Describe an acute and temporary loss of consciousness followed by spontaneous recovery resulting from a short-term cerebral oxygen deficiency

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Subject: Essays

Medicine and Health

Case Study


The term syncope is used to describe an acute and temporary loss of consciousness followed by spontaneous recovery resulting from a short-term cerebral oxygen deficiency or any other essential nutrient. Syncope usually accounts for about 3 percent of emergency room visits in humans (Bergfeldt, 2011). However, the cause or the diagnosis of syncope episodes commonly becomes elusive. Despite performing extensive tests, 25 to 30 percent of syncope in individuals remain undiagnosed. Diagnosing syncope often becomes a challenge because it must be differentiated from similar episodes including episodic weakness, seizures, and rarely cataplexy/narcolepsy syndromes. Differential diagnosis for syncope include reflex vagal and hypotensive syndromes, cardiac disorders, metabolic abnormalities and nervous system diseases (Davidow, Proulx, & Woodfield, 2007). Equally important is understanding the pathophysiology of the different syncope episodes as well as the stepwise management especially in paramedic practice. In this case, two differential diagnosis, cardiac syncope and convulsive syncope after blood loss, shall be discussed in addition to their paramedic intervention and rationale.


The discussion shall revolve around a patient, Lily – a 57-year-old woman who has experienced a syncope episode after complaints of feeling increasingly unwell for the past 24 hours with chest pains. She has also been bruising easily for the past 3 months. She appears pale, clammy, cool and distressed. Lily has was diagnosed with angina 2 years ago with successful angioplasty, hypertension, asthma and GORD. She is on atenolol, GTN spray, transiderm-nitro patch, atorvastatin, salbutamol inhaler, symbicort inhaler, Omeprazole, aspirin and paracetamol. She is also allergic to morphine. She has no communicable diseases and her vaccinations are up to date. She lives with her partner, her father died of heart disease while the mother died of breast cancer. She is a social consumer of alcohol and she quit smoking 10 years. Before quitting, she smoked about 30 sticks a day. Her vital signs are as follows blood pressure 90/60 mmHg, pulse 105 b/min, respiration 28 b/min, SpO2 96 percent and a temperature of 35.1 degrees Celsius.

Differential Diagnosis

Cardiac syncope due to Unstable Angina

Lily was in the office when she suffered syncope. Additionally, she had been complaining of chest pain for the past 24 hours suggestive of an angina development. Unstable angina commonly occurs during rest such as is the case with this patient (Bergfeldt, 2011). The syncope could therefore have been due to decreased cardiac output due to the unstable angina. Usually, evidence from pathologic, angiographic and angioscopic studies reveal that the key physiologic mechanism through which unstable angina occurs is atherosclerotic disruption of a plaque with a superimposed thrombus formation resulting in progression of coronary disease.

Angiographic investigations reveal that it is difficult to differentiate unstable angina from stable angina through quantitatively analysing coronary lesions. Patients with unstable angina have a high incidence of left main coronary artery stenosis. Seventy five percent of coronary artery disease patients progress from stable angina to unstable angina, which shows that unstable angina develops from progression of coronary artherosclerosis. Coronary angiosgrams have also been qualitatively analysed to supply critical information on the role played by thrombosis and plaque rupture in unstable angina pathophysiology (Kapoor, 2007). Based on pathologic and post-mortem angiographic observations, stenoses with irregular borders or complex stenoses demonstrate partially occluding thrombus, plaque rupture or both. Plaque rupture is therefore a precondition for acute progression of CAD into unstable angina.

Further, angioscopic studies provide insight into unstable angina pathophysiology by directly visualizing coronary lesions. About 90 percent of unstable angina cases have been found with thrombi and rest pain similar to Lily’s presentation of chest pain at rest. According to Forrester, CAD is a dynamic process with two cycles, which are interlocking – (1) stable atheroma progressing endothelial ulceration, aggregation of platelets and healing of the ulcer; and (2) endothelial ulceration, followed by partial thrombosis, then complete occlusion, lysis and finally thrombus incorporation (Shukla & Zimetbaum, 2007). Therefore, accelerated angina, which is associated with disruption of the plaque and partially occlusive thrombus are culprits in unstable angina associated with rest pain is evidenced.

