A Case of Pediatric Cardiac Arrest

A Case of Pediatric Cardiac Arrest – EM Reflections November 2021

Authored and Copyedited by Dr. Mandy Peach

Big thanks to Dr. Paul Page for leading this month’s discussions

All cases are imaginary but highlight important learning points.

Case

You are working a day shift at a tertiary hospital that sees both adult and pediatric patients. You receive dispatch for a 2 year-old female with potential sepsis. Parents report high fevers for 4 days and poor intake. EMS report a somnolent child, febrile and tachycardic. ETA of 5 minutes.

On arrival the child appears mottled and drowsy, paramedics have placed a non-rebreather and are supporting the airway. You rapidly complete an assessment while the patient is being placed on cardiorespiratory monitoring and nurses attempt access. The patient responds to voice with whimpers. A paramedic is performing a jaw thrust while another bags. Breathing is shallow and rapid. She is mottled with cool extremities and delayed capillary refill.

Vitals: BP 60 SBP, HR 160 sinus tachycardia, T 39.7 RR 50 O2 88% on 100% NRB.

Gulp. You ask the nurse to page the pediatrician on call as you are worried about this patient.

Pediatric vitals are interpreted by weight or age, but you don’t need a table to see that these vitals are abnormal and this kid is altered. Frankly, this patient is pre-arrest if intervention doesn’t take place soon.

Not so sick kid? Here’s a reminder of expected vitals per age1.

Pediatric patients tend to compensate and compensate – until finally they don’t. Are there earlier signs of sepsis to be on alert for when assessing a patient1?

  • tachycardia out of proportion to fever – fever can give an expected increase in HR by 10 bpm,

  • tachypnea – RR tends to increase by 5 breaths/min for every 1 deg over 38°C.

  • poor perfusion – this can range from poor cap refill to altered level of consciousness.

When it’s later stages – it’s obvious. But sepsis doesn’t always have all these signs – a high suspicion is needed to recognize sepsis before it gets to critical stages.

What is the most concerning vital sign of our patient1?

Hypotension – this is a late sign of sepsis and if untreated the patient will arrest.

You suspect this child has septic shock given the brief history and temperature. Currently, their airway is being well managed by paramedics who have added NC under the mask and with continued jaw thrust they have improved oxygen saturation – but this is temporary.

You want to initiate management for sepsis and potentially need to intubate this child.

But before any of that can occur you need IV access.

Nurses have attempted twice and failed – it’s been 2 minutes. What next?

Do not hesitate to move to intraosseous (IO). This child may imminently arrest. Fluid resuscitation and administration of antibiotics are vital. If you can’t obtain IV access in 60 secs – obtain IO1

Preferred sites in pediatric patients (altered from EMdocs.net)2

Worried about hurting the child? Flush lidocaine through the IO – evidence suggests pain is more from infusions and medications through the IO than the insertion itself.1

Have more time with a relatively stable patient? Consider using PoCUS to help obtain peripheral lines

You obtain IO access and immediately request fluids. You want them to run in as fast as possible, but the child is too small for a level 1 infuser. What’s your approach?

First, choose the fluid type. Normal saline or Ringer’s lactate is fine to start. 20cc/kg is the typically starting bolus over the first 5 minutes of resuscitation. This can be repeated twice more up to 60cc/kg in the first hour. For this patient, and any patient under 2, load a 30-60cc syringe with crystalloid and manually bolus.

Signs of fluid overload?

Hepatomegaly and crackles auscultated in the lungs

A better sign – pulmonary edema seen on PoCUS3.

Normal vs B lines

IO assess has been obtained in both tibia, a nurse is pushing fluid manually while another asked you what antibiotics you want drawn up.

What are the broad-spectrum antibiotics suggested by age1?

You go back to reassess the patient’s airway. They are now satting 92% on 100% NRB + 5L NC. There is still some spontaneous whimpering. You estimate the GCS to be 9: E- 3 V- 2 M -4. This patient’s respiratory status is worsening and they have a low GCS. You feel they need intubation. Repeat vitals are obtained after first bolus.

