxicity

1.     Classic Findings

a. This is Bidirectional V-Tach, classic for digoxin toxicity

b. Like David Elkin talked about a few weeks ago in M&M, lots of different arrhythmias possible with digoxin

c. Beware of atrial arrythmias and dangerous bradycardias

d. Classic EKG finding of scooped, down-sloping, Salvador Dali moustache ST segment

Screen Shot 2019-09-27 at 3.17.25 PM.png

Remember the theoretical phenomenon of stone heart – dig tox may give you hyperK. When you treat with calcium, the theory is that it may cause tetany of the myocardium and precipitate cardiac arrest. Digifab (antidote) will treat hyperK, so consider your options.

 

Dig Toxicity EKG - https://litfl.com/digoxin-toxicity-ecg-library/

Treatment - https://www.wikem.org/wiki/Digoxin_toxicity

 

References

https://litfl.com/tricyclic-overdose-sodium-channel-blocker-toxicity/

http://brownemblog.com/blog-1/2018/6/20/the-poor-mans-tox-screen

http://www.tamingthesru.com/blog/diagnostics/ekg-toxicology

http://hqmeded-ecg.blogspot.com/2014/06/acquired-long-qt-do-not-trust.html


ECMO

 

 

Extracorporeal Membrane Oxygenation

 

What:

Prolonged cardiopulmonary support is called extracorporeal membrane oxygenation (ECMO), extracorporeal life support, or extracorporeal lung assist.

 

Criteria for the initiation of ECMO include acute severe cardiac or pulmonary failure that is potentially reversible and unresponsive to conventional management. Examples of clinical situations that may prompt the initiation of ECMO include the following:

 

Who:

·       Hypoxemic respiratory failure with a ratio of arterial oxygen tension to fraction of inspired oxygen (PaO2/FiO2) of <100 mmHg despite optimization of the ventilator settings, including the tidal volume, positive end-expiratory pressure (PEEP), and inspiratory to expiratory (I:E) ratio. The Berlin consensus document on acute respiratory distress syndrome (ARDS) suggests ECMO in severe respiratory failure (PaO2/FiO2 <70)

·       Hypercapnic respiratory failure with an arterial pH less than 7.20

·       Ventilatory support as a bridge to lung transplantation.

·       Cardiac/circulatory failure/Refractory cardiogenic shock

·       Massive pulmonary embolism.

·       Cardiac arrest

 

How:

During ECMO, blood is drained from the native vascular system, circulated outside the body by a mechanical pump, and reinfused into the circulation. While outside the body, the blood passes through an oxygenator and heat exchanger. In the oxygenator, hemoglobin becomes fully saturated with oxygen, while carbon dioxide (CO2) is removed. Oxygenation is determined by flow rate, where elimination of CO2 can be controlled by adjusting the rate of countercurrent gas flow through the oxygenator

There are two types of ECMO – venoarterial (VA) and venovenous (VV).

 

Both provide respiratory support, but only VA ECMO provides hemodynamic support

 

VV or Veno-Venous - blood is extracted from the vena cava or right atrium and returned to the right atrium. VV ECMO provides respiratory support, but the patient is dependent upon his or her own hemodynamics.

·       Venous drainage from large central veins -> oxygenator -> venous system near RA

·       Support for severe respiratory failure (no cardiac dysfunction)

·       Pathology: pneumonia, ARDS, acute GVHD, pulmonary contusion, smoke inhalation, status asthmaticus, airway obstruction, aspiration, drowning

·       Specific contraindications: unsupportable cardiac failure, severe pulmonary hypertension, cardiac arrest, immunosuppression (severe)

·       For VV ECMO, venous cannulae are usually placed in the right or left common femoral vein (for drainage) and right internal jugular vein (for infusion). Alternatively, a double lumen cannula is available 

VV.jpeg

 

VA or Veno-Arterial: peripheral or central- During VA ECMO, blood is extracted from the right atrium and returned to the arterial system, bypassing the heart and lungs. VA ECMO provides both respiratory and hemodynamic support

 

·       For VA ECMO, a venous cannula is placed in the inferior vena cava or right atrium (for drainage) and an arterial cannula is placed into the right femoral artery (for infusion). Femoral access is preferred for VA ECMO because insertion is relatively easy. The main drawback of femoral access is ischemia of the ipsilateral lower extremity

