The Case of the Perplexing Crepitations

perplexing crepitations

Occam’s Razor – the simplest explanation is most likely to be correct.

In the Emergency Room, we are faced with a multitude of cases, and Occam’s Razor serves best when we need to narrow down on the differential diagnoses.

Sometimes, a few cases may evade this category and continue to baffle us even after a thorough history is obtained or a detailed clinical examination is performed. If we are lucky enough to get the point-of-care (POC) lab tests in time (or the mere availability of POC), they aid in the diagnosis and decision-making. At times, these POC lab tests also may not provide much help.

I have described one such case – a 21-year-old male with fever, dyspnea, desaturation, and multiple petechiae of 3 days duration.

Case Presentation

A 21-year-old male came at 9.30 pm to the ER with fever and breathlessness for three days. Being a healthcare worker himself, he had suspected pneumonia and started oral Amoxiclav, oral Clarithromycin, and Paracetamol. Despite this, there was no improvement in clinical status. He had progressively worsening breathlessness and continuous low-grade fever. On day 3, he developed a few petechial spots over his arms and minimal subconjunctival hemorrhage.

He recalls having myalgia in the lead up to these symptoms, for which he had received several injections of intramuscular Diclofenac. The injection sites now had developed small hematomas. There were no other visible bleeding manifestations. He clearly said that he had had no contact with any infectious patients and had self-isolated after developing these symptoms. His workplace had sent blood and sputum cultures – which came back negative. Their only concern was a continuous rise in the WBC count and sent to our hospital for further management.

Assessment

The patient was very ill-looking and extremely dyspneic with obvious usage of accessory respiratory muscles. He was profusely diaphoretic, had bilateral subconjunctival hemorrhage, multiple petechiae, anasarca, dyspnea, and 99.6⁰F. His Vitals were heart rate – 134/min, blood pressure – 110/70mmHg, respiratory rate – 34/min, SpO2 – 72% in room air; 98% with NIV. There were bilateral crepitations in all lung fields + no obvious abnormalities on CVS, CNS, and abdominal examination. POC ultrasound revealed multiple B-lines in all lung areas. Dilated IVC. The remaining cardiac, abdomen, and limb USGs were normal. ABG revealed Type 1 respiratory failure with elevated lactates. Bedside CXR and chest CT revealed diffuse bilateral lung infiltrates – not typical of pulmonary edema or pneumonia. Probable ARDS was mentioned. Blood samples had been sent for necessary investigations, including cultures and peripheral blood smear.

Management

Meanwhile, opinions were obtained from critical care consultants and pulmonologists regarding further management. Based on the clinical findings, it was decided to start the patient on broad-spectrum antibiotics (BSA), albumin transfusion, diuretics for the fluid overload status, and NIV for respiratory failure [all in suspicion of sepsis with MODS]. The patient was started on BSA before shifting to the ICU. Meanwhile, the blood reports arrived, suggestive of possible Myelodysplastic Syndrome (WBC – 95,000 cu.mm), Hb – 7g/dl. Peripheral Blood Smear report was Acute Myeloid Leukemia – possible M2 or M3.

The patient was immediately started on IV fluids, and oncology consultation was immediately obtained for chemotherapy initiation. Albumin and diuretics were withheld in suspicion of blast crisis and leukostasis / leukemic infiltration of the lungs. The patient was started on Cisplatin and other chemotherapeutic agents; bicarbonate infusion for urine alkalinization; allopurinol to treat hyperuricemia due to cytolysis; aggressive IV fluids for prevention of AKI due to chemotherapy and hyperuricemia [Tumour Lysis Syndrome]. Bone marrow biopsy was done during his hospital stay, which confirmed blast crisis AML-M3. His clinical condition improved considerably, and he was discharged from the hospital on Day 7.

Lessons Learnt

  1. Recognising leukostasis and hyperviscosity in the ED in an undiagnosed AML patient is extremely difficult. https://link.springer.com/chapter/10.1007/978-3-030-22445-5_3
  2. While considering different diagnoses based on clinical findings, always keep an open eye. Rare diseases present to the ED just like all others. https://www.medscape.com/viewarticle/860747_3
  3. Aggressive fluid management is needed in hyperviscosity syndrome. If we had started this patient on diuretics as planned, the blood would have become more viscous and lead to multisystem thrombosis. https://pubmed.ncbi.nlm.nih.gov/22915493/
  4. Increased metabolism in AML can present as pyrexia. With the other features of anemia, leucocytosis, petechiae, and anasarca, we are likely to diagnose this as sepsis. When in doubt, look through other causes of pyrexia (PUO). https://onlinelibrary.wiley.com/doi/full/10.1111/imj.13180
  5. Anasarca in leukemia does not warrant albumin transfusion as this may worsen fluid status. They may actually be in need of steroid therapy. https://www.hindawi.com/journals/crihem/2012/582950/
  6. Point of Care Lab testing is essential to reduce the number of diagnostic errors in the ED. https://acutecaretesting.org/en/articles/
Cite this article as: Gayatri Lekshmi Madhavan, India, "The Case of the Perplexing Crepitations," in International Emergency Medicine Education Project, June 14, 2021, https://iem-student.org/2021/06/14/the-case-of-the-perplexing-crepts/, date accessed: September 25, 2021

Recent Blog Posts By Gayatri L. Madhavan

Physiologically Difficult Airway – Metabolic Acidosis

Physiologically Difficult Airway - Metabolic Acidosis

Case Presentation

A 32-year-old male with insulin-dependent diabetes mellitus came to your emergency department for shortness of breath. He was referred to the suspected COVID-19 area. His vitals were as follows: Blood pressure, 100/55 mmHg; pulse rate, 135 bpm; respiratory rate, 40/min; saturation on 10 liters of oxygen per minute, 91%; body temperature, 36.7 C. His finger-prick glucose was 350 mg/dl.

The patient reported that he had started to feel ill and had an episode of diarrhea 1 week ago. He developed a dry cough and fever in time. He started to feel shortness of breath for 2 days. He sought out the ER today because of the difficulty breathing and abdominal pain.

The patient seemed alert but mildly agitated. He was breathing effortfully and sweating excessively. On physical examination of the lungs, you noticed fine crackles on the right. Despite the patient reported abdominal pain, there were no signs of peritonitis on palpation.

An arterial blood gas analysis showed: pH 7.0, PCO2: 24, pO2: 56 HCO3: 8 Lactate: 3.

The point-of-care ultrasound of the lungs showed B lines and small foci of subpleural consolidations on the right.
At this point, what are your diagnostic hypotheses?

Two main diagnostic hypotheses here are:

  • Diabetic ketoacidosis (Hyperglycemia + metabolic acidosis)
  • SARS-CoV2 pneumonia

We avoid intubating patients with pure metabolic decompensation of DKA if possible, as they respond to hydration + insulin therapy + electrolyte replacement well and quickly. 