BP 64 SBP, HR 158 sinus tach, T 39.8, RR 48 O2 as above.

Do you immediately intubate?

This patient is in profound shock, their catecholamine surge is deplete and any induction agents, even ketamine, would likely still worsen their hypotension and potentially precipitate arrest. If successfully intubated there is then the complication of increasing intrathoracic pressure – thus reducing blood flow back to the heart and decreasing cardiac output1.

The principle of resuscitate before you intubate is especially true in this situation.

You order repeat bolus of fluid to be manually given while antibiotics are being infused in the other IO. A nurse has now achieved peripheral IV access.

You prepare drugs and airway equipment for RSI – you plan to intubate once fluid boluses are complete if vitals have improved.

What drugs will you use? What drugs would you avoid5,6,7,8,9?

Avoiding worsening hypotension is key – ketamine is the drug of choice for sedation in children as it is considered hemodynamically neutral, but again expect drop in BP when the body is in shock. Ketamine also preserves airway reflexes and ventilatory drive.
Conversely propofol creates vasodilation and suppresses the myocardium – causing hypotension. It also can cause respiratory depression and apnea.

There is some evidence that etomidate is associated with less adverse events in septic patients, specifically hypotension. In one observational study in an adult population, ketamine was shown to be complicated by post-intubation hypotension more frequently when compared to etomidate.

In the pediatrics population etomidate for intubation in the ED setting has also been shown to be associated with minimal change in blood pressure – but this was a small, retrospective study. Currently etomidate is not recommended in patients < age 10 and more evidence is needed. One could also consider the potential for adrenal suppression post etomidate (etomidate inhibits functioning of an enzyme required to make cortisol, aldosterone and corticosterone). There are various studies – some in pediatric patients showing decreased plasma cortisol levels at 24 hours post etomidate. A similar effect was seen in other critically ill adult patients. The CORTICUS trial indicated a higher 28 day mortality in patients who received a single dose etomidate vs those that did not, regardless of being given exogeneous steroid.

For paralytics succinylcholine should be used cautiously in pediatric patients – it can precipitate hyperkalemia, bradycardia and even arrest. Rocuronium does have fewer side effects and contraindications, but it’s duration of action lasts approximately 50 mins – compared to approximately 6-10 minutes with succinylcholine. So strongly consider your choice – if you feel this is a ‘can’t intubate, can’t ventilate’ situation rocuronium is a dangerous choice.

You decide to go with ketamine and rocuronium and the drugs are being drawn up – what doses will you use?

In an adult population a safe choice in the shocked patient is to half the sedative and double the paralytic. The reason being even with ketamine you can get myocardial suppression and potential apnea.

For the paralytics use higher dose as the onset of action will be slower – double the dose.

For pediatric patients there is no evidence in the literature to support this practice, currently practice is to choose agents that have the least effect on hemodynamics – typically ketamine and rocuronium.

The RT is asking what size tube and airway equipment you would like.

Quick answer – Broslow tape. In this unstable patient this is the easiest way to get what you need without having to do any mental math. You request a cuffed tube – decreases the need  for ET tube changes4.

While airway equipment is being set up you move now to prepare the patient. How do you position this 2 year old5,10?

Children have larger heads that naturally lies in flexion when supine. To align the mouth, larynx and trachea often the position has to be changed. You can roll up a towel to help with placement. As a rule of thumb:

Keeping a patient supine can also worsen hypoxemia as children have increased chest wall compliance and therefore increased work at baseline to maintain tidal volume. This can eventually lead to intrapulmonary shunting.

So although this patient doesn’t require additional positioning with a towel based on age we would still put the head of the bed up.

Someone asks if they can remove the additional oxygen mask or nasal cannula in preparation for intubation so it’s out of your way. Your response5?

