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Patient with Chest Pain

Last reviewed: July 10, 2018 ~8 min read

1. Subjective
Patient’s chief complaint: A man aged 69 comes to the emergency room with a sharp pain to his chest’s left side, lasting between 30 and 40 mins and then subsiding.
History of present illness: The pain has woken him up thrice in the last 7 days. He claims the pain first started roughly six months ago. Initially, however, the pain used to surface only occasionally, commonly while he was doing gardening. The patient’s past medical history reveals a diagnosis of hypertension twenty-five years back.
Precipitating/alleviating factors: The patient has been smoking a half-cigarette pack daily for the last forty-five years.
Family History: The patient has lost two brothers and his dad to heart disease. The patient does not report any other significant illness history in the family.
Social History: His typical pastimes include sharing a drink with pals and gardening.
Review of Systems: From a physical examination of the patient, no heaves, acute distress, hepatojugular, carotid bruits appreciated, abnormal pulsations, thrills or tenderness to palpation have been observed. All lung fields reveal clear breathing sounds.
2. Objective
Diagnostic Study: Acute Coronary Syndrome (ACS)
ACS constitutes a continuum of states of myocardial ischemia including unstable angina, ST-elevated and non-ST elevated MI (myocardial infarction). ACS has been linked to significant mortality and morbidity, significantly burdening the US healthcare system financially. Its diagnosis commences with an in-depth clinical evaluation of presenting patient symptoms, cardiac troponin level, electrocardiogram, and prior medical history examination. Early stratification of risk may help providers ascertain which approach ought to be adopted: initial conservative or early invasive, besides facilitating ascertainment of appropriate pharmacologic treatments (Smith JN, 2015).
ACS’s characteristic symptom include substernal chest pain, described typically as a pressing or crushing feeling, that radiates to the left arm and jaw. This doesn’t, however, manifest in all cases. Presenting symptoms may be highly subtle and vague with the main complaints commonly being breathing difficulties, isolated pain in the left arm or jaw, light-headedness, nausea, diaphoresis, weakness, and epigastric pain (Singh & Grossman, 2017).
3. Assessment
Pathophysiology: ACS’s underlying pathophysiology is partial reduction in heart musculature blood flow, normally secondary to thrombus formation and plaque rupture, or occasionally to vasospasm without or with underlying atherosclerosis. This leads to reduced flow of blood to heart musculature (partially), subsequently leading to ischemia and infarction of the area (Singh & Grossman, 2017).
Such syndromes’ underlying pathophysiological mechanisms commence with atherosclerosis, developing and progressing for several decades before acute event occurrence. Atherosclerosis is a low-grade inflammation of mid-sized arteries’ inner lining (intima), speeded up by widely-recognized risk factors like elevated cholesterol levels, elevated blood pressure, diabetes, genetics and smoking. This gradual development in coronary atherosclerosis results in slow thickening of coronary arteries’ inner layer that can, with time, narrow the arterial lumen to various extents. Atherosclerosis resulting in the grave SCD (sudden cardiac death) and AMI (acute myocardial infarction) syndromes has a preference for major coronary arteries’ proximal segments, typically arterial bifurcation sites altering arterial flow (Wang et al, 2004). Such gradual atherosclerotic progression can be disrupted by at least one swift progression cycle linked to either plaque haemorrhage or asymptomatic disruption of plaque with intraluminal non-occlusive thrombus formation (Ambrose & Singh, 2015). 
Differential Diagnosis
Pulmonary Embolism: Electrocardiograms are a swift, inexpensive diagnostic test to detect pulmonary embolism (PE), but they have certain limitations when it comes to differentially diagnosing acute PE and ACS (Gul, Nikus, Erdogan, & Ozdemir, 2016). The clinical symptoms of APE and ACS patients can be similar, with myocardial necrosis biochemical markers potentially elevated in case of both ailments. Besides lab and clinical findings and medical history, 12-lead electrocardiogram is vital though it has been linked to certain limitations when it comes to PE and ACS’s differential diagnosis. ECG changes suggesting myocardial ischemia have been noted among 7 out of 10 APE patients, with aggravated progression and one-month mortality predicted (Gul, Nikus, Erdogan, & Ozdemir, 2016).
Myeloperoxidase (MPO): This recognized activated neutrophil-released enzyme has strong pro-inflammatory and pro-oxidative properties. Of late, it has been recommended as a valuable ACS diagnostic tool and risk marker for patients brought to the emergency department with chest pain. Inflammation and oxidative stress contribute significantly to pathogenesis of CAD (coronary artery disease) destabilization causing ACS. Infiltrating neutrophils and macrophages engage in transforming stable coronary artery plaque into unstable lesions (Loria, Dato, Graziani, & Biasucci, 2008). Furthermore, MPO consumes nitric oxide (endothelial-derived), thus decreasing its bioavailability and weakening its anti-inflammatory and vaso-dilating properties (Loria, Dato, Graziani, & Biasucci, 2008).
4. Plan
Diagnostic:
Electrocardiogram: ECGs facilitate prognosis, diagnosis establishment, and provision of useful information on reperfusion failure/success and infarct location. Occlusion of the artery at specific anatomical sites has been linked to distinct ECG patterns, imparting correspondingly differing degrees of long or short run mortality risk (Kumar & Cannon, 2009).
Echocardiography: This forms the backbone of MI complication diagnosis; unexplained hemodynamic deterioration patients ought to be instantly assessed. An important point to note is that transthoracic and transoesophageal echocardiography are complementary, with the performance of the former by a qualified echocardiographer facilitating instant diagnosis. Among the critically ailing, image acquisition might prove hard and in such situations, transoesophageal echocardiography proves highly useful (Greaves, 2002).
Thoracic CT (computed tomography): For excluding fatal causes, radiologists increasingly encounter thoracic CT scans which include great vessel and heart CT angiography. ECG-gated or dual rule-out CT, adapted for excluding pulmonary embolism and aortic dissection, and triple rule-out CT, for excluding significant CAD, have proven to be valuable diagnostic tools. In the right setting that uses the right scanning protocols, triple rule-out can decrease patient triage time, costs and radiation dose (Hammer, Kroft, Hidalgo, Leta, & Roos, 2015).
Therapeutic Plan
Coronary angioscopy and angiography findings’ severity parallels ACS’s clinical severity. While Unstable Angina/ Non St-Elevation Myocardial Infarction (UA/NSTEMI) patients only show white clots, STEMI patient tests reveal red clots. Differences in STEMI and UA/NSTEMI’s underlying pathophysiology necessitate different therapeutic strategies and goals. In the latter, antithrombotic therapy aims at preventing additional thrombosis and allowing reduced coronary stenosis and endogenous fibrinolysis dissolution of the thrombus; revascularization is often utilized for increasing flow of blood and preventing recurrent ischemia or re-occlusion. By contrast, the infarct-connected artery in STEMI is normally completely occluded. The initial strategy is instant catheter-based or pharmacological reperfusion, aiming to obtain normal flow of blood. Anti-ischemic therapy, lipid-lowering, and other treatment approaches facilitate long-term plaque stabilization in every instance (Kumar & Cannon, 2009).
Education
Inclusive health education initiatives are delivered by healthcare providers to their patients for improving clinical outcomes by increasing positive health behaviour maintenance. In addition to medication-related education, for instance, these initiatives help increase behaviors like a nutritious diet and physical exercise, thereby lowering mortality and morbidity rates. Education is largely provided via initiatives within physician practices or outpatient services. Numerous new educational initiatives are targeted at meeting international or national educational standards; ACS education is being personalized taking into account patients’ existing health conditions and needs (Liu, Shi, Willis, Wu, & Johnson, 2017).
Community Resources
The community would greatly benefit from the creation of a larger number of interventional initiatives (at healthcare centers lacking cardiac surgery facility) meeting rigorous standards. Protocol development helps ensure timely, more frequent ACS-risk patient transfer to intervention centers for revascularization and coronary angiography (Wharton & McNamara, 2001).
Referral
Timely ACS diagnosis and referral to the appropriate health facility is extremely urgent and salient as swift treatment can save lives and improve patients’ quality of life and life expectancy (Gul, Nikus, Erdogan, & Ozdemir, 2016).
Follow-up
ACS patients not showing culprit lesions exhibit excellent prognosis following three-year follow-up in comparison to obstructive ACS patients. Diabetes predicts adverse outcomes among ACS patients (Kumar & Cannon, 2009).























