The airway is divided into two broad sections, namely the upper and lower airway. 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. Normal natural breathing occurs through the nose, this is for a number of reasons. One of the most important reasons is the role of structures within the nasal passage and nasopharynx. Within the nasal passage, structures called turbinates moisten and humidify the air that is breathed before it travels into the lower airway, this ensures that inspired air is warmed when it reaches the lower airway (Tortora and Derrickson, 2014). 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, but unfortunately due to the difficulty they have to drink while breathless they tend to be chronically dehydrated.
The undulated surfaces within the nose cause a great deal of turbulence in the air that is inspired, this enables particles within the inspired air to become trapped on hairs and mucous that line the nasal passage and pharynx (Hall, 2011). These offer a protective mechanism, ensuring that infectious particles are filtered out of the air before it enters 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, 2014). This rapid breathing increases air flow, which leads to infectious particles being suspended in the inspired air for longer, and penetrate deeper into the lung, increasing the risk of lower respiratory infections (Lumb, 2010). Again this is one possible reason individuals who suffer from asthma or COPD are prone to respiratory infections. One other primal reason for nose breathing is to enable a human to smell for predators while they eat (Hagberg, 2007).
Moving further back in the upper airway, a wall of muscle makes up the posterior structure of the airway; this wall is called the pharynx and is divided into three areas. The nasopharynx is situated posteriorly to the nose, the oropharynx is the back of the oral cavity, while the laryngopharynx connects 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), which correlates tongue size to pharyngeal size, with a classification being assigned according to the extent the base of the tongue is able to mask the visibility of pharyngeal structures. While this method is routinely used in planned intubations, it is obviously unrealistic in emergency intubation within paramedic practice. Therefore patients with Down's syndrome and children can be difficult to intubate, and this must be anticipated when attending to these patients. When attempting endotracheal intubation the optimal position is achieved by extending the patient's neck. This is done due to the fact that the upper airway has three axes, these are the oral axis, laryngeal axis and 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 with the assistance of a laryngoscope provides a more or less straight view from the mouth to the larynx.
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, 2014). Anterior to the epiglottis and at the base of the tongue is a space called the vallecular, and 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).
Case Study 1
You and a colleague attend an emergency call to Mr Harrison, a 55-year-old teacher. Mr Harrison visited his GP 3 days ago with shortness of breath on exertion. This was causing him to rest after walking 10–15 metres, having previously had no problems with exercise. He has no cough but complains of a sharp right-sided chest pain which ‘gets worse’ on inspiration. He stated that he had recently taken a flight back to London from Hong Kong after a holiday with his wife.
Mr Harrison is overweight at 130 kg and measures 180 cm in height. Aside from suffering mild arthritis, he has no significant past medical history. Initially his GP believed he was suffering from a viral illness but this morning his wife phoned for an ambulance because his condition had ‘quickly deteriorated’.
On arrival you obtain a full set of observations (see below) and the following clinical information: he is quite uptight and is tachypnoeic and sweating. His jugulour venous pressure cannot be seen. The test for the presence of Homan's sign is positive, with his left leg being swollen, painful and hot to touch. He has evidence of peripheral cyanosis.
| Blood pressure | 90/50 mmHg |
| Pulse rate | 105 (regular) |
| Respiratory rate | 22 per minute |
| Tympanic temperature | 27.8°C |
| Oxygen saturation | 87% on air |
| Random blood glucose | 12.1 mmol/L |
The presence of Homan's leads you to diagnose a deep vein thrombosis (DVT) and along with Mr Harrison's recent travel and GP visit you suspect a pulmonary embolism (PE).
Lung physiology
The main role of the pulmonary system is to enable gas exchange, this involves the movement of oxygen into the pulmonary circulation and the removal of carbon dioxide for exhalation. In order for this process to occur there needs to be a number of functional factors in place. Essentially gas exchange relies on adequate ventilation of the alveoli, a functioning respiratory membrane and perfusion of the pulmonary circulation (Lumb, 2010).
Alveolar ventilation is dependent upon adequate depth and rate of breathing, measured as tidal volume (Tv) and rate (RR), respectively (Raoof et al, 2009). These two factors can be multiplied to calculate minute volume (MV) as follows:
Tv x RR = MV
Reductions in either Tv or RR will result in impaired ventilation and therefore have an effect on gas exchange.