  • support for cardiac failure (+/- respiratory failure)

  • pathology: graft failure post heart or heart lung transplant, non-ischemic cardiogenic shock, drug OD, sepsis, PE, cardiac or major vessel trauma, massive pulmonary hemorrhage, pulmonary trauma, acute anaphylaxis

  • specific contraindications: aortic dissection and severe AR

 

VenoarterialECMO.jpeg



 

  

GENERAL CONTRAINDICATIONS

Absolute

  • progressive non-recoverable cardiac disease (not transplant candidate)

  • progressive and non-recoverable respiratory disease (irrespective of transplant status)

  • chronic severe pulmonary hypertension

  • advanced malignancy

  • >120kg

  • unwitnessed cardiac arrest

 

Relative

  • age > 75

  • multi-trauma with multiple bleeding sites

  • CPR > 60 minutes

  • multiple organ failure

  • CNS injury



Procedure: Once it has been decided that ECMO will be initiated, the patient is anticoagulated (usually with intravenous heparin) and then the cannula are inserted. ECMO support is initiated once the cannula are connected to the appropriate limbs of the ECMO circuit. Cannulas are usually placed percutaneously by Seldinger technique. The largest cannulas that can be placed in the vessels are used.  

Things to consider for the Emergency Physician

  • Emergency Physicians have an important role in identifying patients that might benefit from ECMO

  • Be cognizant of central line placement choice

  • Transfer out to center with ECMO capabilities earlier

  • Make sure patient is not bleeding (recent surgeries, recent hemorrhagic CVA)

  • When calling for ECMO, try to figure out what type of ECMO would benefit the patient

  • Perform Bedside POCUS to determine cardiac function

  • Consider certain therapies with caution if you anticipate ECMO initiation- Lipid Emulsion therapy likely a contraindication as it affects the ECMO circuit

  • Be familiar with the common contraindications to ECMO- Age, BMI etc

 

 

References:

LITFL

UptoDate



 

 · 

POTD- EFAST

What:

Extended Focused assessment with sonography in trauma

Trauma evaluation for blunt or penetrating chest/abdomen/back/pelvic trauma as well as in the evaluation of the unexplained hypotensive patient as part of the RUSH protocol and the patient with a possible ruptured ectopic pregnancy.

 

Why:

FAST has 82% sensitivity and 99% specificity for blunt intraabdominal injury in adult patients

 

When:

·      Usually performed as a part of the primary survey but that is not an absolute.

·      Use your clinical judgement to decide whether the FAST should performed during the primary survey or secondary survey.

·      For example, if patient had a penetrating trauma to the extremity, secondary survey might be more important and urgent than performing an EFAST.

 

Who:

Adults and Pediatric patients with blunt or penetrating trauma

 

How:

Your patient should be kept supine to increase your accuracy
Sequence of EFAST

1.     Subxiphoid

2.     RUQ/ R thorax

3.     LUQ/ L thorax

4.     Pelvic

5.     Anterior Lung view bilaterally

 

Subxiphoid first

·      Traumatic cardiac tamponade/pericardial effusion is the first thing you want to rule out. Acute accumulation for a very small amount of fluid can put the patient in severe obstructive shock and cause cardiopulmonary collapse so make sure to rule that out first

·      Increase the depth and go to the RUQ

·      Next, RUQ- Why? It is the most sensitive location for identification of free fluid in the abdomen because the posterior peritoneum attaches in such a way that free fluid from any injury anywhere will travel to the right upper quadrant in a supine patient

·      Place probe on the Horizontal Subxiphoid line with the marker towards patient head in the Mid Axially line

·      The RUQ  can be divided into 3 zones.

o   Above/Below the diaphragm

o   Morrison’s pouch (hepato-renal recess)

o   Paracolic gutter: Around the inferior hepatic edge/inferior pole of kidney

·      Evaluate above the diaphragm to evaluate for intrathoracic free fluid

Picture1.jpg

 



 

·      Evaluate below the diaphragm to evaluate for intraperitoneal fluid

Picture2.jpg

 




 

·      Evaluate between the liver and the entire superior pole of the kidney – Morrisons Pouch view. Make sure you visualize the liver tip- It is the most sensitive area for free fluid on the FAST Exam;

Picture3.jpg

 






 

·      Evaluate between the left edge of the liver and the entire inferior pole of the kidney.