But in this scenario, the patient is extremely sick and has complicating medical issues, such as an acute lung disease decompensating the diabetic condition, probably COVID19. Considering these extra issues may complicate the recovery time and increase the risk of respiratory failure, you decide to intubate the patient in addition to the treatment of DKA.

You order lab tests and cultures. You start hydration and empirical antibiotics while starting preoxygenation and preparing for intubation.

Will this be a Difficult Airway?

Evaluating the patient for the predictors of a difficult airway is a part of the preparation for intubation. Based on your evaluation, you should create an intubation plan. 

This assessment is usually focused on anatomical changes that would make it difficult to manage the airway (visualization of the vocal cords, tube passage, ventilation, surgical airway), thereby placing the patient at risk.

“Does this patient have any changes that will hinder opening the mouth, mobilizing the cervical region, or cause any obstruction for laryngoscopy? Does this patient have any changes that hinder the use of Balloon-Valve-Mask properly, such as a large beard? What about the use of the supraglottic device? Does this patient have an anatomical alteration that would hinder emergency cricothyroidotomy or make it impossible, like a radiation scar? ”

So the anatomically difficult airway is when the patient is at risk if you are unable to intubate him due to anatomical problems.

The physiologically difficult airway, however, is when the patient has physiological changes that put him at risk of a bad outcome during or shortly after intubation. Despite intubation. Or because of intubation, because of its physiological changes due to positive pressure ventilation.

These changes need to be identified early and must be mitigated. You need to recognize the risks and stabilize the patient before proceeding to intubation or be prepared to deal with the potential complications immediately if they happen.

5 main physiological changes need attention before intubation are: hypoxemia, hypotension, severe metabolic acidosis, right ventricular failure, severe bronchospasm.

Back to our patient: Does he have physiologically difficult airway predictors?

  • SI (Shock Index): 1.35 (Normal <0.8) – signs of shock
  • P / F: 93 (Normal> 300) – Severe hypoxemia
  • pH: 7.0: Severe metabolic acidosis – expected pCO2: 20 (not compensating)
  • qSOFA: 2 + Lactate: 3 (severity predictor)

Physiologically Difficult Airway

"Severely critical patients with severe physiological changes who are at increased risk for cardiopulmonary collapse during or immediately after intubation."

Sakles JC, Pacheco GS, Kovacs G, Mosier JM. The difficult airway refocused.

Severe Metabolic Acidosis

In this post, we will focus only on the compensation of the metabolic part, but do not forget that this is a patient who needs attention on oxygenation and hemodynamics as well. That is, this is intubation with very difficult predictions.

What happens during the rapid sequence of intubation in severe metabolic acidosis?

To perform the procedure, the patient needs to be in apnea. During an apnea, pulmonary ventilation is decreased and the CO2 is not “washed” from the airway. These generate an accumulation of CO2, an acid, decreasing blood pH. In a patient with normal or slightly altered pH, this can be very well-tolerated, but in a patient with a pH of 7.0, an abrupt drop in this value can be ominous.

We know that the respiratory system is one of the most important compensation mechanisms for metabolic acidosis and it starts its action in seconds, increasing the pH by 50 to 75% in 2 to 3 minutes, guaranteeing the organism time to recover. So, even seconds without your proper actions can be risky for critical patients.

In addition, it must be remembered that increased RF is the very defense for the compensation of metabolic acidosis, and most of the time the organism does this very well. So if after the intubation the NORMAL FR and NORMAL minute volume are placed in the mechanical ventilator parameters, again there is an increase in CO2 and a further decrease in pH.

And what’s wrong? After all, a little bit of acidosis even facilitates the release of oxygen in the tissues because it deflects the oxyhemoglobin curve to the right, right?

Severe metabolic acidosis (pH <7.1) can have serious deleterious effects:

  • Arterial vasodilation (worsening shock)
  • Decreased myocardial contractility
  • Risks of arrhythmias
  • Resistance to the action of DVAs
  • Cellular dysfunction

What to do?

Always the primary initial treatment is: treating the underlying cause! In patients with severe metabolic acidosis, it is best to avoid intubation! Especially in metabolic ketoacidosis, which as hydration and insulin intake improves, there is a progressive improvement in blood pH.

Sodium bicarbonate

The use of sodium bicarbonate to treat metabolic acidosis is controversial, especially in non-critical acidosis values ​​(pH> 7.2). If you have acute renal failure associated, its use may be beneficial by postponing the need for renal replacement therapy (pH <7.2).

As for DKA, where sodium bicarbonate is used to the ketoacidosis formed by erratic metabolism due to the lack of insulin and no real deficiency is present, its use becomes limited to situations with pH <6.9.

The dose is empirical, and dilution requires a lot of attention (avoid performing HCO3 without diluting!)

NaHCO3 100mEq + AD 400ml

Run EV in 2h

If K <5.3: Associate KCl 10% 2amp

I would make this solution and leave it running while proceeding with the intubation preparations.

Attention: Remember, according to the formula below, that HCO3 is converted to CO2, and if done in excess, is associated with progressive improvement of the ketoacidosis and recovery of HCO3 from the buffering molecules. In a patient already with limited ventilation, its increase can cause deviation of the curve for the CO2 increase, which is also easily diffused to the cells and paradoxically decrease the intracellular pH, in addition to carrying K into the cell.

H + + HCO3 – = H2CO3 = CO2 + H2O

Mechanical ventilation

I think the most important part of the management of these patients is the respiratory part.

If you choose the Rapid Sequence Intubation: Prepare for the intubation to be performed as quickly as possible: Use your best material, choose the most experienced intubator, put the patient in ideal positioning, decide and apply medications skillfully, to ensure the shortest time possible apnea.

You will need personnel experienced in Mechanical Ventilation and you must remember to leave the ventilatory parameters adjusted to what the patient needs and not to what would be normal!

I found this practice very interesting: First, you calculate what the expected pCO2 should be for the patient, according to HCO3:

Winter’s Equation (Goal C02) = 1.5 X HCO3 + 8 (+/- 2)

And then, according to this table, you try to reach the VM Volume Minute value.
Goal CO2 Minute Ventilation
40 mmHg
6-8 L
30 mmHg
12-14 L
20 mmHg
18-20 L

These are just initial parameters. With each new blood gas analysis repeated in 30 minutes to an hour, you re-make fine adjustments using the formula below:

Minute volume = [PaCO2 x Minute volume (from VM)] / CO2 Desired

With the treatment of ketoacidosis, new parameters should be adjusted, hopefully for the better.

Another safer option for these patients would be to use the Awake Patient Intubation technique so that you would avoid the apnea period. However, Awake Patient Intubation Technique is contraindicated in suspected or confirmed COVID-19 cases due to the risk of contamination.

That’s it, folks, send your feedback, your experiences, and if you have other sources!