No – pre-oxygenation is vital in the intubation of any patient, especially a child as they desaturate so quickly. In this 2 year old patient we expect a time of less than 4 minutes to desaturate to 90%. Children have much less surface area or ventilation channels as the alveoli continue to develop until the age of 8. In this patient with potential underlying respiratory illness there could be areas of atelectasis, worsening lung ventilation.

What other airway considerations are going through your head for a pediatric patient10?

Remember CHILD

For a great overall review see this infographic5

 

 

You are about to reassess the airway and obtain new vitals when the patient’s breathing changes to agonal and her whimpering has ceased. There is cardiac activity on the monitor, it be appears to be tachycardia with a widened QRS. Someone yells – check a pulse!

Do you need a pulse to initiate CPR in this patient?4

No – given the frequency of bradycardia and hypovolemia, pulse checks are not reliable. If apnea and unresponsive, initiate CPR.

At what rate should CPR be initiated in this patient4?

Use the encircling hands technique for infant CPR – it is shown to give better hemodynamics. Push hard (>1/3 AP diameter of chest) and fast (100-120 bpm), minimizing interruptions and allowing full recoil of the chest between compressions.

As this is an in-hospital cardiac arrest an LMA is immediately inserted to prevent interruption in compressions and to provide oxygenation.

Aim for 20-30 breaths/minute when an advanced airway is in place.

Out of hospital cardiac arrest4? Resuscitation with bag valve mask results in the same resuscitation outcomes as advanced airways -don’t underestimate the value of a good seal and a 2 person technique.

CPR is ongoing, an LMA has been inserted. The initial rhythm did not appear to be shockable. This is a PEA arrest.

What is your priority?

Determining the cause and in the meantime administering epinephrine – early administration within 5 minutes of non-shockable rhythms increases survival4.

You review your H’s and T’s.

You are pushing fluids for hypovolemia, the patient maintained oxygenation throughout with 2 sources of oxygen and had a normal oxygen saturation before arrest, the patient could be acidotic – but you are drawn to hypoglycemia. You rack your brain but can’t remember the glucose. You verbalize to the room, but no one knows if a glucose was done.

You quickly obtain one – 0.5.

You must correct glucose rapidly:

5cc/kg D10W IV push followed by an infusion of D10NS at 5cc/kg/hr (max at 250cc/hr)11

After the correction of glucose and additional round of CPR you get ROSC.

Obtaining a glucose is VITAL in any pediatric patient – something you know but failed to recognize as you had an unstable patient in front of you.

ABC + DEFG = ABC and DON’T EVER FORGET GLUCOSE1

What other metabolic abnormality must you consider1?

Hypocalcemia is commonly seen in critically ill pediatric patients, even without clinical signs like seizure or arrythmia it is recommended to treat.

Calcium gluconate 10% 0.5-1 cc/kg slowly over 5 minutes (max of 20 cc)

You reassess the vitals and the patient is still hypotensive and tachycardic despite 3 boluses and fluid circulating throughout the arrest. The oxygen saturation is 100%. The RT is still bagging via LMA. Clinically they appear cool and mottled with pulses weaker distally.

The patient is in cold shock. What is the vasopressor of choice11?

You initiate epinephrine at 0.05 mcg/kg/min IV and titrate up by 0.02 mcg/kg/min.

You assess cardiac function and lung fields via bedside ultrasound – the heart is hyperdynamic, lung fields are clear. You continue another bolus.

The patient’s GCS post arrest is back to 9. They are being easily bagged. You plan to wait until vitals have stabilized to switch out the tube.

At this point a pediatric attending arrives and you give an update.Immediately the staff begins verbalizing orders to the room for pressors, fluids and antibiotics. They begin questioning RT and direct them to intubate. The staff look to you for direction.

What do you do at this point?

This can be an uncomfortable situation to be in – this patient is still your patient; they are still unstable at this point and you have been guiding resuscitation. You have developed a sense of trust with your team and more than one leader can often lead to confusion.

