Where do we measure ST elevation?

This was just another ACS for me, but it is really amazing how "Dr. Mattu" took out some great teaching points from it. 

Check out this resource for more EM/ECG stuff..
https://ecgweekly.com

Capnography beyond ROSC

What is Capnography?

It is a non-invasive technique where CO2 is analysed continuously, in the gases entering and leaving the lungs. Look at it like a non-invasive way of estimating the PaCO2. Normal ETCO2 ranges between 35-45mmHg.

Different ways of estimating ETCO2:

1. Waveform capnography (Quantitative): When ETCO2 is graphically displayed and analysed quantitatively (real time quantitative waveform as depicted below). Capnograph is the device that measures and displays the waveform. It gives us a number i.e very close to the PaCO2 (typically underestimates PaCO2 by 5mmHg in healthy adults). Therefore, a high ETCO2 is almost always associated with hypercapnia. 

Normal Capnograph (Adults)

2. Capnometry (Quantitative): When only the numerical value is displayed without the waveform.

                         

3. Qualitative: Does not tell us one fixed number instead gives a range of ETCO2 using the calorimetric device. Ex. 21-30mmHg. Hence, utility is limited to ET tube placement verification.

Calorimeter device

How is it different from SpO2?

SpO2 measures O2 saturation in the blood whereas ETCO2 measures CO2 in the airway. ETCO2 reflects the elimination of CO2 by the lungs and thus paints an immediate picture of patient's condition on the monitor, in contrast to SpO2 that remains normal for several minutes (even when you hold your breath).

SpO2 and ETCO2                             

When interpreting ETCO2, look at both, the numeric value as well as the waveform. If you look only at the numeric value, this is like only looking at the heart rate without the ECG wave pattern!

Normal ETCO2 waveform:

Phase I aka Dead space ventilation/ Inspiratory baseline: Beginning of exhalation, no gas exchange here. There is almost no CO2 in airway during inspiration, so baseline is normally zero.

Phase II aka Ascending/Expiratory upstroke/ Early exhalation phase: CO2 from alveoli reaches the upper airway and causes a rapid rise in the amount of CO2 that is detected on the monitor.

Phase III aka Expiratory plateau phase: CO2 rich air is exhaled out

ETCO2 i.e. end of exhalation contains the highest concentration of CO2 (normal value is about 35-45 mmHg).

Phase IV aka Descending/ Expiratory downstroke: Inspiration begins and CO2 in the airways drops down to zero.

Normal capnograph wave

Note: The baseline represents the inspiratory phase (not expiratory)

Normal capnograph

Increase in ETCO2 (See the waveform below)

Hypoventilation

Increased muscular activity

Malignant hyperthermia

Increased Cardiac Output or Bicarbonate infusion

Relief from bronchospasm

Increasing ETCO2 (Ex. Hypoventilation during procedural sedation)

Decrease in ETCO2 (See the waveform below)

Hyperventilation

Muscle relaxants and hypothermia

Decrease cardiac output

Pulmonary embolism 

Bronchospasm

Decreasing ETCO2

Clinical Applications:

1. Airway management: To confirm the ET tube placement, also for continuous confirmation of the airway
2. Monitoring CPR efficacy: Target ETCO2 >20 during CPR
3. Estimates prognosis during CPR: An end-tidal CO2 value < 10 mm Hg after 20 min of resuscitation has been shown to be very accurate in predicting death
4. Confirming ROSC without stopping chest compressions: With ROSC ETCO2 shows as a sudden increase
5. Monitoring PaCo2 in a Traumatic Brain Injury/ Post Cardiac Arrest care
6. Guide to ventilation during procedural sedation: Shows hypoventilation i.e increasing ETCO2 at least 60 seconds prior to hypoxia 
7. Fluid responsiveness (5% or greater increase in ETCO2 following a passive leg raise is a non invasive way of predicting fluid responsiveness)
8. Diagnosing other pathologies (PE, DKA)

ETCO2 waveform in other pathologies:

Airway obstruction pattern (Bronchospasm)

Rebreathing

Esophageal intubation

On Muscle relaxants

Take Home

• ETCO2 is a surrogate marker for arterial CO2. If increased, it confirms hypercapnia.
• ETCO2 changes immediately with changes in the amount of CO2 in the airway (unlike SpO2 that shows a lag)
• When using waveform capnography, look at the ETCO2 numeric value as well as the waveform.
• Eliminate pulse checks during CPR, use ETCO2 instead.

