LEARNING OUTCOMES
After completing this module, the paramedic will be able to:
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You are called to a 65-year-old female, who has a painful leg. Upon arrival, you are greeted by the patient's husband who takes you inside the house. The patient is sat up in bed and reports waking up this morning with acute lower left leg pain, about which she had become increasingly concerned prior to a GP appointment later that afternoon. The patient also complains of some shortness of breath on exertion. Upon clinical assessment you observe the following:
From the clinical assessment, you suspect that the patient has a potential pulmonary embolism (PE). Treatment is initiated with high-flow oxygen therapy, intravenous cannulation and rapid transportation to the nearest emergency department. En route, the patient appears to deteriorate and you believe that cardiac arrest is likely. You inform the hospital staff, who have a team waiting for your arrival.
Pathophysiology
PE is a potentially life-threatening condition, which presents with a variety of non-specific clinical symptoms (Torbicki, 2010; Peate and Jones, 2014). The true incidence of PE remains unclear, with statistics in the literature ranging from 21/10 000 population to 20–70/100 000 population (Kurt et al, 2018; Joint Royal Colleges Ambulance Liaison Committee (JRCALC), 2016).
Evidence suggests that PE is commonly misdiagnosed and often only found upon post-mortem examination (Kurt et al, 2009). Peate and Jones (2014) identify a PE as an obstruction within the pulmonary circulation. York et al (2015) further describe an embolus as a foreign body within the circulatory system, with the most common being:
A breakdown of risk factors associated with thrombus and emboli formation, otherwise referred to as Virchow's triad, is given in Figure 1. It has been noted that a thrombus is most commonly seen in PE (York et al, 2015). Blood clots form in the deep leg veins, as a result of a period of immobility, increased coagulopathy of blood, or the occurrence of blood vessel disorders (Peate and Jones, 2014). In patients with varicose veins, the stagnated blood flow around valves can lead to clot formation, which is similar to that seen in the turbulent blood flow in the atria of patients with atrial fibrillation. When a blood clot becomes dislodged, it can travel through the systemic circulation and enter the right side of the heart. The blood clot can then continue to travel with de-oxygenated blood into the pulmonary circulation. It is where the vessels narrow from the pulmonary artery, through the arterioles and capillary beds that the clot can become trapped, causing an occlusion (Peate and Jones, 2014).
As a result of the occlusion, blood will begin to back up into the pulmonary circulation. Depending upon the size and location of the clot, this will then lead to a back-up of blood into the right ventricle, which will be under increased strain to effectively pump blood through the pulmonary circulation. Hypoxia will be present in patients with a significant PE, where deoxygenated blood returns in the pulmonary circulation to the left side of the heart.
Furthermore, the occlusion will cause the release of a number of hormones including histamine, angiotensin II and other inflammatory mediators—all of which increase vasoconstriction in the pulmonary circulation, thus impeding blood flow. This, coupled with the back flow of blood will increase the pulmonary artery pressure, and increase strain on the right side of the heart in order to maintain cardiac output (McCance and Heuther, 2006).
The level at which the clot becomes occlusive will have an effect on the patient presentation. For example, a large clot which occludes the pulmonary artery will almost always result in rapid deterioration and death; whereas a clot which occludes a small vessel, or even a capillary, will present with subtle signs and symptoms. Patients can also present with multiple small PEs, which is a condition normally only detected on a computed tomography (CT) scan or post mortem (Edwards and Sabato, 2009).
Clinical presentation in PE
Patients frequently present with non-specific signs and symptoms, and diagnosis is based upon a thorough clinical assessment and history. Common signs and symptoms are listed in Box 1. However, when considering the underlying pathophysiological processes, clinicians should be able to identify suspected cases with a degree of certainty. This is dependent upon the patient being a good historian and the drawing together of clinical information with sound clinical reasoning skills.
| Unexplained tachycardia |
| Unexplained tachypnoea |
| Dyspnoea |
| Chest pain (increased on inspiration and often sharp in nature) |
| Referred pain—shoulder tip |
| Low SpO2 / tissue hypoxia Severe cyanosis in large PE prior to arrest |
| Hypotension |
| Ventilation/perfusion mismatch (low ETC02) |
| ECG changes (S1, Q3, T3—this is uncommon) |
| Red/swollen/painful calf (i.e. Homan's sign) |
| Anxiety |
| Cardiogenic shock |
Cyanosis Kurt et al, 2010; Marshall et al, 2010; Peate and Jones, 2014; York et al, 2015
Cardiogenic shock
The right side of the heart is under increased strain as a result of vasoconstriction in the pulmonary circulation, back flow of blood, and increased pulmonary artery pressure. To maintain an effective cardiac output, the heart rate begins to increase, in an attempt to pump more blood through the pulmonary circulation and around the body. The systemic response to this manifests as cardiogenic (obstructive) shock. An increased heart rate and narrowing pulse pressure is evident; an unexplained tachycardia may be the only sign present. As shock progresses, cardiac output can no longer be sustained by the failing heart and, in the late stages, the patient will present as bradycardic and hypotensive.