Pathologic studies also offer valuable insight into unstable angina pathogenesis with histopathologic correlations between histologic sections and post-mortem coronary angiographic morphology of coronary lesions of patient suffering acute coronary syndrome being evaluated (Brignole, Alboni, & Benditt, Guidelines on management (diagnosis and treatment) of syncope, 2007). They observed that eccentric lesions having irregular borders and similar appearance to type II eccentric stenosis were stenoses, which were histologically ‘complicated’ demonstrating plaque rupture and hemorrhage, superimposed and partially occlusive thrombus in addition to recanalized thrombus. The ‘complicated’ lesions appeared to result in higher risk for acute myocardial infarction (AMI). People dying from unstable angina have also been found with acute coronary thrombosis (Chang-Sing & eter, 2008). The thrombus have been found to be multilayered, which signifies formation through successive and repeated mural deposition resulting in gradual luminal narrowing. The growing thrombus intermittently fragmented resulting in peripheral embolization and occlusion of tiny myocardial arteries.

Progression of CAD consequently leads to reduced myocardial oxygen supply and ischemia. Ischemia leads to decreased efficiency and function of the myocardium, which impairs the overall cardiac function including the cardiac output (Heaven & Sutton, 2010). Syncope in unstable angina is therefore due to decreased cardiac output as well as blood pressure with resultant reduction in cranial perfusion pressure (CPP). A reduction in CPP reduces oxygen delivery to the brain with subsequent syncope.

Ideally, a 12-lead ECG ought to be obtained in the first ten minutes of a patient’s arrival in the emergency unit. In patients with angina but momentarily without feelings of chest pain, unless there have been prior cardiac problems, the electrocardiogram (ECG) will typically be normal as seen in the first image. However, when there is chest pain, elevation or depression of the ST segment shall be observed. An ST elevation represents the highest risk in ECG findings and necessitates immediate triage for revascularization. A peaked T wave may also signify early MI.

The next high risk level is represented by a ST depression of more than 1 mm on an ECG. About 50 percent of patients presenting with such a finding suffer subendocardial myocardial necrosis. Moreover, a ST-segment depression portends a relatively high in-hospital as well as 30-day and 1-year mortalities regardless of the cardiac biomarker levels.

Ideally, Lily should be referred for a cardiac catheterization because her angina seems to be refractory to medical therapy. She has been on atenolol, aspirin, GTN spray and transiderm-nitro patch, which do not seem to improve her situation for the past 24 hours after developing chest pains (Bergfeldt, 2011). Similarly, all the vasodilator medications such as GTN spray and transiderm-nitro patch as well beta-blockers including atenolol should be halted considering that the blood pressure is low at 90/60 mmHg to prevent development of cardiogenic shock and further decrease in CPP. She should also be put on oxygen therapy to improve her partial pressure for oxygen to above 96 percent.

Revascularization should then be done to restore myocardial perfusion to relieve myocardial ischemia and restore heart function including the cardiac output. In cardiac revascularization, searching for the blocked coronary artery segments is done using a catheter guided through the leg or arm into the coronary artery (Bergfeldt, 2011). A liquid dye is then injected through the catheter and a high-speed X-ray records the dye’s course/flow to identify blockages. Based on the extent of coronary artery blockage the physician may prescribe a percutaneous coronary intervention or a coronary artery bypass.

Differential Diagnosis II: Convulsive Syncope

The patient had a history of easy bruising for the past three months, which could have resulted in hypovolemia. Empirical research has shown that acute hypovolemia due to hemorrhage or dehydration can lead to decreased preload and hence decreased cardiac output (CO). Decreased preload consequently results in sympathetic stimulation, which results in increased heart rate, vasoconstriction as well as increased contractility in order to preserve MAP and CO. With an empty ventricle, a very acutely decreased preload leads to a vigorous contraction of ventricles (Lin, Ziegler, Lai, & Bayer, 2009). This may result in excessively stimulated ventricular mechanoreceptors with consequent paradoxical vasodilation, bradycardia as well as syncope. These are typical signs, which Lily presented with at the ED – increased heart rate (tarchycardia) of 105 b/min, decreased blood pressure (hypotension) of 90/60 mmHg.

