References

Adam S, Osbourne S. Critical Care Nursing.Oxford, UK: Oxford University Press; 2005

Allman KG, McIndoe AK, Wilson IH. Emergencies in Anaesthesia, 2nd ed. Oxford: Oxford University Press; 2009

Amerman EC Human Anatomy and Physiology.Chicago Press, USA: Pearson Publishers; 2016

Cornet AD, Kooter AJ, Peters MJ, Smulders YM. The potential harm of oxygen therapy in medical emergencies. Crit Care. 2013; 17:(2)

Hagberg CA. Benumof's Airway Management, 2nd ed. Philadelphia: Mosby Elsevier; 2007

Hall JE. Guyton and Hall textbook of medical physiology, 12th ed. Philadelphia: Elsevier Saunders; 2011

Knudsen K, Högman M, Larsson A, Nilsson U. The best method to predict easy intubation: a quasi-experimental pilot study. J Peri-Anaesthesia Nurs. 2014; 29:(4)292-297

Law JA, Broemling N, Cooper RM The difficult airway with recommendations for management--part 2--the anticipated difficult airway. Can J Anaesth. 2013; 60:(11)1119-1138

Lumb AB. Nunn's applied respiratory physiology, 7th ed. Edinburgh: Churchill Livingstone; 2010

National Institute for Health and Care Excellence. Pulmonary Embolism. 2007. https//cks.nice.org.uk/pulmonary-embolism (accessed December 2017)

Patton KT, Thibodeau GA. Anatomy & physiology, 8th ed. St Louis: Elsevier; 2013

Riedel M. Education in Heart: venous thromboembolic disease; Acute pulmonary embolism 1: pathophysiology, clinical presentation and diagnosis. Heart. 2001; 85:(2)229-240

Tortora GJ, Derrickson BH. Principles of Anatomy and Physiology, 14th ed. New Jersey: John Wiley & Sons; 2014

Continuing Professional Development: Vital airway management skills when treating a pulmonary embolism

02 January 2018
Volume 10 · Issue 1

Abstract

Overview

A pulmonary embolism (PE) is an occlusion of the pulmonary artery that occurs because of a thrombus originating from a deep vein thrombosis. In this CPD module, we will highlight key steps in performing respiratory assessment of a patient with PE, and outline paramedic treatment and management of this condition. A PE results in ventilation with a reduced perfusion. Early intervention to maintain the airway and facilitate oxygen delivery can reduce PE-associated mortality.

LEARNING OUTCOMES

After completing this module, the paramedic will be able to:

  • Provide a definition of pulmonary embolism (PE)
  • Identify the common causes of PE
  • Identify the key steps in performing a respiratory assessment in PE
  • Outline how the paramedic can treat and manage a patient with a PE
  • If you would like to send feedback, please email jpp@markallengroup.com

    A 999 call was received for a 54-year-old female collapsed in a public toilet, cardiopulmonary resuscitation (CPR) in progress. On arrival, you and a colleague are met with a patient who is unresponsive and a security guard performing CPR.

    After assessing the patient, your colleague immobilises the c-spine. The patient is unresponsive to voice and stimuli, the airway is clear and unobstructed, but the respiratory rate is 0 breaths per minute, with no rise and fall of the chest for 10 seconds.

    After asking the security guard to continue compressions at a rate of 30 compressions to 2 inflations, you secure the airway using a size three supraglottic airway device (i-gel) and a bag-valve mask, attached to 100% O2.

    Your colleague applies the defibrillator patches and you note the presence of electrical activity; you find that the patient has a pulse, at a rate of 68 beats per minute. Chest compressions are discontinued and you continue ventilating the patient once every 6 seconds.

    You make the decision to move the patient to the ambulance and secure the patient's airway further using a stepwise approach, with a size six endotracheal tube, secured with ribbon gauze.