Further Reading

  1. Frank Lodeserto MD, “Simplifying Mechanical Ventilation – Part 3: Severe Metabolic Acidosis”, REBEL EM blog, June 18, 2018. Available at: https://rebelem.com/simplifying-mechanical-ventilation-part-3-severe-metabolic-acidosis/.
  2. Justin Morgenstern, “Emergency Airway Management Part 2: Is the patient ready for intubation?”, First10EM blog, November 6, 2017. Available at: https://first10em.com/airway-is-the-patient-ready/.
  3. Salim Rezaie, “How to Intubate the Critically Ill Like a Boss”, REBEL EM blog, May 3, 2019. Available at: https://rebelem.com/how-to-intubate-the-critically-ill-like-a-boss/.
  4. Salim Rezaie, “RSI, Predictors of Cardiac Arrest Post-Intubation, and Critically Ill Adults”, REBEL EM blog, May 10, 2018. Available at: https://rebelem.com/rsi-predictors-of-cardiac-arrest-post-intubation-and-critically-ill-adults/.
  5. Salim Rezaie, “Critical Care Updates: Resuscitation Sequence Intubation – pH Kills (Part 3 of 3)”, REBEL EM blog, October 3, 2016. Available at: https://rebelem.com/critical-care-updates-resuscitation-sequence-intubation-ph-kills-part-3-of-3/.
  6. Lauren Lacroix, “APPROACH TO THE PHYSIOLOGICALLY DIFFICULT AIRWAY”, https://emottawablog.com/2017/09/approach-to-the-physiologically-difficult-airway/
  7. Scott Weingart. The HOP Mnemonic and AirwayWorld.com Next Week. EMCrit Blog. Published on June 21, 2012. Accessed on July 15th 2020. Available at [https://emcrit.org/emcrit/hop-mnemonic/ ].
  8. IG: @pocusjedi: “Pocus e Coronavirus: o que sabemos até agora?”https://www.instagram.com/p/B-NxhrqFPI1/?igshid=14gs224a4pbff

References

  1. Sakles JC, Pacheco GS, Kovacs G, Mosier JM. The difficult airway refocused. Br J Anaesth. 2020;125(1):e18-e21. doi:10.1016/j.bja.2020.04.008
  2. Mosier JM, Joshi R, Hypes C, Pacheco G, Valenzuela T, Sakles JC. The Physiologically Difficult Airway. West J Emerg Med. 2015;16(7):1109-1117. doi:10.5811/westjem.2015.8.27467
  3. Irl B Hirsch, MDMichael Emmett, MD. Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. https://www.uptodate.com (Accessed on July 15, 2020.)
  4. Cabrera JL, Auerbach JS, Merelman AH, Levitan RM. The High-Risk Airway. Emerg Med Clin North Am. 2020;38(2):401-417. doi:10.1016/j.emc.2020.01.008
  5. Guyton AC, HALL JE. Tratado de fisiologia medica. 13a ed. Rio de Janeiro(RJ): Elsevier, 2017. 1176 p.
  6. Kraut JA, Madias NE. Metabolic acidosis: pathophysiology, diagnosis and management. Nat Rev Nephrol. 2010;6(5):274-285. doi:10.1038/nrneph.2010.33
  7. Calvin A. Brown III, John C. Sakles, Nathan W. Mick. Manual de Walls para o Manejo da Via Aérea na Emergência. 5. ed. – Porto Alegre: Artmed, 2019.
  8. Smith MJ, Hayward SA, Innes SM, Miller ASC. Point-of-care lung ultrasound in patients with COVID-19 – a narrative review [published online ahead of print, 2020 Apr 10]. Anaesthesia. 2020;10.1111/anae.15082. doi:10.1111/anae.15082
Cite this article as: Jule Santos, Brasil, "Physiologically Difficult Airway – Metabolic Acidosis," in International Emergency Medicine Education Project, November 25, 2020, https://iem-student.org/2020/11/25/physiologically-difficult-airway-metabolic-acidosis/, date accessed: September 25, 2021

More Posts by Dr. Santos

Oxygenation and Oximetry

Oxygenation and Oximetry

Authors: Job Rodríguez Guillén, Chief of Emergency Department. Hospital H+ Querétaro, México. Regina Pineda Leyte Internal Medic, Anahuac Querétaro University, Mexico. 

Introduction

One of the main goals of mechanical ventilation is oxygenation. Both hypoxemia and hyperoxemia must be avoided and the objectives must be individualized according to the clinical situation and comorbidities of each patient. Oxygenation monitoring is possible at the bedside by physical examination (late clinical signs), pulse oximetry (non-invasive continuous monitoring), and arterial blood gas analysis (gold standard for arterial oxygenation analysis).

Determinants of oxygenation

The main determinant of oxygenation is the mean airway pressure (Paw) and the inspired fraction of oxygen (FiO2). Paw is the average pressure to which the lung is exposed during inspiration and expiration mechanical ventilation (Figure 1). Paw improves oxygenation by allowing the redistribution of oxygen from highly compliant alveoli to less compliant alveoli.(1,2)
Oxygenation and Oximetry - figure 1
Figure 1: Mean airway pressure (Paw) is the integral (area under the curve) of pressure and time. PIP: peak inspiratory pressure; PEEP: positive pressure at the end of expiration; Ti: inspiratory time; Te: expiratory time.
According to the determinants of Paw and the relationship between them, there are five different ways to increase it (Figure 2)
Oxygenation and Oximetry - figure 2
Figure 2: Maneuvers to increase the mean airway pressure (Paw). PEEP: positive pressure at the end of expiration. Only maneuvers 3 and 4 are used in clinical practice to increase Paw and improve oxygenation.

The second determinant of oxygenation is Inspired Oxygen Fraction (FiO2). The use of supplemental oxygen at the hospital level is a common practice and a critical element of intensive care in patients with mechanical ventilation for the management of hypoxemia. However, in recent years it has been shown that higher oxygenation is not the goal. (3) In the same way that hypoxemia should be avoided, hyperoxia should be prevented. (4)

Although the FiO2 can be adjusted in ranges of 21% and up to 100% the lowest value required must be set (preferably <60%) to reach the desired oxygen saturation (SO2) target.

Oxygenation monitoring

Pulse oximetry allows non-invasive monitoring of oxygenation (SpO2), it is simple and reliable in many areas of clinical practice. SpO2 has a confidence rate of 95% ± 4%, so readings ranging between 70% and 100% are considered reliable.(5) In patients with mechanical ventilation, the objective is to identify hypoxemia.

It is important to remember that oximeters do not measure arterial oxygen pressure (PaO2), for this reason, they cannot directly diagnose hypoxemia or hyperoxemia (PaO2 <60 mmHg and PaO2> 120 mmHg respectively).(6)  What they do is “estimate” hypoxemia when SpO2 falls <90%, which would correspond to a PaO2 <60 mmHg according to the oxyhemoglobin dissociation curve (Table 1). (7)  However, it must be taken into account that changes in temperature and pH cause changes in this relationship. As the pH increases (alkalosis) or the temperature decreases (hypothermia), the shift of the curve is to the left since hemoglobin binds more strongly with oxygen, delaying its release to the tissues. Acidosis and fever shift the curve to the right as the hemoglobin molecule decreases its affinity for oxygen, facilitating the release of oxygen to the tissues.

