Case Study #7: AMI or Pulmonary Embolism?
by Alan Batt. Last modified: 28/03/14
Patient & Apparent Chief Complaint
A 79 year old female presents to ambulance crew after emergency call for an episode of vomiting, weakness and collapse.
Patient became very weak that morning, had an episode of collapse, vomiting, weakness. Previous history of hypertension, hypercholesterolaemia, and clinical depression.
Initial Clinical Findings
- Airway – clear & patent
- C Spine – not indicated (MOI/NOI: episode of weakness, collapse, vomiting)
- Breathing – regular, shallow
- Circulation – Pulse present, regular, tachycardic; skin colour pale, cap refill normal
- Disability – LOC before ambulance arrival x approximately 10 mins (according to NOK). Patient alert on arrival.
- ? AMI
- ? APE
- ? aortic aneurysm
- ? vasovagal episode
- A – No known allergies
- M – Currently taking Aspirin, Furosemide
- P – History of HTN, hypercholesterolaemia, depression
- L – Last oral intake 8pm the evening previous, vomiting since
- E – NOK reports patient was very weak this am, feeling nauseated. Collapsed this afternoon with LOC.
- Pulse rate 105bpm
- Pulse rhythm Regular
- ECG rate 104
- ECG rhythm NSR with regular PVCs
- Resp rate 20 per minute, regular, shallow
- Resp quality Normal, equal bilateral air entry
- SpO2% 85% @ room air
- Cap Refill <2secs
- BP 110/80
- Pupils PEARRL, size 3
- GCS 15/15
- BGL 11.3mmol/l
- Physical examination Nil of significance, nil pedal oedema. Patient diaphoretic and anxious.
Pre-hospital care & management
ECG showed alternating ventricular bigeminy, no other apparent pathological changes. O2 @15lpm commenced via non-rebreather mask. Patient reported a “lump” like feeling behind her xiphoid sternum, rating it at 3/10 on pain scale. This is consistent with a ? myocardial infarction, and was treated as such under Acute Coronary Syndrome care guidelines. Aspirin 300mg PO administered. GTN 800mcg administered sublingually. Pain/”lump feeling” resolved after second dose of GTN.
In-hospital care & management
Patient triaged as Category 1 (Life-Threatening Condition) with ? AMI. Brought directly to Resus room. 12 lead ECG repeated. Blood tests taken. Urinary catheter inserted. Multiple bilateral PE’s seen on CT Thorax. Patient thrombolised, developed haematoma on scalp, thrombolysis discontinued. Emboli resolved. Patient transferred to CCU department. and made significant recovery.
Multiple bilateral pulmonary embolisms (PE)
Identification of all interventions initiated and rationale
- Pulse oximetry – to monitor oxygen saturation levels in the blood
- Vital signs (HR, RR, SpO2, BM) – to gain a baseline set of vital signs for reference
- Supplemental oxygen – to re-oxygenate patient
- 3 Lead ECG – to identify any life-threatening arrhythmias
- 12 Lead ECG – to identify any life-threatening arrhythmias or ECG changes indicative of myocardial damage (secondary to hypoxia etc.)
- GTN – to reduce preload and in turn reduce myocardial oxygen demand.
- Aspirin – to decrease the risk of further clots developing and causing further myocardial damage
- Semi-recumbent position – comfortable for patients with chest pain, allows for relaxation of abdominal muscles, and allows for use of intercostals muscles of the back to aid breathing
- IV access – to allow for IV medications to be administered
- CXR – to identify pneumonia, pneumothorax, pleural effusion etc. that may increase morbidity
- Blood tests – to identify any electrolyte imbalances, cardiac enzymes released due to myocardial damage, clotting factors present in blood etc.