Bibliography
Ambrose, J., & Singh, M. (2015). Pathophysiology of coronary artery disease leading to acute coronary syndromes. F1000Prime Rep.
Greaves, S. C. (2002). Role of echocardiography in acute coronary syndromes. Heart., 419–425.
Gul, E. E., Nikus, K., Erdogan, H., & Ozdemir, K. (2016). Differential diagnostic dilemma between pulmonary embolism and acute coronary syndrome. J Arrhythm, 160–161.
Hammer, S., Kroft, L., Hidalgo, A., Leta, R., & Roos, A. d. (2015). Chest CT examinations in patients presenting with acute chest pain: a pictorial review. Insights Imaging., 719–728.
Kumar, A., & Cannon, C. (2009). Acute Coronary Syndromes: Diagnosis and Management. Mayo Clin Proc., 917–938.
Liu, X. L., Shi, Y., Willis, K., Wu, C. J., & Johnson, M. (2017). Health education for patients with acute coronary syndrome and type 2 diabetes mellitus: an umbrella review of systematic reviews and meta-analyses. BMJ Open.
Loria, V., Dato, I., Graziani, F., & Biasucci, L. (2008). Myeloperoxidase: A New Biomarker of Inflammation in Ischemic Heart Disease and Acute Coronary Syndromes. Mediators Inflamm.
Singh, A., & Grossman, S. (2017). Acute Coronary Syndrome. Treasure Island: StatPearls Publishing.
Smith JN, N. J. (2015). Diagnosis and management of acute coronary syndrome: an evidence-based update. J Am Board Fam Med, 283-93.
Wang JC, L. S. (2004). Coronary artery spatial distribution of acute myocardial infarction occlusions. Circulation, 278–84.
Wharton , T., & McNamara, N. (2001). Management of acute coronary syndromes in the community hospital without cardiac surgical capability: how can access to interventional therapy be improved? Am J Cardiovasc Drugs, 375-85.


 

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PaperDue. (2018). Patient with Chest Pain. PaperDue. https://www.paperdue.com/essay/patient-with-chest-pain-essay-2171866

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