References:

1. Heradstveit BE, Heltne JK. PQRST - A unique aide-memoire for capnography interpretation during cardiac arrest. Resuscitation 2014; 85:1619-20.
2. Monnet, X. et al. ETCO2 is better than arterial pressure for predicting volume responsiveness by PLRT. Intensive Care Med. 2013 Jan;39 (1): 93-100
3. http://www.medscape.com/viewarticle/812011
4. http://edtech2.boisestate.edu/meganjacobson/502/capno.html
5. http://www.carefusion.com/pdf/Center_for_Safety/Documents/RC1706-L3017-Capnography-Handbook.final.pdf

Running the code

This week, lets go through some key points on cardiac arrest. Some of these form the fundamentals of CPR in addition to other important points which are not talked about when we do the routine life support courses.

1. High quality CPR
Well, we all know this, Right?

• Rate:100-120/min
• Depth: 5cm approximately
• Allowing full chest recoil
• Not to hyperventilate
• Minimising interruptions

This is something that is really stressed on during the life support courses. Well, this is because survival is linked to the quality of CPR and there should not be any excuses here. This is very basic simple stuff that can make a difference. So how are doing it so far?

Current literature says we are slow/ shallow with chest compressions and do not allow adequate recoil. So next time when you run a code, make sure that you stick to these points and especially stay away from interruptions.

Reasons for interruptions: 

a) Airway: Securing the airway should be individualised for every patient. There is no magic number here. For a witnessed arrest with presumed cardiac cause, airway can be delayed for 8-10 minutes whereas early airway control should be done for a hypoxic arrest (drowning, pulmonary edema). In India, pre-hospital intubations are rare and by the time patients are brought to a hospital, airway should be secured ASAP on arrival with minimal interruptions to chest compressions. This is not the time for a novice to try intubation, it should be done by the most experienced provider around. 

b) Pulse Checks: Checking pulse during CPR is unreliable and should not be done, instead use ETCO2 to look for the ROSC. DO NOT STOP COMPRESSIONS TO CHECK FOR PULSE. 

c) Peri shock pauses: Shock can be delivered with transcutaneous pads or paddles and in India, the use of paddles is far more common than pads. 
With every 5 seconds of peri shock pause, there is an 18% decrease in survival. It is recommended to continue to deliver compressions while charging the defibrillator and once it is charged, only then hold the chest compressions for probably < 5 seconds, deliver the shock and resume compressions. It is painful to see those providers, who stop compressions as soon as they touch the paddles, then charge the defibrillator and then deliver the shock. This way it roughly takes about 20-30 seconds.

If there is expertise available, use intra arrest ECHO to pick up a tamponade or dilated RV, but again minimise compressions (Transesophageal ECHO is coming to the ED's soon..)


2. Hemodynamics Guided Resuscitation
Choose one of these three to judge your performance and hemodynamic status:

a) Coronary Perfusion Pressure (needs an arterial line and central line to monitor CPP)

• Our goal is to achieve an adequate Coronary Perfusion Pressure (CPP) i.e. CPP > 20mm Hg
• CPP = Aortic DBP - Right Atrial Pressure (RAP) 

OR

b) Diastolic Blood Pressure (needs just an arterial line)

• Insert a intra arrest femoral arterial line and target DBP > 40mm Hg 
• If < 40, improve CPR or give epinephrine
• If > 40, no need to give epinephrine, continue high quality CPR