    The patient is immobilised on a spinal board and transported to the rear of the ambulance where she is placed on the stretcher and secured. On the way to the hospital, ventilations are continued throughout—one ventilation every 6 seconds— and her vital signs monitored until arrival to the emergency department (ED). In addition, you obtain a full set of observations (Table 1) and the following clinical information: 2 days previously, the patient returned from overseas on a long-haul flight and was complaining of sharp chest pains and difficulty breathing the morning of the collapse.


    Blood pressure 90/50 mmHg
    Pulse rate 105 (regular)
    Respiratory rate 22 breaths/minute
    Tympanic temperature 37.8 C°
    SpO2 87% on air
    Random blood glucose 12.1. mmols/litre

    The presence of Homan's sign (calf pain at dorsiflexion; calf swollen and ‘warm’) leads you to diagnose a deep vein thrombosis (DVT) and along with the patient's recent travel and collapse, you suspect a pulmonary embolism (PE).

    Airway anatomy and physiology

    The airway is divided into two broad sections: the upper and lower airways. In the case of airway management, it is vital that the paramedic has a good working knowledge of the anatomy and physiology of the upper airway (Figure 1). Normal natural breathing occurs through the nose for a number of reasons, with the structures within the nasal passage and nasopharynx being the most important. Within the nasal passage, structures called turbinates moisten and humidify the air that is breathed in before it travels into the lower airway, ensuring that inspired air is warmed when it reaches the lower airway (Tortora and Derrickson, 2011). Without this mechanism, inspired air would be cold and have a profound effect on core body temperature. In order to humidify inspired air during normal breathing, the turbinates will use 1 litre of fluid a day (Hagberg, 2007). Therefore, patients in respiratory failure, such as chronic obstructive pulmonary disease (COPD), will use a great deal more fluid. Unfortunately, owing to the difficulty patients with COPD have when drinking while breathless, they tend to be chronically dehydrated.

    Figure 1. Anatomy of the airway

    The undulated surfaces within the nose cause a great deal of turbulence in the air that is inspired, enabling particles within the inspired air to become trapped on the hairs and mucous that line the nasal passage and pharynx (Hall, 2011). This is a protective mechanism ensuring that infectious particles are filtered out of the air before entering the trachea. However, mouth breathing is adopted when an individual needs to inspire and expire greater volumes of air, in situations such as exercise or respiratory distress (Tortora and Derrickson, 2011). This rapid breathing increases air flow, leading to infectious particles being suspended in the inspired air for longer, and enabling them to penetrate deeper into the lung, increasing the risk of lower respiratory infections (Lumb, 2010). This is another possible reason individuals who suffer from asthma or COPD are prone to respiratory infections.

    Moving further back in the upper airway, a wall of muscle makes up the posterior structure. This wall is the pharynx and is divided into three areas:

  • The nasopharynx, situated posteriorly to the nose
  • The oropharynx, the back of the oral cavity
  • The laryngopharynx, connecting the larynx and the oesophagus (Hall, 2011).
  • It is worthy to note that the palatine and lingual tonsils are situated in the oropharynx, which provides an immune response to infections or periods of illness (Patton and Thibodeau, 2013). These tonsils will of course become enlarged when activated during illness, and can become a hindrance to airway management—particularly to endotracheal intubation.

    Indeed, many other structures can lead to challenges in airway management. For instance, the degree of mouth-opening can dictate the difficulty in inserting a laryngeal mask airway (LMA) or performing endotracheal intubation (Hagberg, 2007). The size of the patient's tongue in relation to their mouth can also pose a challenge when attempting airway management. The larger the tongue, the less room there is to insert a laryngoscope and endotracheal tube. These factors can be assessed using the Mallampati classification (Knudsen et al, 2014). While this method is routinely used in planned intubations, it is unrealistic in emergency intubation within paramedic practice. Therefore, children and patients with Down's syndrome can be difficult to intubate, and this must be anticipated. When attempting endotracheal intubation, the optimal position is achieved by extending the patient's neck. This is done as a result of the upper airway having three axes:

  • The oral axis
  • The laryngeal axis
  • The tracheal axis (Hagberg, 2007).
  • When the head is in a neutral position, the oral axis is perpendicular to the pharyngeal and tracheal axis; extending the neck dramatically reduces this perpendicular angle. This aligns the three airway axes and can provide a more or less straight view from the mouth to the larynx with the assistance of a laryngoscope.