·      Move on to the LUQ next; The LUQ can also be divided into 3 zones:

o   Above/Below the diaphragm,

o   Spleno-Renal recess

o   3. Paracolic gutter: Around the inferior pole of kidney

 

·      The only difference between the RUQ and LUQ here is that you should place your probe at the posterior axillary line on the left, instead of midaxillary line of the right. Have your “knuckles on the gurney”.

 

·      Beware of the stomach Sabotage ??

Picture4.jpg

 






 

·      Evaluate above the diaphragm to evaluate for intrathoracic free fluid like the RUQ

 

·      Evaluate below the diaphragto evaluate for intraperitoneal fluid. This is where free intraperitoneal fluid will usually develop first in the left upper quadrant (LUQ) (different from the RUQ where the first area of free fluid is usually around the inferior pole of the kidney and right paracolic gutter).

 

Pelvic View

·      Make sure you obtain the pelvic view before the RN places the foley because you will loose the acoustic window that the bladder provides

·      Always obtain a longitudinal and Transverse view

·       Rectovesical pouch (male patients)

·       Rectouterine / pouch of Douglas in female patients

·       Do not be fooled by the seminal vesicles in males  

 

Remember

·      New blood is anechoic (black).

·      Ascites is anechoic (impossible to differentiate.

·      Clotted blood is echogenic (shades of gray)

 

Limitations

·      Not a diagnostic test but a screening tool

·      Injuries that do not cause free fluid

·      Injuries causing retroperitoneal free fluid

·      Injuries that cause <300 cc intraperitoneal free fluid (the lower the fluid amount the more likely to miss)

·      Injuries causing free fluid where the FAST scan is done too early in free fluid accumulation, and, therefore, will not detect it

·      Lower sensitivity in kids about 60-85%. Specificity 90-99%

 

References:

Dr Eitan Dickman

EmCrit

SonoSpot

Rozycki, Grace S., et al. "Early detection of hemoperitoneum by ultrasound examination of the right upper quadrant: a multicenter study." Journal of Trauma and Acute Care Surgery 45.5 (1998): 878-883.

 

Shokoohi, Hamid, Keith S. Boniface, and Audra Siegel. "Horizontal subxiphoid landmark optimizes probe placement during the Focused Assessment with Sonography for Trauma ultrasound exam." European Journal of Emergency Medicine 19.5 (2012): 333-337.

 

 · 

Targeted Temperature Management

Great job on resuscitating that V fib cardiac arrest and achieving sustained ROSC. 

Now what? Cool them!

Whether you cool them or not could determine whether your patient goes into multisystem organ failure in the ICU or walks out of the hospital few weeks later.

 

What:

Targeted temperature management (TTM) to improve survival and neurological outcomes among comatose survivors of patients with cardiac arrest

 

Who:

Adults with out-of-hospital cardiac arrest with an initial shockable rhythm and nonshockable rhythm

 

Inclusion criteria (must meet all criteria)

  • Postcardiac arrest status (any rhythm as a cause of arrest is eligible)

  • ROSC < 30 minutes from EMS/code team arrival

  • Time at induction < 6 hours from ROSC

  • Comatose status (patient does not follow commands)

  • MAP ≥ 65 mm Hg (may include use of vasopressor drugs)

Exclusions may include

  • DNR advanced directive, MOLST, poor baseline status, or terminal disease

  • Traumatic etiology for the arrest

  • Active bleeding or known intracranial bleeding (relative)

  • Cryoglobulinemia (relative)

  • Pregnancy (relative; consider obstetrician/gynecologist consultation)

  • Recent major surgical procedure (relative)

  • Severe sepsis/septic shock as cause of arrest (relative)

Why:

  • Decreased fever-related tissue injury

  • Reduction in ischemic-reperfusion injury

  • Cerebral metabolic rate decreases by a 6-7% for every 1ºC drop in body temperature which reducing oxygen demand, preserving phosphate compounds and preventing lactate production and acidosis

  • Bernard, et al (2002) found an Absolute Risk Reduction (ARR) for death or severe disability of 23%, NNT was 4.5