During ventilation the alveoli will contain a mixture of gases, namely nitrogen, oxygen and carbon dioxide, all of which exert a pressure onto the alveolar membrane playing a part in maintaining alveolar opening (Tortora and Derrickson, 2011). Cells within the alveolar walls, called type II pneumocytes, secrete surfactant which reduces the surface tension on the alveolar membrane (Hall, 2011). Surface tension exists in any air and water interface; that is, water will have a ‘surface’ when it is facing air. This surface has a tension which pulls the water molecules together, surfactant reduces this tension thus keeping the alveoli open, a loss of surfactant would result in alveolar collapse (Lumb, 2010). Maintaining alveolar opening is fundamental in gas exchange, as open alveoli results in a large surface area for gas exchange to occur. Any losses of surface area will have a detrimental effect on gas exchange, resulting in hypoxia and hypercapnia.
Further to surface area, the respiratory membrane, which is the alveolar membrane and pulmonary capillary membrane, is fundamental to gas exchange, with issues such as minimal diffusion distance from alveoli to capillary being influential in gas exchange (Lumb, 2011). Any increases in diffusion distance due to tissue oedema will have an adverse effect on gas exchange, as oxygen has a low potential to dissolve in fluid and therefore will not cross into the capillary very effectively (Hall, 2011).
As previously mentioned, the need for adequate perfusion of the pulmonary circulation is fundamental to ensure effective gas exchange. The rate of perfusion essentially depends on cardiac output (CO), which is reliant on stroke volume (SV) and heart rate (HR), which can be expressed as follows:
SV x HR = CO
70 x 72 = 5040 ml
Perfusion is dependent on adequate circulating volume, with blood loss having obvious detrimental effects on perfusion. Furthermore, the flow of blood though the pulmonary system is vital to ensure that adequate volumes of deoxygenated haemoglobin passes through, thus maintaining a concentration gradient for oxygen to pass from alveoli into the circulation. If the flow is too fast the haemoglobin will pass through the pulmonary system too rapidly to allow full saturation with oxygen. If on the other hand the flow is too slow, the haemoglobin will become fully saturated, but the supply to tissue will be too slow to meet demand (Lumb, 2011). Both these situations will obviously lead to hypoxia.
The relationship between ventilation (V) and perfusion (Q) can be calculated via the V/Q relationship. Perfusion (i.e. CO) is normally 5 litres/min, while ventilation is 4 litres/min (Glenny, 2008). By dividing these two figures the V/Q ratio can be established:
V ÷ Q = V/Q
4 ÷ 5 = 0.8
0.8 is considered a normal V/Q ratio and would ensure optimal gas exchange, but any reductions in either figure will have effects:
Pulmonary obstruction due to pulmonary embolus
4 ÷ 1 = 5
In this example ventilation remains unchanged as the PE only affects the perfusion aspect, therefore the V/Q ratio increases.
Pneumonia
3 ÷ 5 = 0.4
In pneumonia on the other hand, ventilation is affected by the pneumonic area of lung, perfusion is unchanged, but the V/Q ratio is reduced.
Airway assessment
The ability to correctly diagnose a PE necessitates a thorough respiratory assessment. The quick 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 (Bernsten and Soni, 2013). If the patient can only speak in short sentences or with one or two words then 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 suspicion of cervical spine injury a jaw thrust should be used and consideration given to protecting the cervical spine.
In addition to the airway manoeuvres mentioned above a compromised airway can be maintained by using an artificial airway, such 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. In medical terms 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. These are listed in Table 1.
| Colour | The colour of the patient's skin and mucus membranes is a useful indicator of haemoglobin saturation. Note 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 and 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 (AP) diameter may change for a number of reasons and not just because of an underlying respiratory problem. |
The paramedic should look for effective, equal and bilateral chest wall expansion without any paradoxical movements. Paradoxical movements might include:
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. Further, any of these observations might indicate respiratory disease/pathology.
When undertaking a respiratory assessment it is not only important to consider the above but also to perform and record vital signs.
Oxygen saturation monitoring
Blood oxygen saturations looks at the haemoglobin (Hb) in the red blood cells (erythrocyte) and measures 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 98–100% (Cornet et al, 2013). Oxygen saturations below normal is 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. Thus it may be necessary to use an ear probe to obtain accurate readings. In order to obtain O2 saturations successfully, the probe should be placed in the best possible position so as to obtain the best possible reading. There are a number of places where the probe can be attached and these include:
Normally a person's O2 saturation (abbreviated as SpO2) will range between 98%–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 that, 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 partial pressure of carbon dioxide, which currently paramedics don't record.
Paramedic management of pulmonary embolism
Essentially the management of a PE in the pre-hospital setting is one of symptom management and rapid transfer to a treatment facility. It is important to emphasise that PE is a time-critical condition that must be treated definitively as a matter of urgency, therefore it is imperative that an alert/information call is made on scene (Association of Ambulance Chief Executives (AACE), 2016). Furthermore, the patient suffering a PE is at significant risk of cardiac arrest at any time, so this should be anticipated when attending to the patient (Resuscitation Council (UK), 2011).