- Urinary catheter – to monitor urinary output to ensure adequate renal function
- CT Scan – to identify pathological processes that may result in increased morbidity/mortality
- Thrombolysis – to dissolve any clot that may be present in the pulmonary arteries, causing pulmonary ischemia
A Premature Ventricular Complex that occurs every 2nd beat is known as Ventricular Bigeminy; every 3rd beat is known as Ventricular Trigeminy and every 4th beat is known as Ventricular Quadrigeminy. In general they are considered to be non-pathological, and not life-threatening.
However these rhythms need to be observed for continuous runs (couplets, triplets etc.) which may progress to VT. In general they are not treated with anti-arrhythmics unless symptomatic. They normally signify myocardial irritation, due to hypoxia, AMI, electrolyte disturbance, medication administration or drug use.
(Hebbar & Heuston, 2002)
The Wells score is a clinical tool used in aiding a diagnosis of pulmonary embolism.
- clinically suspected DVT – 3.0 points
- alternative diagnosis is less likely than PE – 3.0 points
- tachycardia – 1.5 points
- immobilisation/surgery in previous four weeks – 1.5 points
- history of DVT or PE – 1.5 points
- haemoptysis – 1.0 points
- malignancy (treatment for within past 6 months, palliative) – 1.0 points
- Score >6.0 – High (probability ~59%)
- Score 2.0 to 6.0 – Moderate (probability ~29%)
- Score <2.0 – Low (probability ~15%)
- Score > 4 – PE likely. Consider diagnostic imaging.
- Score 4 or less – PE unlikely. Consider D-dimer to rule out PE
(Soderberg et al., 2009)
Diagnosing a PE in the ED
- 1. Typical history:
- Chest pain, may be described as sharp, stabbing.
- Wells score >6.0
- ECG changes:
- Tachycardia (~69%)
- RBBB (8-60%)
- Large S wave in I, large Q wave in III, inverted T wave in III – “S1Q3T3” (rarely seen, can be seen with other pathologies, not useful)
- Radiological Imaging:
- CXR – to rule out other causes of dyspnoea (CHF, # ribs etc.). PE specific signs such as Westermark sign (a focus of vasoconstriction distal to the PE) and Hamptons hump (a wedge shaped consolidation in the lung field) are unreliable and not always present (~2% of PE patients)
- Blood Tests:
- Raised D-dimer level
- Abnormal clotting factor test, FBC, LFT, U&E may be indicative of secondary cause of PE
Pre-Hospital Thrombolysis for MPE
The Thrombolysis during resuscitation for out-of-hospital cardiac arrest trial (TROICA Study – a double-blind, multicenter trial) did not detect an improvement in outcome when tenecteplase was used without adjunctive antithrombotic therapy (heparin, aspirin) during advanced life support for out-of-hospital cardiac arrest.Böttiger BW1, Arntz HR, Chamberlain DA, Bluhmki E, Belmans A, Danays T, Carli PA, Adgey JA, Bode C, Wenzel V; TROICA Trial Investigators; European Resuscitation Council Study Group. Thrombolysis during resuscitation for out-of-hospital cardiac arrest. N Engl J Med. 2008 Dec 18;359(25):2651-62. PMID: 19092151.
A case study by Perkins & Mitchell (2008) documented a case of a patient who was thrombolised pre-hospital for a Massive Pulmonary Embolism. The patient presented with sudden onset dyspnoea and tachypnoea, with no associated chest pain.
The patient was diaphoretic, distressed, and peripherally shut-down (no distal pulses etc.) He was tachycardic at 148bpm, his BP was unobtainable as was his SpO2%. He received 1000ml of crystalloid with no improvement. A 12 lead ECG showed a classic S1Q3T3 pattern of APE. The patient consented to thrombolysis, there were no contraindications present. The patient received a standard dose of reteplase for AMI. Within minutes the patient s condition improved. He was transferred to ED without further event, admitted to CCU and discharged following a complete recovery.