Oxygenation and Oximetry - Table 1
Table 1: Estimation of the oxygenation state according to SpO2. SpO2: oxygen saturation by pulse oximetry; PaO2: arterial oxygen pressure.

SpO2 values <70% are not reliable. If necessary, the oxygenation assessment should be supplemented by arterial gas analysis. The arterial oxygen saturation (SaO2) is the oxygen saturation obtained by this test.

Oxygenation Goals

According to the oxyhemoglobin dissociation curve, the goal of oxygen titration is to achieve a PaO2 in the range of 60-65 mmHg or an SpO2 of approximately 90-92%. However, the objectives must be individualized and the current recommendations for oxygen therapy in critically ill patients. (8) are as follows (Table 2).

Table 2: Recommendations for oxygenation by SpO2. O2: oxygen; SpO2: oxygen saturation by pulse oximetry; AMI: Acute myocardial infarction; EVC: Cerebral vascular event; VM: mechanical ventilation; SIRA: Acute respiratory distress syndrome. Some exceptions apply like carbon monoxide poisoning.

It has been suggested that critically ill patients can tolerate lower levels of PaO2 (“permissive hypoxemia”) (9-10), however, studies are limited to make a recommendation to routine clinical practice.

Conclusions

Oxygenation goals should be established once the requirement for mechanical ventilation is indicated according to the clinical condition of each patient and monitoring that these objectives are met. Pulse oximetry allows continuous, non-invasive monitoring at the bedside. It should be remembered that hyperoxemia, as well as hypoxemia, should be avoided.

References

  1. Marini JJ,Ravenscraft SA. Mean airway pressure: physiologic determinants and clinical importance–Part 1: Physiologic determinants and measurements. Crit Care Med. 1992 Oct;20(10):1461-72.
  2. Marini JJ,Ravenscraft SA. Mean airway pressure: physiologic determinants and clinical importance–Part 2: Clinical implications. Crit Care Med. 1992 Nov;20(11):1604-16.
  3. Girardis M, Busani S, Damiani E, et al. Effect of conservative vs conventional oxygen therapy on mortality among patients in an intensive care unit: the Oxygen-ICU Randomized Clinical Trial. JAMA. 2016;316(15):1583-1589.
  4. Bitterman, Haim. “Bench-to-bedside review: oxygen as a drug.” Critical Care1 (2009): 205.
  5. Chan MM,Chan MM, Chan ED. What is the effect of fingernail polish on pulse oximetry?. Chest. 2003 Jun;123(6):2163-4.
  6. Wandrup JH. Quantifying pulmonary oxygen transfer deficits in critically ill patients. Acta Anaesthesiol Scand Suppl 1995;107:37–44
  7. Allen J. Photoplethysmography and its application in clinical physiological measurement. Physiol Meas 2007;28:R1–39
  8. Siemieniuk Reed A C, Chu Derek K, Kim Lisa Ha-Yeon, Güell-Rous Maria-Rosa, Alhazzani Waleed, Soccal Paola M et al. Oxygen therapy for acutely ill medical patients: a clinical practice guideline BMJ 2018;  363 :k4169
  9. Gilbert-Kawai ET, Mitchell K, Martin D, Carlisle J, Grocott MP. Permissive hypoxaemia versus normoxaemia for mechanically ventilated critically ill patients. Cochrane Database Syst Rev 2014;5:CD009931.
  10. Capellier G, Panwar R. Is it time for permissive hypoxaemia in the intensive care unit? Crit Care Resusc 2011;13:139–141.
Cite this article as: Job Guillen, Mexico, "Oxygenation and Oximetry," in International Emergency Medicine Education Project, October 5, 2020, https://iem-student.org/2020/10/05/oxygenation-and-oximetry/, date accessed: September 25, 2021

19 Questions and Answers on the COVID-19 Pandemic from a Emergency Medicine-based Perspective

covid 19 - from a Emergency Medicine-based Perspective

1) What is COVID-19?

Corona Virus Disease 2019 (COVID-19) is the disease caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).

2) What is SARS-CoV-2?

SARS-CoV-2 is a virus belonging to the Coronaviridae family. Spike proteins (S proteins) on the outer surface of SARS-CoV-2 are arranged in a way that resembles the appearance of a crown when viewed under an electron microscope (see Figure 1). S proteins facilitate viral entry into host cells by binding to the angiotensin-converting enzyme 2 (ACE2) host receptor. Several cell types express the ACE2 receptor, including lung alveoli cells. [1].

Morphology of the SARS-CoV-2
Figure 1 - Morphology of the SARS-CoV-2 viewed under an electron microscope.Note the spikes that adorn the outer surface of the virus, which impart the look of a corona surrounding the virion. (https://phil.cdc.gov/Details.aspx?pid=23312)

3) How is SARS-CoV-2 transmitted?

Viral particles can spread from person-to-person through airborne transmission (e.g., large droplets) or direct contact(e.g., touching, shaking hands). We have to remember that large droplets are particles with a diameter > 5 microns and that they can be spread by coughing, sneezing, talking, etc., so do not forget to wear full PPE in the Emergency Department (ED). Other potential routes of transmission are still being investigated.

4) What is the incubation time?

In humans, the incubation period of the SARS-CoV-2 varies from 4 days to 14 days, with a median of about 4 days [2].

5) Can we say the COVID-19 is like the seasonal flu?

No, we can’t say that. COVID-19 differs from the flu in several ways:

  • First of all, SARS-CoV-2 replicates in the lower respiratory tract at the level of the pulmonary alveoli (terminal alveoli). In contrast, Influenza viruses, the causative agents of the flu, replicate in the mucosa of the upper respiratory tract.
  • Secondly, SARS-CoV-2 is a new virus that has never met our adaptive immune system.
  • Thirdly, we do not currently have an approved vaccine to prevent infection by SARS-CoV-2.
  • Lastly, we do not currently have drugs of proven efficacy for the treatment of disease caused by SARS-CoV-2.

6) Who is at risk of contracting the COVID-19?

We are all susceptible to contracting the COVID-19, so it is essential that everyone respects the biohazard prevention rules developed by national and international health committees. Elderly persons, patients with comorbidities (e.g., diabetics, cancer, COPD, and CVD), and smokers appear to exhibit poor clinical outcome and greater mortality from COVID-19 [3]

7) What are the symptoms of the COVID-19?

There are four primary symptoms of COVID-19: feverdry coughfatigue; and shortness of breath (SOB).

Other symptoms are loss of appetite, muscle and joint pain, sore throat, nasal congestion and runny nose, headache, nausea and vomiting, diarrhea, anosmia, and dysgeusia.

8) What is the severity of symptoms from COVID-19?

In most cases, COVID-19 mild or moderate symptoms, so much so it can resolve after two weeks of rest at home. However, onset of severe viral pneumonia requires hospital admission.