    The larynx itself is made up of nine cartilages and connects the laryngopharynx and trachea. The most important structures of note within the larynx during intubation are the epiglottis; the true vocal chords; and corniculate cartilage. The epiglottis is a flap of tissue that covers the opening to the trachea (glottis) during swallowing, thus protecting against aspiration (Tortora and Derrickson, 2011). Anterior to the epiglottis and at the base of the tongue is a space called the vallecular; it is in this space that the tip of a laryngoscope is placed in order to lift the mandible and tongue forward to enable endotracheal intubation. It is important that the patient is pharmacologically paralysed prior to intubation in order to relax the vocal chords—this enables both easy passage of an endotracheal tube into the trachea and reduces the risk of vocal cord injury (Allman et al, 2009).

    Airway assessment

    The ability to correctly diagnose a PE necessitates a thorough respiratory assessment. The quickest assessment of whether an airway is clear or not is to ask the patient a question. A normal verbal response from the patient immediately informs the assessor that the patient has a patent airway, is breathing and is perfusing his/her brain (Law et al, 2013). If the patient can only speak in short sentences or with one or two words, they are in respiratory distress and require a further in-depth assessment of their respiratory function.

    Airway assessment should also involve a visual assessment for airway obstructions, such as foreign bodies; vomit; secretions; or facial, mandible and laryngeal fractures. One of the most common causes of airway obstruction is an altered level of consciousness—this will cause the mandible and oropharyngeal muscles to relax and collapse over the larynx, thus obstructing the airway. Providing there is low suspicion of cervical spine injury, a ‘head tilt chin lift’ should be performed to open the airway. However, if there is a suspicion of cervical spine injury, a jaw thrust should be used and consideration given to protecting the cervical spine.

    In addition to these airway manoeuvres, a compromised airway can be maintained using an artificial airway, such as a guedel airway. A severely compromised airway can be treated by intubation and in, certain circumstances, cricothyroidotomy and emergency tracheotomy.

    Breathing assessment

    Breathing assessment is required to ascertain the patient's ability to adequately ventilate. The first step is to observe the patient and simply watch how they breathe. This aspect of assessment is termed inspection, with clinical staff adopting a logical progression of inspection, palpation, percussion and auscultation. What this means for paramedics is observe (look), feel and listen.

    Observations

    When assessing a patient's respiratory system, it is important that the paramedic make a number of important observations (Table 2). The paramedic should look for effective, equal and bilateral chest wall expansion without any paradoxical movements, which includes:

  • Observing only one side of the chest moving up and down
  • Greater movement of one side of the chest when compared with the other
  • One side of the chest moving up and the other side moving down.

  • Colour The colour of the patient's skin and mucus membranes is a useful indicator of haemoglobin saturation. Noting that cyanosis is a late indicator of hypoxia.
    Ability to speak Increased effort to speak and/or inability to speak as well as only being able to speak in monosyllables indicates respiratory distress.
    Use of accessory muscles A patient who is in respiratory distress uses additional muscles to breathe. These include, sterno-mastoid, scalene and abdominal muscles. With advanced training the paramedic should be able to assess whether a patient is using these additional muscles or not.
    Rate, rhythm and depth of breathing The paramedic should assess whether the patient's respiratory rate is above or below normal level. In an emergency situation, it is difficult to assess lung volumes, so observing depth of breathing is an important indicator.
    Shape and expansion of chest When performing a respiratory assessment it is important to consider both the shape and expansion of the chest. For example, the anteroposterior diameter may change for a number of reasons and not just because of an underlying respiratory problem.