Kuisma et al. (1998) present the case of a 52-year-old previously healthy man who experienced acute severe dyspnoea after suffering from gastroenteritis for 3 days. After arrival of the ambulance, cardiac arrest with an initial rhythm of electro mechanical dissociation (PEA) occurred. Circulation was restored after 10 min of cardiopulmonary resuscitation but soon cardiac arrest reoccurred.
Based on a strong clinical suspicion of massive pulmonary embolism, thrombolytic treatment with heparin 5000 IU and reteplase 20 U, given as single boluses and heparin was continued as an infusion 1000 IU h(-1). After 7 min of continued resuscitation, circulation was restored and after 40 min the vital functions began to stabilize, thus indicating pulmonary reperfusion.
The diagnosis of pulmonary embolism was confirmed by a ventilation-perfusion scan and by spiral computerised tomography. The patient was discharged from intensive care after 2 days with a cerebral performance category I.Kuisma M1, Silfvast T, Voipio V, Malmström R. Prehospital thrombolytic treatment of massive pulmonary embolism with reteplase during cardiopulmonary resuscitation. Resuscitation. 1998 Jul;38(1):47-50. PMID: 9783510.
Wang, L. (2012) Thrombolytic therapy for pulmonary embolism: lessons from recent clinical trials. Australasian Journal of Paramedicine (3) 4 (PDF)
Incidence of mortality associated with Acute/Massive Pulmonary Embolism
Massive Pulmonary Embolism has a fatality rate of between 30-70% (Perkins & Mitchell, 2008). It can prove immediately fatal in some cases.
- The incidence of PE in Ireland is approximately 60-70 per 100,000. With a population of approximately 4.4 million this means an average annual occurrence of approximately 2400-2800 PEs per annum in Ireland, with approximately 700-1900 fatalities as a result.
- The incidence of PE in the USA is approximately 600,000 per annum, with approximately 60,000 fatalities as a result.
AAOS (2005) Emergency Care and Transportation of the Sick and Injured 9th Edition. Massachusetts: Jones & Bartlett
Elling B, Caroline N, Smith M (2007) Nancy Caroline’s Emergency Care in the Streets, 6th Edition (UK Edition). London: LWW
Perkins ZB1, Mitchell C, Donald O. Prehospital thrombolysis of a massive pulmonary embolus. Emerg Med J. 2008 May;25(5):303-4. PMID: 18434474.2.
Kuisma M1, Silfvast T, Voipio V, Malmström R. Prehospital thrombolytic treatment of massive pulmonary embolism with reteplase during cardiopulmonary resuscitation. Resuscitation. 1998 Jul;38(1):47-50. PMID: 9783510.
Böttiger BW1, Arntz HR, Chamberlain DA, Bluhmki E, Belmans A, Danays T, Carli PA, Adgey JA, Bode C, Wenzel V; TROICA Trial Investigators; European Resuscitation Council Study Group. Thrombolysis during resuscitation for out-of-hospital cardiac arrest. N Engl J Med. 2008 Dec 18;359(25):2651-62. PMID: 19092151.
Söderberg M1, Brohult J, Jorfeldt L, Lärfars G. The use of D-dimer testing and Wells score in patients with high probability for acute pulmonary embolism. J Eval Clin Pract. 2009 Feb;15(1):129-33. PMID: 18759753.
Hebbar AK1, Hueston WJ. Management of common arrhythmias: Part II. Ventricular arrhythmias and arrhythmias in special populations. Am Fam Physician. 2002 Jun 15;65(12):2491-6. PMID: 12086238.
The following two tabs change content below.Paramedic, educator, researcherAlan is a critical care paramedic, paramedic educator and prehospital researcher, currently working around the world as an educator and researcher. He has previously worked and studied across Europe, North America and the Middle East. He holds a Graduate Certificate in Intensive Care Paramedic Studies, and an MSc in Critical Care. His main interests are in care of the elderly, end-of-life care, patient safety, professionalism (including role and identity), and paramedic education.
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Case Study #7: AMI or Pulmonary Embolism?
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