Intubating Asthmatic Patients

Asthma is Greek for panting, which is a fitting translation for a patient that presents with a severe asthma exacerbation. We try to avoid intubating these patients because they are prone to compilations such as pneumothorax, mucus plugging, and increased morbidity and mortality. 

However, there are specific situations when you may consider intubating an asthmatic patient. One reason is that your patient may not be improving despite maximal medical therapy, such as BIPAP, albuterol, ipratropium, magnesium, epinephrine/terbutaline, ketamine, etc. Another reason is that your patient may now be altered, and have worsening work of breathing, and vital sign abnormalities. Remember that a “silent chest” is a poor prognostic indicator; you may not hear wheezing because they are not moving any air. 

If you choose to intubate, there are tricks to maximize your success and optimize your management of your patient on the vent. 

  • Use a large ETT (8-9) because it reduces airflow resistance and can facilitate procedures later (such as bronchoscopy). 

  • Ketamine is a useful induction agent because of its bronchodilatory effects. It may also be useful if you choose delayed sequence intubation. 

  • High airway pressures can cause hypotension after intubation, so consider giving volume if there is a current or prior history of hypotension. 

  • If hemodynamics are compromised consider giving an epinephrine drip. It is considered a systemic bronchodilator that can provide hemodynamic support as well as bronchodilation. 

  • Keep a low respiratory rate when bagging or on the vent (6-8 breaths/min). Giving them time to exhale will decrease the chances of air trapping and pneumothorax. Another way to do this is to increase the I:E time (1:4 or 1:5). 

  • If the vent is alarming, troubleshoot (DOPES mnemonic) but be suspicious for mucus plugs, pneumothorax, or breath stacking. If they are breath stacking, disconnect them from the vent and push on their chest to help them fully exhale.  

A quick note about auto-PEEP and breath stacking: Auto-PEEP refers to trapping gas in the lungs during respiration. This occurs when one breath can’t be fully exhaled before the next inhalation. This trapped gas causes additional positive pressure, known as “auto-PEEP” in the chest which is typically higher than the PEEP set on the ventilator. This process predisposes patients to develop a pneumothorox. 

Thanks for reading!

Ariella


CXR- Consolidation or Atelectasis?

Here is a quick guide on differentiating consolidations vs atelectasis on chest x-ray.

The reason that we can differentiate structures on x-rays is due to differences in density. For example, the lungs are air-filled and appear black whereas the ribs, vertebrae, and heart are solid and appear white. 

Consolidation: consolidation represents the replacement of alveolar air with fluid, blood, pus, or other substances. There are 3 lobes of the right lung, the upper, middle, and lower lobes. The right middle lobe sits next to the heart border. The left lung has 2 lobes, the upper and lower lobe. The left upper lobe sits next to the heart (image 1). If you have an obscured right heart border, it may indicate consolidation of the right middle lobe (image 2). Similarly, an obscured left heart border may indicate a consolidation in the left upper lobe (image 3). The lower lobes of each lung sit next to the hemidiaphragm. If you cannot make out a hemidiaphragm, it may suggest that there is something of similar density, such as a consolidation, in that lower lobe.

On a normal lateral chest x-ray, the vertebrae should get progressively darker as you get closer to the bases, known as the "more black sign". The vertebrae located near the apex of the lung have overlying muscles, making them appear white, compared to those at the bases that have overlying air, which makes them appear darker (image 4). You should also be able to make out 2 hemidiaphragm on the lateral x-ray with sharp costophrenic angles.

Atelectasis: Atelectasis refers to the collapse of a lung portion. On a normal x-ray, ⅓ of the heart is located on the right and ⅔ of the heart is located on the left side of the chest (image 5). In atelectasis, you will see the mediastinum shift towards the affected side due to volume loss, causing the heart and trachea to shift (image 6). In addition, the unaffected lobe on the ipsilateral side will be hyperlucent as a result of compensatory hyper-expansion. The rib spaces on the affected side may also be closer together when compared to the contralateral side and there may be an elevation of the ipsilateral hemidiaphragm. 

Tip: don’t be fooled by a rotated cxr. Rotation can be assessed by measuring the distance between the medial edges of the clavicles to the vertebral spinous processes. They should be equal or near equal.

 

Thanks for reading! 

Ariella 

References: 

https://radiopaedia.org/courses/emergency-radiology-course-online/pages/1417

https://radiopaedia.org/articles/lung-atelectasis


POTD: ECMO

Hello everyone! Let's talk about ECMO. I was first introduced to ECMO in the era of pre-vaccine COVID, where it was often hailed as the Hail Marry of solutions for severe COVID cases in younger patients. But ECMO can be used for so much more, including a recently discussed topic - hypothermia.

What is ECMO?

ECMO, or extracorporeal membrane oxygenation, is a prolonged cardiopulmonary support technique that allows oxygenation of the blood bypassing the heart and lungs. It differs from cardiopulmonary bypass in that it requires less anticoagulation and allows for longer duration of treatment. 

Who qualifies for ECMO?

Criteria for ECMO include acute severe cardiac or pulmonary failure that is potentially reversible and has failed conventional treatment and carries a high risk of death. Conditions include:

  • ARDS and severe respiratory failure (severe hypercapnia pH < 7.20, or P/F ratio < 70)

  • poor gas exchange/obstruction (massive PE)

  • acute pulmonary injury: smoke inhalation, contusion, drowning

  • nonischemic cariogenic shock, cardiac/pulmonary trauma, massive PE

  • bridge to lung or cardiac transplant or LVAD

Who does not qualify for ECMO?

Absolute contraindications include:

  • unwitnessed cardiac arrest

  • non-reversible, progressive lung or cardiac disease that is not a transplant candidate

  • pulmonary hypertension

  • advanced cancer

  • >120 kg

Relative contraindications include:

  • older than 75 years

  • CPR > 60 minutes

  • CNS injury

  • multi organ failure or trauma

What types of ECMO exist?

VV or veno-venous: the most common access, typically central vein IVC access (femoral, IJ), passes through oxygenator, and deposits in a large vein near RA (IJ, subclavian)

  • provides respiratory support but not circulatory support

  • pathologies: COPD, ARDS, PNA, smoke inhalation injury, status asthmatics, airway obstruction, drowning

VA or veno-arterial: can be peripheral or central, access is central vein, passes through oxygenator, and deposits in arterial access around pulmonary artery

  • provides both respiratory and cardiac support

  • pathologies: non-ischemic cardiogenic shock, heart/lung transplant, LVAD failure, PE, sepsis

Complications:

  • clot formation

  • bleeding

  • vessel trauma, LV distension

  • North-south syndrome - hypoxia and cyanosis in cephalic and lower extremities outside of range of circuit access

https://wikem.org/wiki/Extracorporeal_membrane_oxygenation

https://www.emra.org/emresident/article/ecmo-in-the-ed/