You ask the attending to step out and together you review the management up to that point. This was a complex case with a lot of intervention. You discuss each medication given and the outcome. You make your suggestions on pressor support and fluid and reinforce what has been given. Together you are on the same page and go back in to reassess with the team.

It’s important to respectfully gain additional input from consultants and work together to ensure optimum care, but still realize that you are running the room. In other cases you may be at a loss for what to do and need guidance for what to do next – but again, once a plan is decided with your consultant it’s important that you verbalize to the room and give clear instruction to your team.

Overwhelmed and need to pass off? No problem – once you have help verbalize to the room that the consultant will now be leading resuscitation and stay nearby to assist and learn.

Lastly, what other medication should you consider if the patient’s hemodynamics or clinical picture do not improve1?

Steroid – up to 25% of pediatric patients with septic shock have adrenal insufficiency. This may be from the infectious process itself, from previous steroid use or from primary adrenal insufficiency.

You administer hydrocortisone 2mg/kg IV.

What markers of a successful resuscitation will you look for1?

  • Capillary refill < two seconds
  • Normal blood pressure
  • Normal pulses with no differential betweencentral and peripheral pulses
  • Warm extremities
  • Urine output > 1 ml/kg/hr
  • Normal mental status
  • Normal lactate

The patient gets admitted to the ICU for Pneumococcal sepsis and after a prolonged admission does well.

 

Pediatric patients are scary – use the resources you have, verbalize your thought process to the room and ask for help. Continuously reassess 

ABC + DEFG = ABC and DON’T EVER FORGET GLUCOSE1

 

References and further reading:

  1. EM Cases Digest – Vol 2. Pediatric Emergencies. Chapter 2: Sepsis and septic shock. Helmon, A. Lloyd, T. 2016. Toronto, ON.
  2. Image altered from http://www.emdocs.net/feelin-it-in-my-bones-a-review-of-intraosseous-access-in-the-emergency-department/
  3. Images from https://www.thepocusatlas.com/
  4. Highlights of the 2020 American Heart Association Guidelines for CPR and ECC
  5. Tolmie, A 2021. PEM Pearls01: Pediatric Airway Differences. CanadiEM. Retrieved Jan 20, 2022 from https://canadiem.org/pem-pearls-01-pediatric-airway-differences/
  6. Scheirer, O. 2018. CRACKCastE192 – Airway. CanadiEM. Retrieved Jan 20, 2022 from https://canadiem.org/crackcast-e192-airway-9th-edition/
  7. Mohr NM, Pape SG, Runde D, Kaji AH, Walls RM, Brown CA 3rd. Etomidate Use Is Associated With Less Hypotension Than Ketamine for Emergency Department Sepsis Intubations: A NEAR Cohort Study. Acad Emerg Med. 2020 Nov;27(11):1140-1149. doi: 10.1111/acem.14070. Epub 2020 Jul 20. PMID: 32602974; PMCID: PMC8711033.
  8. Guldner G, Schultz J, Sexton P, Fortner C, Richmond M. Etomidate for rapid-sequence intubation in young children: hemodynamic effects and adverse events. Acad Emerg Med. 2003 Feb;10(2):134-9. doi: 10.1111/j.1553-2712.2003.tb00030.x. PMID: 12574010.
  9. Sprung CL, Annane D, Keh D, Moreno R, Singer M, Freivogel K, Weiss YG, Benbenishty J, Kalenka A, Forst H, Laterre PF, Reinhart K, Cuthbertson BH, Payen D, Briegel J; CORTICUS Study Group. Hydrocortisone therapy for patients with septic shock. N Engl J Med. 2008 Jan 10;358(2):111-24. doi: 10.1056/NEJMoa071366. PMID: 18184957.
  10. Hsu, J. 2021. Tiny Tips: Pediatric Airway Anatomy Considerations CanadiEM. Retrieved Jan 20, 2022 from https://canadiem.org/tiny-tips-pediatric-airway-anatomy-considerations/
  11. Pediatric Severe Sepsis Algorithm 2018. A PedsPac from Translating Emergency Knowledge for Kids (TREKK).