  • The Hypothermia After Cardiac Arrest (HACA) Group (2002) found an ARR for unfavourable neurological outcome of 24%, and NNT of 4


How:

  • IV cold saline 2-3 mL/kg

  • Cooling vest and cooling machine- Arctic Sun

  • If shivering does not occur, do not use neuromuscular blockade

  • If paralysis employed, titrate to degree of shivering- do not need train-of-four monitoring

  • Sedation of choice is institution dependent (MMC CICU uses Fentanyl and Midazolam)

When:

Initiation of TTM within122 minutesof hospital admission was associated with improved survival.
Most guidelines recommend initiation within6 hours

What temperature should be targeted:

This remains controversial, with guidelines accepting a range of temperature targets from 33-36C. Available evidence shows no benefit to hypothermia (33C) compared to normothermia (36C). In the absence of evidence, targeting 36C is prudent

  • TTM36 is more hemodynamically stable than TTM33, which is relevant because these are often very unstable patients.

  • TTM36 avoids electrolytic shifts associated with raising and lowering the temperature.

  • Hypothermia at 33C suppresses immune function and associates with increased rates of pneumonia.

  • TM33 will induce bradycardia, which is dangerous in patients with underlying torsades de pointes.

References

Bernard SA et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med 2002;346:557-63. PMID 11856794

Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002;346:549-56. PMID 11856793

Nielsen N et al. Targeted temperature management at 33 degrees C versus 36 degrees C after cardiac arrest. N Engl J Med 2013; 369: 2197-206. PMID 24237006

Stanger, Dylan, et al. "Door‐to‐targeted temperature management initiation time and outcomes in out‐of‐hospital cardiac arrest: insights from the Continuous Chest Compressions Trial." Journal of the American Heart Association 8.9 (2019): e012001.

Donnino, Michael W., et al. "Temperature management after cardiac arrest: an advisory statement by the advanced life support task force of the international liaison committee on resuscitation and the American Heart Association emergency cardiovascular care committee and the council on cardiopulmonary, critical care, Perioperative and Resuscitation." Circulation 132.25 (2015): 2448-2456.

REBEL EM
LITFL
EB Medicine
Mayo Clinic Florida TTM Guideline

 · 

Status Epilepticus

Status Epilepticus

 

Background

  • Definition

    • >5 min of seizure activity without response to treatment // recurrent seizure without return to baseline mental status

  • mortality is 22%

  • can be convulsive or non-convulsive (tricky)

    • non-convulsive can be change in behavior/complete loss of consciousness with signs such as twitching/blinking/eye deviation

    • eeg shows continuous epileptiform discharges

  • get a fingerstick/BGM

  • ABCs

    • try to place in left lateral decubitus position (can aspirate)

    • place a NC/NRB/LMA early

      1. intubate if benzos are not breaking the seizure

        • this is obviously at the discretion of the team, best to consider all circumstances…intubate if you need to

        • standard RSI is fine but if at all possible, then try to use induction agent only

          • paralytic can mask seizures and put them in non-convulsive state

            • if must use, then succ is quicker on/off

    • IV line for meds (IO/IM/IN if desperate)

 

Treatment

  • First line: Benzos

    • Not controversial, should be first line

    • Versed

      1. If no IV, then give versed IM or IN

    • Ativan

    • Valium

    • Try to use weight based dosing the way we do in peds

    • *if no response after 4 min, give another dose

  • Second line: depends

    • Traditionally:

      • Phenytoin 20 mg/kg IV

      • Fosphenytoin 20-30 mg/kg IV (/IM)

      • Keppra 40 mg/kg IV (max 4.5g)

    • BUT, consider anesthetic instead

      • Propofol 1.5-2mg/kg IV

        • followed by 20-200mcg/kg/min drip

        • can add Ketamine 1mg/kg IV to propofol

      • Phenobarb 15-20 mg/kg over 10 min

        • followed by 5-10mg/kg after 10 min

        • followed by .5-4mg/kg/hr drip

        • May not be as readily available as propofol/ketamine is in your ED

      • **still hang the phenytoin/keppra even though you’re giving them an anesthetic, will need long term anticonvulsant on board anyway

  • Eclampsia

    • give 4g magnesium IV

**management slightly different in peds 

 

stat2.png


Find the cause

  • infectious

  • eclampsia

  • INH

    • Give pyridoxine (1g for every 1g of INH taken….or can just give the max of 5g empirically)

  • Hyponatremia

    • 3% NaCl 2ml/kg q 10 min

      1. if in a pinch, then give amp of bicarb (consists of 6% NaCl) which will always be available somewhere in a code cart

bicarb.png

  • Alcohol withdrawal

    • High dose benzos, but also consider propofol/phenobarb if need to

  • Drugs

  • Metabolic

 

First10EM

wikiEM

 · 

EKG in Syncope

Why did each of these patients pass out?