9) Which COVID-19 patients we should admit to the hospital?

The onset of severe viral pneumonia requires hospital admission. COVID-19-associated pneumonia can quickly evolve into respiratory failure, resulting in decreased gas exchange and the onset of hypoxia (we can already detect this deterioration in gas exchange with a pulse oximeter at the patient’s home). This clinical picture can rapidly further evolve into ARDS and severe multi-organ failure.

The use of the PSI/PORT score (or even the MuLBSTA score, although this score needs to be validated) can help us in the hospital admission decision-making process.

10) Do patients with COVID-19 exhibit laboratory abnormalities?

Most patients exhibit lymphocytopenia [11], an increase in prothrombin time, procalcitonin (> 0.5 ng/mL), and/or LDH (> 250 U/L).

11) Are there specific tests that allow us to diagnose COVID-19?

RT-PCR is a specific test that currently appears to have high specificity but not very high sensitivity [12]. We can obtain material for this test from nasopharyngeal swabs, tracheal aspirates of intubated patients, sputum, and bronchoalveolar lavages (BAL). However, the latter two procedures increase the risk of contagion.

However, since rapid tests are not yet available, RT-PCR results may take days to obtain, since laboratory activity can quickly saturate during epidemics. Furthermore, poor pharyngeal swabbing technique or sampling that occurs during the early stage of COVID-19 can lead to further decreased testing sensitivity.

Consequently, for the best patient care, we must rely on clinical symptoms, labs, and diagnostic imaging (US, CXR, CT). The use of a diagnostic flowchart can be useful (see Figure 2).

diagnostic flow chart
Figure 2 - A possible diagnostic flow chart for an ill patient admitted to hospital with suspected COVID-19 (from EMCrit Blog)

12) Can lung ultrasound help diagnose COVID-19?

Yes, it can help! The use of POCUS lung ultrasound is a useful method both in diagnosis and in real-time monitoring of the COVID-19 patient.

In addition, we could monitor the patient not only in the emergency department (ED) or intensive care unit (ICU), but also in a pre-hospital setting, such as in the home of a patient who is in quarantine.

In fact, POCUS lung ultrasounds not only allows one to anticipate further complications such as lung consolidation from bacterial superinfection or pneumothorax, but it also allows detection of viral pneumonia at the early stages. Furthermore, the use of a high-frequency ultrasound probe, which is an adoption of the 12-lung areas method [4] and the portable ultrasound (they are easily decontaminated), allow this method to be repeatable, inexpensive, easy to transport, and radiation-free.

There are no known pathognomonic patterns of COVID-19.

The early stages COVID-19 pneumonia results in peripheral alveolar damage including alveolar edema and a proteinaceous exudate [5]. This interstitial syndrome can be observed via ultrasound by the presence of scattered B lines in a single intercostal space (see videos below).

Subsequently, COVID-19 pneumonia progression leads to what’s called “white lung”, which ultrasound represents as converging B lines that cover the entire area of the intercostal space; they start from the pleura to end at the bottom of the screen.

Finally, the later stages of this viral pneumonia lead to “dry lung”, which consists of a pattern of small consolidations (< 1 cm) and subpleural nodules. Unlike bacterial foci of infection, these consolidations do not create a Doppler signal within the lesions. We should consider the development from “white lung” to “dry lung” as an unfavorable evolution of the disease.[6]

(the 5 videos above come from the COVID-19 gallery on the Butterflynetwork website)

13) Can CXR/CT help us in the diagnosis of COVID-19?

Yes, it can help! There are essentially three patterns we observed in COVID-19.

In the early stages, the main pattern is ground-glass opacity (GGO)[7]. Ground glass opacity is represented at the lung bases with a peripheral distribution (see videos below) .

The second pattern is constituted by consolidations, which unlike ground-glass opacity, determine a complete “opacification” of the lung parenchyma. The greater the extent of consolidations, the greater the severity and the possibility of admission in ICU.

The third pattern is called crazy paving[8]. It is caused by the thickening of the pulmonary lobular interstitium.

However, we should consider four things when we do a CXR/CT exam. First, many patients, especially in the elderly, exhibit multiple, simultaneously occurring pathologies, so it is possible to clinically observe nodular effusions, lymph node enlargements, and pleural effusions that are not typical of COVID-19 pneumonia. Secondly, we have to be aware that other types of viral pneumonia can also cause GGO, so they cannot be excluded during the diagnostic process. Thirdly, imaging can help evaluate the extent of the disease and alternative diagnoses, but we cannot use it exclusively for diagnosis. Lastly, we should carefully assess the risk of contagion from transporting these patients to the CT room.

14) What is the treatment for this type of patient?

COVID-19 patients quickly become hypoxic without many symptoms (apparently due to “silent” atelectasis). Therapy for these clinical manifestations is resuscitation and support therapy. In patients with mild respiratory insufficiency, oxygen therapy is adopted. In severe patients in which respiratory mechanics are compromised, non-invasive ventilation (NIV) or invasive ventilation should be adopted.

15) How can we non-invasively manage the airways of patients with COVID-19?

In the presence of a virus epidemic, we should remember that all the procedures that generate aerosolization (e.g., NIV, HFNC, BMV, intubation, nebulizers) are high-risk procedures.

Among the non-invasive oxygenation methods, the best-recommended solution is to have patients wear both a high-flow nasal cannula (HFNC) and a surgical mask[9]. Still, we should also consider using CPAP with a helmet interface. Furthermore, we should avoid the administration of medications through nebulization or utilize metered-dose inhalers with spacer (Figure 3).

Figure 3 – General schema for Respiratory Support in Patients with COVID-19 (from PulmCrit Blog)

16) How can we invasively manage the airways of patients with COVID-19?

We should intubate as soon as possible, even in non-critical conditions (Figure 3). Intubation is a high contagion risk procedure. As a result, we should adopt the highest levels of precaution[10]. To be more precise:

  • As healthcare operator, we should wear full PPE. Only the most skilled person at intubation in the staff should intubate. Furthermore we should consider using a video laryngoscope. Last but not least, we should ensure the correct positioning of the endotracheal tube without a stethoscope (link HERE).
  • The room where intubation occurs should be a negative pressure room. When that is not feasible, the room should have doors closed during the intubation procedure.
  • The suction device  should have a closed-circuit so as not to generate aerosolization outside.
  • Preoxygenation should be done using means that do not generate aerosols. Let us remember that HFNC and BVM both can generate aerosolization. So, it is important to remember to turn off the flow of the HFNC before removing it from the patient face to minimize the risk and to use a two-handed grip when using BVM, interposing an antiviral filter between the BVM and resuscitation bag and ventilating gently.
  • Intubation drugs that do not cause coughing should be used. In addition, we should evaluate the use of Rocuronium in the Rapid Sequence Intubation (RSI) since it has a longer half-life compared to succinylcholine and thus prevents the onset of coughing or vomiting.