In larger PEs, gaseous exchange in the capillary beds and alveoli becomes impaired and hypoxia will ensue (Marshall et al, 2010). A mismatch develops between the ventilation and perfusion rates, together with increased physiological dead space owing to poorly perfused and under-ventilated lung tissue (Marshall et al, 2010). This is also known as a ventilation/perfusion (V/Q) mismatch. This in turn reduces the amount of carbon dioxide that is exchanged for oxygen, resulting in two effects: decreased oxygen intake and decreased expired carbon dioxide. Clinically, the patient will therefore present as hypoxic, with hypocapnia.
As CO2 is the byproduct of aerobic metabolism, if the amount of CO2 expired by the lungs decreases (ETCO2), as in a PE, there will be, and must be, a subsequent initial increase in intravascular CO2. This rise is intravascular CO2 may subsequently increase respiratory rate to compensate, leading to ‘normal’ or (if treatment isn't sought) low blood CO2 level.
In a study conducted by Kurt et al (2009), capnography was found to have a 70% sensitivity rate in patients with PE, which suggests a degree of diagnostic ability when used accurately. However, it must also be considered that a patient with increased respiratory rates will also likely be hypocapnic. ETC02 monitoring should therefore be used in conjunction with other clinical examinations to aid the diagnosis of a potential PE in pre-hospital care (Kurt et al, 2009).
Tachypnoea
An increased respiratory rate will occur as a result of the physiological processes associated with cardiogenic shock, described in the previous section. It is noted in the literature that an unexplained tachypnoea is one of the most common signs of a PE (York et al, 2015). However, in isolation (i.e in the absence of other signs and symptoms), this can be considered a somewhat unreliable indicator for diagnosing a potential PE.
ECG changes
ECG changes in PE are uncommon, but have been reported throughout medical literature. ECG changes occur as a result of the increased strain on the right side of the heart (Hitt and Pateman, 2015). The most common patterns seen are described as S1Q3T3 and right-bundle branch block, shown in Figure 2. Acute right axis deviation will also be present on the ECG as a result of right heart strain. Clinicians should be mindful that the ECG patterns are not always apparent, and the emphasis for diagnosis should be on a thorough history-taking and clinical examination.
Pre-hospital management
There is no specific management of PE during the pre-hospital phase, with emphasis placed on diagnosis and timely transportation to an appropriate hospital. However, clinicians are able to provide symptom control to patients with suspected PE. This includes calming measures, supportive therapy and analgesia. Hospital management includes confirming diagnosis with CT scan and thrombolytic therapy (Torbicki, 2010). Thrombolysis in pre-hospital care for PE would not be appropriate because of its inability to confirm diagnosis and its associated risks.
Assessment
Serial monitoring including heart rate, ECG, respiratory rate, oxygen saturations and blood pressure should be carried out. This will enable the clinician to identify any trends in the patient, such as progressive shock (Peate and Jones, 2014). A thorough history should be obtained, which includes an assessment of any previous venous thromboembolism, PE, associated family history and assessment of risk factors as outlined by Virchow's triad in Figure 1 (Wilbeck and Evans, 2015).
The Wells score (Figure 2) (Wilbeck and Evans, 2015; York et al, 2015; JRCALC, 2016) is a tool that can be used to identify the probability of a PE, and can be applied in the pre-hospital field. Although the literature to validate the use of Wells score in pre-hospital care appears sparse, York et al (2015) identify that the criteria are based around the signs, symptoms and risk factors of PE, which remain constant whether in the pre-hospital or hospital setting. Clinicians should use the Wells score when assessing a patient with suspected PE to reinforce the probability of diagnosis, coupled with a history and findings of clinical assessment.
High-flow oxygen
Hypoxia should be corrected with high levels of supplemental oxygen. This should be administered in accordance with local guidelines, aiming for a target saturation of 94–98%, adjusting levels as required (JRCALC, 2016).