 

 

 

 

 

 

 

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EM Reflections – September 2020

Thanks to Dr. Paul Page for leading the discussions this month

All cases in this series are imaginary, but highlight learning points that have been identified as potential issues during rounds

Edited by Dr David Lewis 


Discussion Topics

  1. Incomplete Abortion

    • Unstable patients require staff to staff direct communication. OBGYN staff are always in house.
    • Patients remain responsibility of EM attending staff during and after consult. Transfer of care occurs at admission.
    • Be aware of the pitfalls of handover and possible need to reassess patient depending on clinical situation
  2. Cardiac Arrest – Pulmonary Embolism

    • Be aware of bias when seen patient in low acuity area
    • Alway consider and document a ‘top 3’ differential diagnosis
    • CPR must be extended after thrombolysis for suspected / confirmed PE
    • Consider following a standardized VTE pathway

 


Incomplete Abortion

Case

A 30yr old female presents with a profuse PV bleeding. She is 7 weeks pregnant by dates. She presents with abdominal pain, palor and is hypotensive and tachycardic. During fluid resuscitation, PV exam confirms the presence of blood and clots, the os is open and contains tissue. This is removed. The bleeding appears to stop. CBC identifies a low hemoglobin. The patient is transfused. What are the potential pitfalls in the management of this case?


 

Threatened abortion

Bleeding before 20 weeks’ gestation in the presence of an embryo with cardiac activity and closed cervix

Spontaneous abortion

Spontaneous loss of a pregnancy before 20 weeks’ gestation

 Complete abortion

Complete passage of all products of conception

 Incomplete abortion

Occurs when some, but not all, of the products of conception have passed

 Inevitable abortion

Bleeding in the presence of a dilated cervix; indicates that passage of the conceptus is unavoidable

 Septic abortion

Incomplete abortion associated with ascending infection of the endometrium, parametrium, adnexa, or peritoneum

 

First Trimester Bleeding – American Family Physician

Patient Information Leaflet

 

Management of Unstable Patients with 1st Trimester Bleeding

  • Urgent Consult to OBGYN
  • Management is similar to all unstable bleeding patients (resus room, monitors, vascular access, IV fluid +/- unmatched O neg blood, foley).
  • Investigate for DIC.
  • Tranexamic acid (1g IV) +/- oxytocin (40U by IV in 1L NS at 150cc/hour) can be given to slow bleeding before definitive management (in the OR).
  • **In an unstable patient with massive vaginal bleeding, a pelvic exam is indicated to identify a source and to look for and extract tissue found in the cervix.**
  • Any unstable patient who presents with 1st trimester bleeding and requires blood transfusion should be admitted, even if they stop bleeding in ED and the low Hb is corrected. There is potential for rebleed over next 24 hrs especially if products are retained.

Episode 23: Vaginal Bleeding in Early Pregnancy


Further Reading:

CanadiEM Frontline Primer – Early Pregnancy – First Trimester Bleeding

 

 

 


Cardiac Arrest – Pulmonary Embolism

Case

A 68 yr old male is brought into the emergency department with chest pain and shortness of breath. The patient is diaphoretic and hypotensive. They report a 5 day history of progressive leg swelling prior to these new symptoms. During the initial assessment the patients has a cardiorespiratory arrest. What is the differential diagnosis? What is the management of cardiac arrest when PE is suspected


 

A retrospective study published in Arch Intern Med  – May 2000, found that PE was found as the cause in 60 (4.8%) of 1246 cardiac arrest victims over an 8 year period.The initial rhythm diagnosis was pulseless electrical activity in 38 (63%), asystole in 19 (32%), and ventricular fibrillation in 3 (5%) of the patients. Thrombolysis resulted in significantly higher rate of ROSC, however survival to discharge was very low.