OR

c) ETCO2 

• When you can't get an arterial line, use waveform capnography
• It is the continuous non invasive measurement end tidal CO2 using a sensor, the value is displayed on the monitor as a number.
• ETCO2 acts as a surrogate marker of cardiac output in addition to confirming the ET tube placement and ROSC.
• Target ETCO2 > 20mmHg 

3. Medications
Theoretical benefit: Improve CPP, CPP
Detrimental effects: Increase myocardial O2 demand, post ROSC myocardial dysfunction

Epinephrine (Adrenaline)

• No difference in outcomes, but we are finding it hard to stop using it!!
• Literature says more epi = no change or worse outcomes.
• With epi you are more likely to achieve ROSC, but worsen the neurological outcomes.
• Read more on epinephrine here by Dr. Anand Swaminathan (@EMSwami)

Give q5min epi now if you have been doing q3min so far and watch out for the next ACLS update OR use Hemodynamics Guided Resuscitation. 


3. Team Leadership

• This is by far the most important take home point from this post. Your leadership skills, ability to mobilise resources and getting things done can affect the outcome of a code. With experience we need to learn how to take control of the situation and communicate effectively under stress. Just knowing the algorithms is not enough.
• Good Leadership: Appropriate role assignment, better communication, reduces errors and establishes ROSC faster
• Errors are made due to indecisive and weak leadership which can cost a life.
• If there is time available, brief your team prior to the code and always debrief after you are done with the code regardless of the outcome. This will improve the team dynamics for future resuscitations. 
• 

So take the charge, assign tasks, be decisive, communicate early, clearly and effectively.

Take Home:

• Don't forget the basics, focus on high quality CPR
• Don't flood them with epinephrine instead use Hemodynamics guided resuscitation (CPP, DBP or ETCO2)
• Communicate early, clearly and effectively. Good leadership saves lives..

Thank You

References:

1. Michael Winters, MD: Running the Perfect Code in 2015 (AAEM Scientific Assembly) 
2. Castelao, Ezequiel Fernandez, et al. "Effects of team coordination during cardiopulmonary resuscitation: A systematic review of the literature." Journal of critical care 28.4 (2013): 504-521.CPR quality- Consensus 
3. Panesar, Sukhmeet S., Agnieszka M. Ignatowicz, and Liam J. Donaldson. "Errors in the management of cardiac arrests: An observational study of patient safety incidents in England." Resuscitation 85.12 (2014): 1759-1763.
4. Cheskes, Sheldon, et al. "Perishock Pause An Independent Predictor of Survival From Out-of-Hospital Shockable Cardiac Arrest." Circulation 124.1 (2011): 58-66.
5. Sunde, Kjetil, and Theresa M. Olasveengen. "Towards cardiopulmonary resuscitation without vasoactive drugs." Current opinion in critical care 20.3 (2014): 234-241.
6. Stiell, Ian G., et al. "Advanced cardiac life support in out-of-hospital cardiac arrest." New England Journal of Medicine 351.7 (2004): 647-656.Johnson NJ et al Resuscitation 2014
7. Sutton, Robert M., et al. "Hemodynamic-directed cardiopulmonary resuscitation during in-hospital cardiac arrest." Resuscitation 85.8 (2014): 983-986.

NIV: What’s the big deal about that big mask?

A patient struggling for that ‘satisfying, good, deep breath’ and failing at every attempt is not an uncommon sight in the ED. Shortness of breath/breathlessness is one of the major presentations in the EDs all around the world. The diverse etiologies and the potential complications due to long periods of breathlessness makes it a time critical symptom requiring early intervention. 

Non-invasive ventilation is one of the important modalities of managing a patient with shortness of breath when indicated. Let us review some of the important points about non-invasive ventilation.

So, what is NIV?

It’s a method of giving ventilatory support/delivering oxygen to a patient with respiratory distress using a positive pressure mask so that invasive methods like endotracheal intubation is postponed or avoided.