According to a study of 433 human participants by Kapoor (2007), 18 of them were found to have a low blood pressure secondary to gastrointestinal bleeding and dehydration. Indeed, hypotension has been found to be iatrogenic. Hypotension can also result from or be worsened by medication including hydralazine, enalapril and Nitroglycerindue to extreme vasodilation. Therefore, patients on such medication can be normal during rest and experience syncope following exertion especially if the cardiac output cannot be adequately increased in order to compensate for this decrease in vascular resistance (Sanmartín, Núñez, & Martinón-Torres, 2008). As earlier highlighted, decreased cardiac output results in decreased CPP with consequent deprivation of the brain of adequate oxygen. Syncope is therefore bound to occur.


Holter monitoring is important in diagnosis of convulsive syncope because it excludes significant arrhythmic causes. In fact, Holter monitoring is indicated for patients such as Lily with underlying heart problems, which may cause structural heart changes such as hypertension. A twelve surface electrode is preferable in the ECG investigation of convulsive syncope. Nevertheless, this investigation can be improved by considering correlated symptoms such as the cardiac rhythm and the heart rate (Sanmartín, Núñez, & Martinón-Torres, 2008). The above ECG shows sinus arrhythmia as well as periods of sinoatrial arrest and junctional escape.

Treatment of patients with convulsive therapy usually involves various approaches to enhance venous return. To begin with, patients should be trained on aversive manoeuvres, the simplest of them being lying down as well as bending at the waist, leg crossing and squatting in order to enhance muscle pump and increase the muscle tone of lower extremities. Elastic hose support is also helpful especially for aged adults (Ozkara, Metin, & Kucukoglu, 2009). Additionally, increased salt and fluid intake are helpful in preventing initial thoracic hypovolemia.

In terms of medication, initial treatment of Lily ought to involve withdrawal of vasodilator medication in order to promote restoration of the blood pressure. GTN spray and transiderm-nitro pathch should be withdrawn. It has been demonstrated that beta-1 blockade works well in reduction of putative contractility in addition to blunting rennin and epinephrine release (Lin, Ziegler, Lai, & Bayer, 2009). Fludrohydrocortisone is also an essential medication in promoting retention of water and sodium at the expense of some potassium wasting resulting in systemic volume expansion. Furthermore, fludrohydrocortisone has been shown to assist in sensitization of alpha receptors as well as prevention of vasodilation. Equally important is the administration of volume expanders to restore the blood pressure and brain perfusion.

Prolonged cardiac monitoring is important because it improves the sensitivity of Holter monitoring. Moreover, prolonged monitoring through wireless telemetry enables the review of continuous electrocardiogram records at particular points of access (Ozkara, Metin, & Kucukoglu, 2009). This is particularly important for Lily because of her chronic heart problem.

Reference List

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Brignole, M. 2007. Diagnosis and treatment of syncope. BMJ , 93 (1), 130–136.

Brignole, M., Alboni, P., & Benditt, D. 2007. Guidelines on management (diagnosis and   treatment) of syncope. Eur Heart J , 22 (1), 1256–1306.

Chang-Sing, P., & eter, C. 2008. Syncope: Evaluation and management. A review of         current approaches to this multifaceted and complex clinical problem. Cardiol Clin , 9 (1), 641–651.

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Kapoor, W. 2007. Syncope and hypotension. In E. Braunwald, Heart Disease: A Textbook           of Cardiovascular Medicine (pp. 863–876). Philadelphia: WB Saunders Co.

Krahn, A., Klein, G., & Yee, R. 2007. Randomized assessment of syncope trial:    conventional diagnostic testing versus a prolonged monitoring strategy. Circulation ,            104 (1), 46-51.

Lin, J., Ziegler, D., Lai, C., & Bayer, W. 2009. Convulsive syncope in blood donors. Ann Neurol , 188 (123), 525-28.

Ozkara, C., Metin, B., & Kucukoglu, S. 2009. Convulsive syncope: a condition to be         differentiated from epilepsy. John Libbey Journal , 11 (4), 243-251.

Sanmartín, M., Núñez, A., & Martinón-Torres, F. 2008. Convulsive syncope: characteristics          and reproducibility using the tilt test. An Pediatr , 59 (1), 441-7.

Shukla, G., & Zimetbaum, J. 2007. Syncope. AHA Journal , 34 (2), 2341-2348.