Analgesia
A common symptom of PE is the acute chest pain, often described as sharp in nature (Wilbeck and Evans, 2015). Edwards and Sabato (2009), as well as Peate and Jones (2014), identify that patients presenting in pain are likely to require analgesia, in the form of intravenous morphine. A pain assessment should always be carried out and the patient should always be offered analgesia. In current UK paramedic practice, this would normally be in the form of nitrous oxide, paracetamol (oral or intravenous) and morphine (oral or intravenous).
Nitrous oxide should be used cautiously in patients who present as hypoxic. Although the composition of nitrous oxide is 50% oxygen, the emphasis in these patients must be on maintaining oxygen saturations at 94–98%. Nitrous oxide can be used in short durations, with supplemental oxygen administered in between.
Intravenous paracetamol will provide relief from mild-to-moderate pain and, if given slowly, is considered to be haemodynamically stable (JRCALC, 2016). Owing to its cardiovascular stability and very few other side-effects, intravenous paracetamol should be considered as a first-line analgesic in patients with suspected PE.
Morphine provides effective relief from mild-to-severe pain. However, morphine is associated respiratory and cardiovascular depression and is known to precipitate hypotension (JRCALC, 2016). The cardiovascular effects of morphine in acute PE are not widely described in the literature; however, Richards (2009) identifies several clinical effects of morphine which can be applied to patients presenting with PE. Firstly, Richards (2009) describes that morphine can stimulate the vagus nerve, which can induce bradycardia proceeded by hypotension, compounded by vasodilation. Secondly, a release of histamine from mast cells can also result in vasodilation and hypotension (Richards, 2009). When considering a patient who is in compensatory cardiogenic shock as a result of PE, the use of large boluses of morphine may have a significant detrimental effect; for example, a patient who is tachycardic with narrowing pulse pressure and reduced cardiac output, as a result of the PE, could have a profound hypotension caused by morphine administration and the lack of central reserve to overcome this effect. Morphine should be used cautiously while monitoring the patient.
Intravenous fluid therapy should be used with caution and in patients who present with profound shock. However, York et al (2009) identify that prolonged fluid therapy should be used with caution in patients who have right-ventricular failure, as there is potential to overload the circulatory system, which is already struggling to cope. JRCALC (2016) guidelines further compound this and only advise fluid therapy where perfusion is profoundly affected.
Cardiac arrest
Cardiac arrest as a result of PE is not uncommon; Hitt and Pateman (2015) report up to 70% of all out-of-hospital cardiac arrests being attributed to coronary heart disease or PE. Patients presenting with massive PE are at high risk of cardiac arrest. Hitt and Pateman (2015) report a case series in which two patients with suspected PE at the time of cardiac arrest received pre-hospital thrombolysis and survived to discharge from hospital. In order to be considered effective, patients should be administered thrombolysis on a case-by-case basis at the earliest opportunity. Paramedics should be mindful that in the patient in cardiac arrest, normal resuscitative efforts must continue, and thrombolysis can be used as an adjunctive therapy where available (Hitt and Pateman, 2015).
Emerging therapies
There is evidence to suggest that the profoundly shocked patient with poor cardiac output can benefit from inotropic support (Marshall et al, 2010). The choice of inotrope is dependent upon the cardiovascular status of the patient; however, in paramedic practice, the choice would currently be limited to dilute adrenaline. Further research is required before any recommendation on the use of inotropic support in conscious patients is considered in the pre-hospital field.
Transportation
Rapid transportation to hospital following diagnosis in pre-hospital care is essential in patients with suspected PE (JRCALC, 2016). The literature goes on to suggest that early diagnosis and treatment with thrombolytic therapy can be beneficial on patient prognosis and outcome (Peate and Jones, 2015; York et al, 2015). Therefore, pre-hospital clinicians should aim for minimal on-scene times, while providing effective patient-centred management.
Conclusion
PE is a potentially life-threatening condition which can be challenging to diagnose in pre-hospital care. Clinicians should have a background understanding of the underlying physiological processes of PE and how these can manifest clinically. A thorough history-taking and clinical examination is the key to diagnosis, using clinical reasoning skills to draw together clinical information from a variety of sources to produce differential diagnoses. When diagnosed, PE should be treated as a medical emergency with careful management and timely transportation to definitive care. Clinicians should also be mindful of the patient presenting in cardiac arrest with suspected PE and the potential role of thrombolysis in this group of patients.