What are the types of NIV?

There are 2 modes of NIV: CPAP (Continuous Positive Airway Pressure) and BPAP (Bilevel Positive Airway Pressure). BPAP has IPAP and EPAP (I-Inspiratory, E-Expiratory)

Terminology:

In general,
Type 1 RF requires CPAP type of NIV.

Type 2 RF requires BPAP type of NIV.

PEEP=EPAP=CPAP i.e. they all mean the same!

So you can say in Type 1 RF(Hypoxic failure), the pressure we provide is PEEP or just EPAP or CPAP. 

For Type 2 RF (Hypercapnic), we provide IPAP as well as EPAP. IPAP is greater than EPAP, PS (Pressure Support is the difference between IPAP and EPAP). For instance if IPAP = 15 and EPAP is 10 then PS = 15-10 i.e. 5cm H2O. 

A BPAP machine can be used as a CPAP machine if you set EPAP=IPAP i.e. you deliver the same pressure during inspiration as well as expiration.

Did you just say BPAP instead of BiPAP?

Yes! If you know that ‘Xerox’ is a trademark/brand while ‘photocopy’ is the actual terminology, you got this one right as well. BiPAP and BIPAP are actually trademarked modes of Bilevel Positive Airway Pressure (BPAP). (Apple fanboys can however use the i :-P)

CPAP:

• Found to be more useful in reducing the need for intubation and reducing the mortality in patients with acute cardiogenic pulmonary edema. 
• A fixed positive pressure is delivered throughout the respiratory cycle without any change during inspiration or expiration. The pressure required can be set on the machine and is measured in cmH₂O.  
• Commonly used pressures range 5-15cm of H₂O. (5-8cm of H2O is a reasonable starting pressure)
• O₂ can be titrated depending upon the SpO2, PaO2.

BPAP:

• Found more effective in acute exacerbation of COPD.
• Different pressures are used during inspiration (IPAP) and expiration (EPAP).
• The commonly used initial settings are EPAP: 3-6 and IPAP: 8-12 with supplemental oxygen of 3-5liters/min.
• The pressure can be adjusted depending upon the clinical condition of the patients and /or values of PaO2, PCO2 and SpO2. 
• To treat persistent hypercapnia increase IPAP by 2cms at a time. To treat persistent hypoxia, increase IPAP and EPAP by 2cms at a time.
• The maximum EPAP/IPAP is 25/15cmH₂0.
• Many comparative studies have demonstrated no significant difference between two modes of NIV when used for either for pulmonary edema or COPD.
• So, just in case the nurse asks you “we do not have a BPAP machine but there’s an old CPAP machine, will that be okay?” the answer should be “Yes!” irrespective of the etiology! (Most modern machines can deliver both CPAP and BPAP)

In whom do we put it on?

• In patients with respiratory failure/respiratory distress (e.g COPD and Acute Pulmonary Edema) without any contraindications.
• Although there’s no clear consensus regarding the indications for the use of NIV, when there are no contraindications, many patients with dyspnea may be suitable candidates for NIV. (Asthma, ARDS, Neuromuscular disease, Chest trauma, Cystic Fibrosis)
• To facilitate extubation in patients with COPD who have failed weaning attempts.
• ‘Do-not-intubate (DNI) patients’    
• Obstructive Sleep Apnea (OSA) – CPAP is commonly used in the night.

Contraindications for the use of NIV:

•    Patients who require immediate endotracheal intubation.
•    Decreased level of consciousness.
•    Inability to fix/position the mask due to past facial surgery.
•    Excessive secretions, vomiting and risk of aspiration.
•    Uncooperative patient.
•    Lack of staff trained/experienced in operating and monitoring the device and        patient the patient on NIV.
•    Hemodynamically unstable patient.
•    Severe hypoxia and/or hypercapnia: PaO2/FiO2 ratio<200mmHg, PaCO2 >      60mmHg.
•    Gastrointestinal bleeding.