EKG#1

Picture1.png

EKG #2

EKG #3

EKG #4

4.png

EKG #5

5.png

EKG #6

6.png

ANSWERS & RESOURCES

This week’s theme was EKG in syncope!

EKG#1

Third Degree Heart Block

Screen Shot 2019-09-20 at 9.22.55 AM.png

EKG#2

Hypertrophic Cardiomyopathy

Screen Shot 2019-09-20 at 9.24.59 AM.png

EKG#3

Wolff Parkinson White

Screen Shot 2019-09-20 at 9.25.19 AM.png

EKG#4

Arrhythmogenic Right Ventricular Dysplasia (ARVD)

Screen Shot 2019-09-20 at 9.25.36 AM.png

EKG#5

Brugada

EKG#6

Prolonged QT

Screen Shot 2019-09-20 at 9.26.21 AM.png

Here’s how you can think through your EKG in syncope!

Start from the left side and
work systematically through the rhythm.

Screen Shot 2019-09-20 at 9.38.37 AM.png

Vaping/VAPI

Vaping and Vaping Associated Lung Injury (VAPI)

Background

  • What is vaping?

    • The process of inhaling/exhaling aerosol (aka vapor) produced by an e-cigarette or other similar (handheld, and now commonly, portable) device.

    • These devices are thought to be “safe” by the general public because they do not produce tobacco smoke. Instead, they produce aerosolized vapor that contains harmful particles, which the public also mistakenly believes is just harmless water vapor (its not...).

  • Around since 2007ish when the e-cig first came out.

    • Now, there are a ton of vaping pens/devices (juul, zip, mods, insert cool name here, etc.)

  • Vape device consists of a mouthpiece, battery, pocket for e-liquid/juice, and a heating component

  • E-liquid contains propylene glycol or vegetable glycerin liquid with nicotine and other chemicals/flavorings (yes, even crème brule...)

    • Again, not tobacco, but don’t be fooled…

      1. One juul pod/cartridge (~200 puffs) has the same amount of nicotine as 1 box of cigarettes.

    • Many people vape THC and synthetic drugs as well

  • Has led to 500+ illnesses and 8 deaths across the US

    • Possibly linked to contaminated THC based vape cartridges

      1. Similar to other drugs, distributors (usually on the black market) are possibly cutting their product with other dangerous and cheaper substances

        1. Specifically, vitamin e acetate, an oil that could cause lung inflammation if not heated up properly during vaping

          • Most recent development linked to two brothers/illegal cannabis vaping ring in Wisconsin. Check it out here.

  • If you have a suspected case, then please call the poison control center and/or call a tox consult depending on where you are working

    • per Dr. Harmouche, our awesome toxicologist (by the way, thanks for the useful info!), the poison control center can report to the DOH who can then decide to investigate/test samples.

      • the national toxicology registry is also collecting cases for research purposes.

  • *if you have a patient (especially young one) who has worsening respiratory symptoms, please be diligent and ask about a vaping history in the last 90 days. They may have the below condition, which can cause them to deteriorate quickly if unnoticed and untreated.