Diagnosis of PE in cases of cardiac arrest is often difficult to establish. Clinical suspicion of PE as a cause of cardiac arrest remains the key in timely diagnosis and treatment. In this study sudden dyspnea and syncope were the most suggestive reported symptoms. Deep vein thrombosis is known to be an important risk factor for PE, but clinical signs of deep vein thrombosis are rare and nonspecific. Right bundle-branch block was present in 67% of these cases, and this should induce a high suspicion for massive PE as cause of cardiac arrest. The authors recommend either transthoracic or transesophageal echocardiography be performed at the bedside in all cases to help establish the diagnosis of PE as the cause of a cardiac arrest.

 

 

Management of Cardiac Arrest in Suspected PE


  1. Commence CPR and follow the ACLS 2018 Algorithm
  2. Suspicion for PE as cause of cardiac arrest?
  3. Bedside Assessment to Increase Suspicion of PE as cause of cardiac arrest
  4. Thrombolysis
  5. VA ECMO + Interventional Radiology / Cardiovascular Surgery

1.  Commence CPR and follow the ACLS 2018 Algorithm

AHA ACLS 2018 Algorithms –  Update Highlights

2.  Suspicion for PE as cause of cardiac arrest?

  • Sudden onset dyspnoea or syncope prior to cardiac arrest
  • Right ventricular strain, new RBBB or other PE suggestive findings on ECG immediately prior to cardiac arrest
  • Initial non-shockable rhythm
  • History of immobilization prior to cardiac arrest (recent surgery, travel, injury)
  • History of thromboembolism
  • History of recent cancer diagnosis and treatment
  • Known hypercoagulation condition (e.g. Factor V Leiden)
  • No history of cardiac disease
  • Age less than 50yrs
  • Female
  • Pregnancy or Birth Control
  • Clinical signs of recent DVT (swollen leg, history of swollen/painful leg)

Improving identification of pulmonary embolism-related out-of-hospital cardiac arrest to optimize thrombolytic therapy during resuscitation

3.  Bedside Assessment to increase likelihood of PE as cause of cardiac arrest

  • Clinical exam for signs of DVT
  • Clinical assessment to exclude other reversible causes of cardiac arrest (5H’s and 5T’s)
  • DVT PoCUS
  • Transthoracic Echo PoCUS – RV dilatation, TV regurge, visible clot, dilated IVC (must not delay CPR)
  • Transesophageal Echo PoCUS – RV dilatation, TV regurge, visible clot, dilated IVC (superior images, does not interfere with CPR)

 

4.  Thrombolysis

An retrospective study published in Chest in 2019 analysed thrombolysis in PE related out-of-hospital-cardiac arrest. They found that thrombolysis was associated with increased 30 day survival but that a good neurological outcome was rare and not significantly improved. This 2019 systematic review and meta-analysis concluded that systematic thrombolysis during CPR did not improve hospital discharge rate.

Despite a weak evidence base, both the European Resuscitation Council (ERC) as well as the American Heart Association (AHA) have recommend the use of fibrinolytic therapy when PE is either known or suspected as the cause of cardiac arrest.

AHA Recommendations – in refractory cardiac arrest where PE has either been confirmed or is suspected, thrombolysis is a reasonable emergency treatment option:

  • Alteplase 50mg peripheral IV bolus
  • Option to repeat the bolus at 15 mins
  • Continue CPR for 30-60 minutes after lytic administration

EMCrit 261 – Thrombolysis during Cardiac Arrest

 

5.  VA ECMO + Interventional Radiology / Cardiovascular Surgery

Interventional and surgical procedures cannot be performed during CPR.