In conclusion, let us remember that intubation, extubation, bronchoscopy, NIV, CPR prior to intubation, manual ventilation etc. produce aerosolization of the virus, therefore, it is necessary that we wear full PPE.

17) What is the drug therapy for COVID-19?

Currently, there is no validated drug therapy for COVID-19. Some drugs are currently under study. They include Remdesivir (blocks RNA-dependent RNA polymerase), Chloroquine and Hydroxychloroquine (both block the entry of the virus into the endosome), Tocilizumab and Siltuximab (both block IL-6).

18) Is there a vaccine available for COVID-19?

No, there is still no vaccine currently available to the public.

19) What precautions should we take with COVID-19 infected patients?

As healthcare professionals, we should wear full personal protective equipment (PPE) and know how to wear them (“DONning”) and how to remove them properly (“DOFFing”) (see video below). Furthermore, we should wear full PPE for the entire shift and when in contact with patients with respiratory problems.

Resources on COVID-19

Cite this article as: Francesco Adami, Italy, "19 Questions and Answers on the COVID-19 Pandemic from a Emergency Medicine-based Perspective," in International Emergency Medicine Education Project, March 27, 2020, https://iem-student.org/2020/03/27/19-questions-and-answers-on-the-covid-19/, date accessed: September 25, 2021

References

[1] Zheng YY, Ma YT, Zhang JY, Xie X. COVID-19 and the cardiovascular system. NatRev Cardiol. 2020 Mar 5.

[2] del Rio C, Malani PN. COVID-19—New Insights on a Rapidly Changing Epidemic. JAMA. Published online February 28, 2020. doi:10.1001/jama.2020.3072

[3] Yee J et al. Novel coronavirus 2019 (COVID-19): Emergence and Implications for Emergency Care. Infectious Disease 2020. https://doi.org/10.1002/emp2.12034

[4] Belaïd Bouhemad, Silvia Mongodi, Gabriele Via, Isabelle Rouquette; Ultrasound for “Lung Monitoring” of Ventilated Patients. Anesthesiology 2015;122(2):437-447. doi: https://doi.org/10.1097/ALN.0000000000000558.

[5] Qian-Yi Peng, Xiao-Ting Wang, Li-Na Zhang & Chinese Critical Care Ultrasound Study Group (CCUSG). Findings of lung ultrasonography of novel corona virus pneumonia during the 2019–2020 epidemic. 12 March 2020 Intensive Care Medicine.

[6]  Chan JF, Yuan S, Kok KH, et al. A familial cluster of pneumonia associated with the 2019 novel coronavirus indicating person-to-person transmission: a study of a family cluster. Lancet 2020.

[7] Chest CT Findings in Cases from the Cruise Ship “Diamond Princess” with Coronavirus Disease 2019 (COVID-19)

[8] Radiographic and CT Features of Viral Pneumonia Hyun Jung Koo, Soyeoun Lim, Jooae Choe, Sang-Ho Choi, Heungsup Sung, and Kyung-Hyun Do RadioGraphics 2018 38:3, 719-739 doi: https://doi.org/10.1148/rg.2018170048

[9]  WHO – Clinical management of severe acute respiratory infection (SARI) when COVID-19 disease is suspected.

[10] Safe Airway Society. Consensus Statement: Safe Airway Society Principles of Airway management and Tracheal Intubation Specific to the COVID-19 Adult Patient Group. MJA 2020.

[11] GUAN WJ, Ni ZY, Hu Y, Liang WH, et al  Clinical Characteristics of Coronavirus Disease 2019 in China. N Engl J Med. 2020 Feb 28. doi: 10.1056/NEJMoa2002032

[12] Tao Ai et al. Correlation of Chest CT and RT-PCR Testing in Coronavirus Disease 2019 (COVID-19) in China: A Report of 1014 Cases. Radiology, published online February 26, 2020; doi: 10.1148/radiol.2020200642

Clinical examination of the hemodynamically unstable patient

Clinical examination of the hemodynamically unstable patient

Authors: Job Rodríguez Guillén. Chief of Emergency Department. Hospital H+ Querétaro. México and Paola Rivero Castañeda. Medical Intern, Anahuac Querétaro University, Mexico. 

Introduction

Clinical examination accounts as a fundamental part in the management of most critical scenarios. Although there are few publications and it remains controversial, its value considered as limited by 50% of medical practicioners (1). None of the well-known semiology books include any section about the physical examination in the critically ill patient (2). Nonetheless, an adequate clinical evaluation at the patient’s bedside may save lives in the context of a serious situation.

Clinical Examination Objectives

The main objectives are identifying and discerning from types of shock, emphasizing in the identification of life-threatening conditions, clinical signs of organic hypoperfusion, as well as to evaluate treatment response regarding therapies employed, and risk stratifying.

Identify hemodynamic instability

  • Life-threatening conditions (Tension pneumothorax, Cardiac tamponade, Pulmonary thromboembolism, Active hemorrhage, etc.)
  • Organ hypoperfusion
    (Altered mental state, decreased uresis, mottled skin, prolonged CFT, etc.)

Evaluate treatment response

  • Vital signs and normalization of the clinical state
    (Mental state improvement, diminished skin mottling, improved uresis, normalization of prolonged capillary filling time, etc.)

Risk stratifying

  • Scale and prognostic scores calculation. Prognostic scores use a combination of clinical and/or laboratoy variables (SOFA: Squential Organ Failure Assessment; APACHE: Acute Physiology and Chronic Health Evaluation; SAPS: Simplified Acute Physiology Score; MPM: Mortality Probability Models, etc.)

Clinical Exam Systematization

The clinician must be able to do a quick and efficient clinical examination to recognize different states of shock as early as possible, or even situations that may compromise organic perfusion. At a given time, it’s suggested to check out the clinical history, re-interrogate the patient and his/her family members, as well as patient’s family/regular physician (or even look for their previous medical notes), in order to help clinical integration, and so for decision making.

Systematization of the evaluating process, based on the previously proposed objectives, can be identified with the following mnemonic: PROA.

PROA - Summary

P - Probabilistic thinking

  • Think about any probability.
  • Look for intentionally.
  • Analyze clinical context and individualize.

R - Risk of dying

Identify life-threatening causes: Cardiac tamponade, Tensionpneumothorax, Pulmonary thromboembolism, Active hemorrhage, etc.

O - Organic hypoperfusion

Cutaneous perfusion signs: examine mottled skin and capillary filling time.

A - Approach of the clinical examination

Clinical exam by regions. Some components may not be relevant for all patients, even requiring other physical maneuvers. Even though laboratory and imaging are not part of the clinical exam, their interpretation must be integrated with the examination findings.

Probabilistic Thinking

Medicine is a science of uncertainty and an art of probability.

— William Osler

Clinical decision making in the emergency department begins with the estimation of the probability of a determined patient to have or do not have specific conditions (Bayesian reasoning or pretest probability).