VAPI

  • Young patients (~20 YOs), but can affect any age group

  • ~75% male

  • ~80% of cases reported vaping with THC

  • ~94% vaped within a week of symptom onset

  • 100% have some sort of constitutional symptom

    • fever, chills, fatigue, weight loss

    • 29% of victims have presented febrile

  • 98% have respiratory symptoms

    • SOB, cough, chest pain, hemoptysis

    • URI symptoms not common (rhinorrhea, sneezing, congestion)

  • 81% have GI symptoms

    • n/v/d, abdominal pain

  • CXR

    • Commonly shows BL infiltrates

    • Worsens quickly

  • CT chest

    • Should be obtained in suspected cases

    • Will show BL groung glass opacities (see below, very impressive)

    • May also see pleural effusions, pneumomediastinum, and tree-in-bud opacities

vape3.png
  • Labs

    • CBC may show leukocytosis

      1. May show eisopnipholia

    • ESR and CRP likely to be elevated

    • RSV, flu, HIV testing if indicated

    • Consider legionella testing

  • Diagnosis of exclusion

    • And may not need a bronchoscopy if the rest of the work up (mainly infectious/malignancy) is negative, and other parts of history don’t provide more likely diagnosis/explanation for respiratory findings

  • Treatment

    • Antibiotics until PNA excluded

    • Steroids (1mg/kg/day)

    • May need intubation (30% of cases already)

  • Takes several days to recover

  • The unknown

    • Pathophysiology of it all unclear

    • Possibly lipoid pneumonia from bad ccannabis oil/liquid being vaped

      1. Vitamin e, mentioned above, has been recently been used as aliquid carrier

        1. This is harmful

    • OR different cases may have different pathophysiological processes going on

      1. Again, unclear

 · 

Second Victim Syndrome

Second Victim Syndrome (SVS)

Background

  • Medical errors are the third leading cause of death in the US

  • Poor outcomes can be due to a larger system failure or a human error

    • Examples include incorrect medication dosages, improper management, harm during a procedure, missed diagnoses, etc.

  • Second victim

    • Defined in 2000 by Albert Wu

    • In situations where medical errors are made or safety is compromised, the first victim is the patient and the second victim is the healthcare professional (EMT, nurse, physician) who can also be affected or traumatized by the event.

SVS

  • Aforementioned events can have a lasting impression on a provider

  • He/she tends to repeat the event over and over in his/her mind leading to emotional distress and scars

  • Immediate symptoms

    • Anxiety, guilt, shame, sadness, fear, anger

    • Can have sympathomimetic manifestations—tachycardic, elevated BP, etc

  • Later symptoms

    • Depression, loss of confidence, loss of job satisfaction, hypervigilance, poor decision making

  • Can develop PTSD like symptoms

    • Insomnia, flashbacks, SI, isolation

Identifying Second Victims

  • Symptoms and behavior can be similar to those who suffer from burn out

  • Different stages of SVS (see below)

SVS.png

Management

  • Support from colleagues is helpful

    • Provides a sense of shared understanding

  • M&Ms/patient safety conferences that are supportive instead of punitive

  • Culture change

    • Shift toward a “Just Culture”

      1. Balancing accountability and support instead of perpetuating a blame/shame culture

  • TRUST mnemonic

    • Treatment that is Just

    • Respect

    • Understanding and compassion

    • Supportive care

    • Transparency and opportunity to contribute

 · 

STEMI Equivalents

STEMI Equivalents

Hyperacute T Waves

  • in ≥ 2 contiguous leads

  • broad and asymmetric

  • concerning when upright T-wave in V1 > V6

  • also need to rule out hyperK

Wellen's Waves

  • Commonly in V/2/V3

  • Type A: biphasic T waves

  • Type B: more common; deep, symmetric T waves inversions

ekg2.png

AVR

  • ST Elevation >1mm in AVR and/or V1 with diffuse depressions

  • LMCA occlusion, LAD occlusion, or triple vessel disease

    • Nonspecific, can also see this EKG with PE, aortic dissection, etc.

ekg4.png


De Winter’s T Waves

  • ST depression with peaked T Waves

    • > 1 mm of upsloping ST depression and tall symmetric T-waves commonly in the precordial leads

  • Proximal LAD occlusion

ekg6.png

Also consider:


Posterior MI

  • ST depressions in V1-V3

  • Get posterior EKG with leads V7V8V9

    • STE ≥ 0.5 mm (≥ 1 mm in men < 40 years) in V7, V8, or V9

  • Left circumflex or RCA occlusion

Right Ventricular MI

  • should consider in your inferior STEMI pts

  • ST elevation in V1 (+/- V2 ST elevation OR depression)

  • ST elevation in lead III > lead II

  • Get a right sided EKG with leads V3V4V5

    • Can have elevations in these

  • RCA occlusion

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