How does it work?

Alveolar recruitment + increased of FiO2 à Reverse hypoxia.

Improves airflow by, Stenting of closed/obstructed airways à Decreases atelectasis or lung collapse à Improves pulmonary compliance à reduces the work of breathing.

The difference between EPAP and IPAP is called pressure support, which augments ventilation and reduces the work of breathing.

Addition of positive pressure to the thoracic compartment also reduces the preload and afterload à Improvement of patients with cardiogenic pulmonary edema.

How to monitor a patient on NIV?  What do I look for?

Once the patient is on NIV, patient has to be monitored closely.

Be prepared for the RSI in case NIV fails. Keep equipment ready and make sure they are working. Involve senior on the shift. Notify anesthesia if necessary.

Parameters to be looked for which are suggestive of NIV failure include:

•   Intolerance to NIV: Restless and irritable, asynchronous breathing with ventilator.
•   Increased secretions, vomiting patient.
•   Altered mental status.
•   Increasing dyspnea/respiratory distress despite optimum settings. (RR>35-40)
•   Persistent hypoxia despite supplemental oxygen.
•   Hemodynamic instability.
•   Worsening blood gases.

Other important things to be taken care of when patient is on NIV

• Explain the patient what NIV is and how air is delivered with pressure. Just forcing that nasty mask on patient’s face without explaining anything would make an already anxious patient more anxious and you will most probably end up with an uncooperative patient and failed NIV.
• Make sure that the mask is of appropriate size and well fitting. An Ill-fitting mask will result in air leak and NIV will be ineffective.  – Dealing with the big mask is indeed a big deal!
• Face Mask is proffered over nasal mask in the ED.
• Use cotton over the nasal bridge/forehead (pressure points) to avoid pressure sores.
• Sitting position / Head end elevation
• Follow up with a blood gas within 30-60 minutes .
• Have an alternative plan for NIV failure. Be prepared for Intubation.
• Be very cautious if you have to use analgesics that are known to cause sedation.

Complications of NIV:

•   Gastric distension
•   Failure of NIV
•   Aspiration (rare)
•   Hypotension with higher pressures (infrequent)
•   Barotrauma (rare)
•   Pressure ulcers over the face.
•   Oral and nasal dryness à Irritation.

Take home points:

•   Consider NIV ASAP in eligible patients (Timing is important).
•   EPAP=CPAP=PEEP, IPAP > EPAP and PS = IPAP-EPAP.
•   Reassure, use an appropriately sized mask .
•   Have a definitive plan for failed   NIV.

       Author:

      Dr. Apoorva Chandra

      Resident – Emergency Medicine 

      Apollo health city

      Hyderabad, India

      @apoorvamagic on twitter 

      Email: apoorvamagic@gmail.com

References and further reading/listening/viewing:

1. http://www.draeger.com/sites/assets/PublishingImages/Segments/Hospital-US/A_Breath_Ahead/02_Contemporary_Clinical_Practice/NIV-FAQs.pdf
2. http://www.ebmedicine.net/topics.php?paction=showTopic&topic_id=271
3. http://bja.oxfordjournals.org/content/early/2013/04/04/bja.aet070.full
4. Ventilation Literature Summaries http://lifeinthefastlane.com/ccc/ventilation-literature-summaries/
5. EMCrit Podcast 19 – Non-Invasive Ventilation: http://emcrit.org/podcasts/niv/
6. BiPAP part 1 on YouTube by David Gibson:  https://www.youtube.com/watch?v=UXWa1r3hEoM
7. BiPAP part 2: https://www.youtube.com/watch?v=gewxf3FopOY
8. British thoracic society guidelines: https://www.brit-thoracic.org.uk/guidelines-and-quality-standards/non-invasive-ventilation-(niv)/
9. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3042478/
10. Oxford handbook of emergency medicine: Page no. 109 (section on COPD).