Example; the probability of septic shock in a young patient after having a car crash is very low compared to the high probability of presenting with hemorrhagic or obstructive shock.

Proposed decisions related to initial probabilistic thinking vary in clinical relevance depending on the patient’s condition. It should always be re-evaluated through available additional data (posttest probability) (Figure 1).

Relationship between probability thresholds and decision‐making zones
Figure 1: Relationship between probability thresholds and decision‐making zones (3).

Risk of Dying

Shock is a momentary pause in the act of death.

— John Collins Warren

Currently, there are four types of shock, all with a common pathophysiological pathway: acute circulatory insufficiency associated with cell oxygen utilization dysfunction (altered-balance between oxygen input and consumption: DO2/VO2 dysfunction), a central situation that takes part in the development of multiorgan dysfunction (4-5).

Initial physical examination should be directed to the identification of immediate life-threating pathologies such as obstructive shock (Tension pneumothorax, cardiac tamponade, pulmonary thromboembolism), hemorrhagic shock etc.

These pathologies require immediate action. Otherwise, early multi-organ dysfunction and death may occur. The Point of Care Ultrasound (PoCUS), is a fundamental tool used for the evaluation of patients with hemodynamic instability of unknown origin.

Organ Hypoperfusion

When assessing the damage an earthquake or fire has caused inside a building, one looks through the windows. Using this analogy, it would be useful to be able to see inside the body to view the damage caused by the shock process.

— Jean-Louis Vincent

The initial approach to clinical examination begins with the skin. It is essential to remember that microcirculation cannot be globally defined through its dependency with macrocirculation, autoregulation mechanisms and organ interactions. Moreover, the availability of devices to evaluate it remains limited. Therefore, the evaluation is done from clinical, biochemical and hemodynamic data integration (6) (Figure 2)

Figure 2: three windows of shock

The correct way of measuring capillary filling time

Approach of The Clinical Examination

Clinical exam is not an art, is an essential ability.

— Leonel Martínez-Ramírez

During the initial evaluation, multiple situations can affect the accomplishment of a detailed physical examination. Therefore, it is recommended to follow a structured exploration method, looking at every main organ system and region. Documenting its results would allow avoiding the inclusion of essential data, and would permit to identify tendencies or any change in the patient’s clinical status.

Clinical examination approach in the critically-ill patient.

7Clinical examination approach emphasized in the critically-ill patient. This examination is realized based on every region in the body. Some components may not be relevant for all patients, or even some other maneuvers shall be executed in the physical examination. The verification list should be modified to be adapted to each patient’s circumstances. Laboratory and other studies analysis does not conform part of the clinical examination, although, their interpretation should be added to exploration findings (7).

  • General appearance

    Introduce yourself to the patient. Evaluate general appearance, physical state, complexity or the presence of particular face patterns, etc.

  • Head

    Inspect pupils' symmetry and reactiveness to light. Look for facial asymmetry and signs of bleeding in nostrils and oropharynx. Inspect lips, mouth and tongue, searching for lesions or signs of ulceration.

  • Neck

    Evaluate neck symmetry, venous distension and tracheal positioning. Palpate searching for adenopathies, subcutaneous emphysema, etc.

  • Thorax

    Expose the thorax, inspect the use of accessory respiratory muscles, diaphragmatic movement, and type of respiration. Also, look for ecchymosis or hematomas. Palpate searching for subcutaneous emphysema or bone crepitations. Auscultate respiratory sounds bilaterally, as well as heart sounds, noting the physiological splitting of the second heart sound, murmurs, friction and gallop rhythm or third heart sound.

  • Upper extremities

    Evaluate upper extremities symmetry. Inspect all arterial and venous line catheters. Evaluate for presence of mottled skin, peripheral pulses and perfusion through capillary filling time.

  • Abdomen

    Take into consideration the diaphragmatic movement during ventilation. Evaluate distension and tympanic sounds during the percussion of the abdomen. Palpate for any rigidity or involuntary guarding. Evaluate abnormal growth of spleen and liver, palpable masses, murmurs or other intestinal sounds.

  • Lower extremities

    Evaluate all sites of vascular accesses and palpate pulses. Evaluate mottled skin, peripheral perfusion and edema.

  • Central Nervous System and Mental State

    Evaluate if the patient is able to follow orders and if his/her four extremities can move equally. Evaluate plantar response as well as withdrawal to pain stimuli. Check pupils and facial symmetry if they were not previously evaluated.

  • Devices and Incisions

    Every possible surgical site should be evaluated, as well as the entrance of every device, including endotracheal tubes, vascular accesses, thoracic tubes, enteral probes and urinary catheters. It should be taken into consideration the characteristics and quantity of urine in the Foley bag.

  • Monitors and waveforms

    The mode, pressures, ventilation per minute and waveforms, hemodynamic monitor (venous pressure, arterial pressure), telemetry and vital signs, as well as any other type of bedside monitor, should be inspected in order to detect any qualitative or quantitative alteration/abnormality.

  • Posterior region

    Exam executed when the patient is in a prone position. Inspect looking for lesions or penetrating wounds. Pressure ulcer appearance should be evaluated.

  • Environment

    Family’s or visitors' moods should be taken into consideration. Light quality, ambient temperature, etc. should be evaluated.

Conclusions

Clinical integration of initial clinical history and the physical examination should be added to the biochemical complementation as well as advanced hemodynamic monitoring parameters, when these are available. Even so, if clinical examination answers raised questions during the initial evaluating process, the clinician must act according to physiological principles. There is no ideal hemodynamic monitoring, meaning that all parameters have to be individualized for each patient and his/her clinical context. Therefore, clinical examination systematization results are an excellent aid for the clinician regarding his/her clinical practice.  

References and Further Reading

  1. Vazquez R, Vazquez Guillamet C, Adeel Rishi M, Florindez J, Dhawan PS, Allen SE, Manthous CA, Lighthall G.  Physical examination in the intensive care unit: opinions of physicians at three teaching hospitals. Southwest J Pulm Crit Care. 2015;10(1):34-43. DOI: http://dx.doi.org/10.13175/swjpcc165-14
  2. Cook CJ, Smith GB. Do textbooks of clinical examination contain information regarding the assessment of critically ill patients?Resuscitation. 2004;60:129–136.
  3. Zehtabchi S, Kline J.A. The Art and Science of Probabilistic Decision‐making in Emergency Medicine. Academic Emergency Medicine, 17:521-523. DOI: http://doi.org/10.1111/j.1553-2712.2010.00739.x
  4. Weil MH, Shubin H. Proposed reclassification of shock states with special reference to distributive defects. Adv Exp Med Biol.1971 Oct;23(0):13-23.
  5. Ince C. The microcirculation is the motor of sepsis. Crit Care. 2005;9 Suppl 4:S13-9. DOI: 1186/cc3753
  6. Vincent JL, Ince C, Bakker J. Clinical review: Circulatory shock–an update: a tribute to Professor Max Harry Weil.Crit Care. 2012 Nov 20;16(6):239. DOI: 10.1186/cc11510.
  7. Metkus TS, Kim BS. Bedside Diagnosis in the Intensive Care Unit. Is Looking Overlooked?. Ann Am Thorac Soc.2015 Oct;12(10):1447-50. DOI: 10.1513/AnnalsATS.201505-271OI.
Cite this article as: Job Guillen, Mexico, "Clinical examination of the hemodynamically unstable patient," in International Emergency Medicine Education Project, December 6, 2019, https://iem-student.org/2019/12/06/clinical-examination-of-the-hemodynamically-unstable-patient/, date accessed: September 25, 2021