    Any asymmetrical chest expansion is abnormal and any form of unilateral lung or pleural disease can cause this asymmetry of chest. Unilateral chest expansion can indicate a pneumothorax which is a life-threatening situation necessitating urgent intervention. Furthermore, any of these observations might indicate respiratory disease/pathology. When undertaking a respiratory assessment, it is not only important to consider the points mentioned in this section, but also to perform and record vital signs.

    Oxygen saturation monitoring

    Blood oxygen saturations look at the haemoglobin (Hb) in the red blood cells (erythrocytes), and measure the extent to which the haemoglobin molecule is bound to oxygen—that is, how ‘saturated’ the haemoglobin molecule is with oxygen. Normally, a person's saturation value is between 98 and 100% (Cornet et al, 2013). Oxygen saturations below normal are referred to as hypoxaemia.

    An effective way to monitor for hypoxaemia is to use a pulse oximeter. This is a good bedside monitor, but its limitations should be recognised, as use on a peripherally cold patient will provide inaccurate readings. Therefore, it may be necessary to use an ear probe to obtain accurate readings. In order to obtain successful readings of O2 saturation, the probe should be placed in the best possible position. There are a number of places where the probe can be attached and these include:

  • Fingers
  • Toes
  • Ears
  • Nose.
  • As noted, a person's O2 saturation (SpO2) will normally range between 98% and 100% (Adam and Osbourne, 2005). However, saturations will fall in many respiratory conditions, including a PE. It is therefore necessary to maintain oxygen saturation as near to normal as possible. In most circumstances, the trend in oxygen saturation is more important than the value per se, as this can indicate whether the patient is responding to therapy or deteriorating.

    Furthermore, it is a continuous and non-invasive monitor. Its principal limitation is in patients who are receiving supplemental oxygen; it will not reliably detect hypoventilation. Hypoventilation must, in the clinical environment, usually be confirmed by measurement of the PaCO2, which paramedics currently don't record.

    Respiratory management skills

    Any deviations discovered during the basic respiratory assessment will need to be acted upon promptly. One of the very first and most basic respiratory management skills essential for good patient care is oxygen therapy. In combination with respiratory assessment and oxygen saturation monitoring, if a patient requires oxygen, it needs to be administered safely and effectively. Therefore, paramedics need to:

  • Know when to initiate oxygen therapy
  • Know how to deliver oxygen safely and appropriately
  • Base oxygen delivery upon patient needs.
  • Administering oxygen

    If a patient's condition necessitates the administration of oxygen, this should be carried out as quickly and as efficiently as possible. Although technically and legally, oxygen is a drug that must be prescribed by a qualified practitioner, in the emergency situation, the absence of a prescription should not delay the administration of this essential intervention. Once the decision to administer oxygen has been made, an appropriate oxygen delivery device will need to be used. There are two types of oxygen delivery system—variable performance and fixed performance.

    Pathophysiology of PE

    A PE is essentially an occlusion in the pulmonary artery—the main blood vessel that carries blood from the heart to the lungs. This occlusion happens because of the presence of an embolus (thromboemboli) that often originates from a thrombus elsewhere in the body, usually the veins of the legs or pelvis (see Clarification Box).

    ‘Thrombotic’ pulmonary embolism, therefore, is not an isolated disease of the lungs; rather, it is a complication of venous thrombosis formation and the development of thromboemboli. These thromboemboli will ultimately travel through the right side of the heart, and up into the pulmonary arteries, eventually occluding. Evidence of leg DVT is found in about 70% of patients who have sustained a PE. As a PE is preceded by DVT, the factors predisposing the two conditions are the same and broadly fit ‘Virchow's Triad’ of venous stasis, injury to the vein wall and/or enhanced coagulability of the blood (Amerman, 2016). DVT and PE are therefore parts of the same process; the development of a venous thromboembolism and thromboemboli formation, with subsequent pulmonary artery occlusion (Riedel, 2001).