Several studies have concluded that ECMO can be beneficial in patients with PE related cardiac arrest

Extracorporeal membrane oxygenation in life-threatening massive pulmonary embolism

Use of extracorporeal membrane oxygenation in patients with acute high-risk pulmonary embolism: a case series with literature review

Resuscitation of prolonged cardiac arrest from massive pulmonary embolism by extracorporeal membrane oxygenation

Massive Pulmonary Embolism as a Cause of Cardiac Arrest: Navigating Unknowns in Life After Death

 

The consensus seems to be that in order to see benefit from the use of ECMO to bridge patients with massive PE / cardiac arrest a protocolized approach is required, including a standby ECMO team and predetermined pathways.

 


Further Reading

Submassive & Massive PE

 

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EM Reflections – December 2019

Thanks to Dr Joanna Middleton for leading the discussions this month

Edited by Dr David Lewis 


Discussion Topics

  1. Cardiopulmonary Resuscitation In Patients With Mechanical Circulatory Support

    • Patient with mechanical circulatory support devices have unique clinical signs of cardiac arrest
    • Understanding the function of these devices ids critical to the management of these complex cases
  2. Aortic Dissection

    • Remains a commonly missed or delayed diagnosis
    • Once diagnosed, meeting the therapeutic goals requires a careful and considered approach

Cardiopulmonary Resuscitation In Patients With Mechanical Circulatory Support

Case

A 70yr male presents with cardiac arrest. He has an LVAD. What are the implications for emergency management and cardiopulmonary resuscitation?


Introduction

Cardiac arrest in patients on mechanical support is a new phenomenon brought about by the increased use of this therapy in patients with end-stage heart failure.

It is important to understand the difference between blood flow and perfusion when assessing any patient with suspected cardiovascular hemodynamic instability, especially patients with an LVAD, in whom the peripheral arterial pulse is not a reliable indicator. Flow represents the forward movement of blood through the systemic circulation. It can be either adequate or inadequate to provide sufficient oxygen delivery to sustain tissue per- fusion. Assessment of adequate tissue perfusion is the most important factor in determining the need for circu- latory assistance such as chest compressions.

What is a Left Ventricular Assist Device?

With an LVAD, blood enters the device from the LV and is pumped to the central aortic circulation, “assisting” the heart.  The outflow cannula is typically anastomosed to the ascending aorta, just above the aortic valve. RA/RV still working

 

Blue Arrow – Important point as patients often present with iGel in place…

 

Unique Patient Properties

  • Pulses often absent
    • BP measured manually with a Doppler – MAP (50-90)
  • SpO2 may not be measurable
  • Anticoagulated
  • Need power!
  • Very reliant on RV function/preload
  • Leading cause of death – sepsis and stroke

Further Reading

Cardiopulmonary Resuscitation in Adults and Children With Mechanical Circulatory Support. A Scientific Statement From the American Heart Association


Aortic Dissection

Aortic dissection remains difficult to diagnosis with 1 in 6 being missed at the initial ED visit. Why? The diagnosis is rare with and incidence of only 2.9/100,000/year, and the presentation is often atypical mimicking other more common diagnoses such as ACS and stroke.

View The SJRHEM  – Aortic Dissection – Resident Clinical Pearl here:

Aortic Dissection

Diagnosis

The most common initial misdiagnoses are acute coronary syndrome, pulmonary embolism, and stroke. Patients with these suspected diagnoses should also be screened for high-risk features of acute aortic dissection. If none are present, they are unlikely to have an acute aortic dissection. If high-risk features are present, balance your clinical suspicion for an aortic dissection with the likelihood of an alternative diagnosis using an approach such as RAPID

How Do I rule Out Aortic Dissection – Just the Facts – CJEM

PoCUS

Early Screening for Aortic Dissection With Point‐of‐Care Ultrasound by Emergency Physicians

A total of 127 patients were enrolled: 72 in the US group and 55 in the control group. In the US group, compared with CTA, the sensitivity of EP POCUS was 86.4%, and the specificity was 100.0%.

 

 

Treatment Goals

From EMCases.com

 

Further Reading

Episode 92 – Aortic Dissection Live from The EM Cases Course

 

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