Massive Pneumothorax Without A Tension

massive pneumothorax

Case Presentation

A 24-years-old male with shortness of breath and chest pain presented to the emergency department. He was alert and oriented. Vitals were as follows; BP: 127/65 mmHg, HR: 101 beats per min, RR: 24 breaths per min, T: 37-degree celsius, SatO2: 94%. Physical examination revealed that normal breathing sounds on the left side, but decreased breath sounds on the right side of the chest. No JVD noted. Other examination findings were unremarkable.

Shortness of breath and chest pain started suddenly while he was playing soccer about 30 minutes ago. Since then, shortness of breath and chest pain increased. He has no known medical disease, allergy.

Bedside ultrasound revealed pneumothorax on the right.

Bedside Ultrasound Examination

Above video shows left side B mode ultrasound examination. Investigation was done in lung settings by using Butterfly iQ portable ultrasound. Lung sliding and comet tail artefacts are seen on examination which is normal findings.

Above video shows right side B mode and M-mode ultrasound examination. There is no lung sliding or comet tail artefacts in B mode, and M-mode revealed “barcode sign” which is seen in pneumothorax.

Pneumothorax - US - Lung - M-mode

Image shows “barcode sign” in M-mode examination. 

Bedside Portable Chest X-ray

spontaneous pneumothorax 1 - 18yo male

Bedside portable anteroposterior chest x-ray shows right sided large pneumothorax.

Cite this article as: Arif Alper Cevik, "Massive Pneumothorax Without A Tension," in International Emergency Medicine Education Project, November 25, 2019, https://iem-student.org/2019/11/25/massive-pneumothorax-without-a-tension/, date accessed: September 25, 2021

Goals in Mechanical Ventilation: Concepts for the Students

Goals in Mechanical Ventilation: Concepts for the Students
Authors: Dr. Job Heriberto Rodríguez Guillén (@job_rdz), Dr. Sergio Edgar Zamora Gómez (@ezg_galeno)

Introduction

Mechanical ventilation (MV) is one of the cornerstones of life support in the emergency department. It provides time for establishing therapeutic management aimed at the triggering cause of injury until the patient improves physiologic balance (1). Therefore, MV can not be a unique and specific treatment for any disease by itself; but it has two general and fundamental goals: to support the injured lung and protect the healthy lung.

Set your goals: Support and Protect

Support

MV supports the respiratory system; meanwhile, the primary disease becomes under control.

Example: A patient with acute respiratory distress syndrome (ARDS) due to pneumonia, where MV provides support to improve gas exchange and reduce work of breathing (WOB) meanwhile antibiotic treatment induces remission of the infectious disease.

Protect

MV is aimed to avoid complications not related to the primary disease. The patient-ventilator relationship becomes of benefit for the patient as his respiratory function is in the risk of injury because the primary disease does not allow him to breathe properly or because therapeutic interventions can reduce protective airway reflexes and lead to respiratory complications.

Example: Patients presenting neuromuscular diseases (Guillain-Barre syndrome), diseases affecting bulbar muscles (myasthenic crisis), decreased consciousness (stroke, poisoning) or severe traumatic brain injury, all these without lung injury at first but in high risk of pneumonitis and pneumonia due to aspiration of gastric content.

Goals of Mechanical Ventilation
Mechanical ventilation has two general and fundamental goals: to support the injured lung and protect the healthy lung.

Specific goals of mechanical ventilation

One of the specific objectives of MV is to promote the optimization of arterial blood gases levels and acid-base balance by providing oxygen and eliminating carbon dioxide (ventilation). MV can reduce the work of breathing by taking effort from respiratory muscles and maintaining the long-term respiratory support for patients with chronic diseases.

MV´s circle (2) begins by recognizing the patient´s need for mechanical ventilatory support. Intubation and ventilation decision making is an essential skill for emergency physicians. Consideration of the patient´s needs is the basis of this decision making. The main indications for intubation and mechanical ventilation are (3):

  1. Refractory hypoxemia
  2. Increased respiratory effort
  3. Apnea/hypopnea leading to inadequate ventilation (Hypercapnia)
  4. The inability for airway protection

The goals should be individualized and established according to the clinical situation that led the patient to required ventilatory support. Although standard criteria traditionally have been specified for the onset of MV (3), we must remember that indication for intubation and ventilation is an essential skill for every physician treating critical care patients and the key is just thinking about what the patient needs.

Standard criteria for starting mechanical ventilation
Acute Ventilatory Failure
pCO2 > 50 mmHg + pH < 7.30
Impending Ventilatory Failure
Maintains normal gasometric levels by increasing respiratory effort.
Severe Hypoxemia
pO2 50%

pCO2 and pO2 values at sea level

In general, we can encompass the specific objectives of MV in three fundamental principles that must be fulfilled in every patient by setting the goals according to the primary disease:

  1. Improve oxygenation (O2) and ventilation (CO2)
  2. Reduce respiratory effort
  3. Minimize ventilator-induced lung injury (VILI)

Conclusions

The goals of MV are established based on the primary disease that led the patient to need MV support, under the concept of protecting and supporting the lungs. Primum non nocere; lung-protective ventilation should be initiated in all patients who need it.

References and Further Reading

  1. Frank Lodeserto MD, “Simplifying Mechanical Ventilation – Part I: Types of Breaths”, REBEL EM blog, March 8, 2018. Available at: https://rebelem.com/simplifying-mechanical-ventilation-part/.
  2. Frank Lodeserto MD, “Simplifying Mechanical Ventilation – Part 2: Goals of Mechanical Ventilation & Factors Controlling Oxygenation and Ventilation”, REBEL EM blog, May 18, 2018. Available at: https://rebelem.com/simplifying-mechanical-ventilation-part-2-goals-of-mechanical-ventilation-factors-controlling-oxygenation-and-ventilation/.
  3. Scott Weingart. EMCrit Lecture – Dominating the Vent: Part I. EMCrit Blog. Published on May 24, 2010. Accessed on August 30th 2019. Available at [https://emcrit.org/emcrit/vent-part-1/ ].
Cite this article as: Job Guillen, Mexico, "Goals in Mechanical Ventilation: Concepts for the Students," in International Emergency Medicine Education Project, September 2, 2019, https://iem-student.org/2019/09/02/goals-in-mechanical-ventilation-concepts-for-the-students/, date accessed: September 25, 2021