    The blockage/occlusion of the pulmonary arteries accounts for the ‘classic’ presentation of a PE, these being the abrupt onset of pleuritic chest pain; shortness of breath; and hypoxia. Note, however, that it is possible for patients with a PE to have no obvious symptoms at initial presentation.

    The effects of a PE, especially the extent of hypoxaemia, depend on the level to which thromboemboli occlude the pulmonary artery; the duration over which this occlusion occurs; and any pre-existing medical history the patient may have.

    Small thromboemboli may have no acute physiologic effects and may begin to lyse immediately, resolving within hours or days. Larger thromboemboli, however, can cause a reflex increase in ventilation (tachypnea); hypoxaemia caused by ventilation/perfusion (V/Q) mismatch; low mixed venous oxygen content as a result of low cardiac output; and atelectasis owing to alveolar hypoxaemia. In addition, there are also abnormalities in surfactant, and an increase in pulmonary vascular resistance (Amerman, 2016).

    The primary pathophysiological mechanism for the hypoxaemia seen in PE is a V/Q mismatch. This is a defect that occurs in the lungs, whereby ventilation (exchange of air between lungs and environment) and perfusion (passage of blood through lungs) are not evenly matched. A normal V/Q ratio value is 0.8. A low V/Q relationship indicates a ventilation problem, whereas a high V/Q relationship indicates a perfusion or CVS problem. Thus, in primary lung diseases such as pneumonia and COPD, the V/Q ratio moves down, towards zero. Where there is adequate respiratory function and ventilation but reduced blood-perfusion, the V/Q ratio moves up, towards infinity.

    A PE V/Q mismatching occurs because of:

  • Intrapulmonary shunting, where un-embolised areas of the lung are relatively over-perfused, so that the ventilation in these areas may be insufficient to fully oxygenate the extra blood flow. Intrapulmonary shunting also occurs through areas of lung collapse and infarction where, again, there is some blood flow but reduced ventilation owing to infarcted lung tissue.
  • An increase in ‘dead space’, defined as an area of lung where gaseous exchange cannot take place. In a PE—because some areas of the lung are underperfused—there is a relative increase in ventilation. However, because this ‘ventilated’ lung cannot facilitate gaseous exchange (because of the reduced blood supply), this leads to an increase in respiratory ‘dead space’.
  • Clarification Box. Thrombus vs. embolus

    A thrombus is a solid mass of platelets and/or fibrin

    An embolus is a piece of a thrombus that has broken free

    The ECG in PE

    The electrocardiogram (ECG) changes associated with acute PE may be seen in any condition that causes acute pulmonary hypertension, including hypoxia, causing pulmonary hypoxic vasoconstriction. In a PE—because the blockage/occlusion of the pulmonary arteries by thromboemboli causes acute pulmonary hypertension—the ECG can show evidence of acute cor pulmonale/right ventricular strain pattern (inverted T-waves) and right-axis deviation (with axis between 0 and -90o). The ‘classic’ SI QIII TIII pattern (a prominent S-wave in lead I and a Q-wave and inverted T-wave in lead III) can result from any cause of acute cor pulmonale including acute bronchospasm, pneumothorax and other acute lung disorders, and is not specific to PE.

    Conclusion

    Airway management is a vital and important skill that all paramedics should possess, and one that plays an important role in the care and management of a PE. Skill in managing a patient's airway forms part of the core emergency skills that the National Institute for Health and Care Excellence (NICE) (2007) has identified as essential for all clinicians. All paramedics should also be competent in performing a respiratory assessment using the look, feel and listen principles.

    Based upon the assessment, paramedics should be able to implement appropriate airway management strategies as outlined in the current CPD article. Using these skills, patients will receive appropriate respiratory care quickly, efficiently and effectively.