The initial management on scene is one of managing life-threatening ABDE issues. First and foremost the airway needs to be managed and oxygen will need to be administered at high flow with the aim of maintaining SpO2 94–98% (AACE, 2016). Achieving this may be problematic depending on the size and location of the PE. Patient positioning may improve the patient's breathing; however, the paramedic needs to be mindful of postural hypotension when sitting the patient upright (Mulryan, 2011). In the case of a patient who is displaying signs of airway compromise and/or inadequate ventilation, intubation should be performed and artificial ventilation should be instigated.
Further to airway and respiratory issues the patient will be experiencing cardiac issues due to the PE dramatically increasing mean pulmonary arterial pressure. This will usually manifest as right-sided ischaemia or simply tachycardia, therefore a 12-lead ECG can be a useful diagnostic tool in preparation for arrival to hospital (AACE, 2016). If the patient is showing signs of significant hypotension (systolic blood pressure ≤90 mmHg), intravenous fluid should be given to support blood pressure.
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 that of oxygen therapy. In combination with respiratory assessment and oxygen saturation monitoring, if a patient requires oxygen, then this needs to be administered safely and effectively. Therefore, paramedics need to know when to initiate oxygen therapy, how to deliver oxygen safely and appropriately and base oxygen delivery upon patient needs.
Administering oxygen
If a patient's condition necessitates the administration of oxygen, then 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 utilised. There are two types of oxygen delivery system: variable performance and fixed performance
Pathophysiology of pulmonary embolism
Essentially, a PE is 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 originate from a thrombus elsewhere in the body, usually the veins of the legs or pelvis. (See clarification box, below).
| A thrombus is a solid mass of platelets and/or fibrin |
| An embolus is a piece of thrombus that has broken free |
‘Thrombotic’ pulmonary embolism, therefore, is not an isolated disease of the lungs but a complication of venous thrombosis formation and the development of thromboemboli. These thromboemboli ultimately travel through the right side of the heart and up into (and eventually occluding) the pulmonary arteries. 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 to 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, 2015). 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 extent to which thromboemboli occludes 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 and resolve within hours or days. Larger thromboemboli, however, can cause a reflex increase in ventilation (tachypnoea), hypoxaemia due to ventilation/perfusion (V/Q) mismatch, and low mixed venous oxygen content as a result of low cardiac output, atelectasis due to alveolar hypocapnia. Additionally, there is also abnormalities in surfactant, and an increase in pulmonary vascular resistance (Amerman, 2015).
The primary pathophysiological mechanism for the hypoxaemia seen in PE is a ventilation–perfusion (V/Q) mismatch. A V/Q mismatch is a defect that occurs in the lungs whereby ventilation (the exchange of air between the lungs and the environment) and perfusion (the passage of blood through the lungs) are not evenly matched. A normal V/Q ratio value is 0.8. Lower than that indicates a respiratory disease, higher a perfusion or cardiovascular disease. Thus, in primary lung diseases such as pneumonia and COPD the V/Q ratio moves down, towards zero (0). Where there is adequate respiratory function and ventilation but reduced blood-perfusion the V/Q ratio moves up, towards infinity.
In a PE V/Q mismatching occurs because of i) intrapulmonary shunting, where un-embolised areas of the lung are relatively over-perfused, so that the ventilation in these areas may be insufficient to oxygenate fully 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 due to infarcted lung tissue. V/Q mismatching in PE can also occur because of ii) 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 provide gaseous exchange (because of the reduced blood supply), this leads to an increase in respiratory dead space.
The ECG in pulmonary embolism
The ECG changes associated with acute pulmonary embolism 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 zero and -90 degrees). 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 so is not specific to PE.
Conclusions
Pulmonary embolism is one of the most preventable deaths in the UK and paramedics play a crucial role in its identification and initial management.
In order to treat a pulmonary embolism in an emergency situation within the community, paramedics must be competent in performing a comprehensive and thorough respiratory assessment, in order to recognise the condition's specific signs and symptoms. Because pulmonary embolisms are most commonly caused by deep vein thrombosis, other physical assessment and history-taking skills are also required, especially noting hydration status and the physical condition of the lower limbs.
Having performed an appropriate assessment, paramedics are then able, and are best placed, to initiate oxygen therapy and facilitate fast transport to hospital.
Once the paramedic fully understands the pathophysiology of a pulmonary embolism and how a pulmonary embolism presents clinically, pulmonary embolism symptom identification can be enhanced and patient care improved.
LEARNING OUTCOMES
After completing this module you should be able to:
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