Acute Myocardial Infarction


Article Author:
Oren Mechanic


Article Editor:
Shamai Grossman


Editors In Chief:
Chaddie Doerr


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Frank Smeeks
Kristina Soman-Faulkner
Radia Jamil
Patrick Le
Sobhan Daneshfar
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi


Updated:
5/22/2019 7:03:40 PM

Introduction

Acute myocardial infarction is one of the leading causes of death in the developed world. The prevalence of the disease approaches three million people worldwide with more than one million deaths in the United States, annually. Acute myocardial infarction can be divided into two categories, non-ST-segment elevation MI (NSTEMI) and ST-segment elevation MI (STEMI). Unstable angina is similar to NSTEMI. However, cardiac markers are not elevated.[1][2][3]

Etiology

The etiology of acute myocardial infarction is decreased coronary blood flow. The available oxygen supply cannot meet oxygen demand, resulting in cardiac ischemia. Decreased coronary blood flow is multifactorial. Atherosclerotic plaques classically rupture and lead to thrombosis, contributing to acute decreased blood flow in the coronary. Other etiologies of decreased oxygenation/myocardial ischemia include coronary artery embolism, which accounts for 2.9% of patients, cocaine-induced ischemia, coronary dissection, and coronary vasospasm.[4][5]

Epidemiology

Among patients suffering from acute myocardial infarction, 70% of fatal events are due to occlusion from atherosclerotic plaques. As atherosclerosis is the predominant cause of acute myocardial infarction, risk-factors for the atherosclerotic disease are often mitigated in the prevention of disease. Modifiable risk factors account for 90% (men) and 94% (female) of myocardial infarctions. Modifiable risk factors include cigarette smoking, exercise, hypertension, obesity, cholesterol, LDL, and triglyceride levels. In contrast, age, sex, and family history are non-modifiable risk factors for atherosclerosis.[6][7]

Pathophysiology

Atherosclerotic rupture leads to an inflammatory cascade of monocytes and macrophages, thrombus formation, and platelet aggregation. This leads to the decreased oxygen delivery through the coronary artery resulting in decreased oxygenation of the myocardium. Inability to produce ATP in the mitochondria leads to the ischemic cascade, and therefore apoptosis (cell death) of the endocardium, or myocardial infarction.

With some exception due to genetic variation, coronary arteries have unique and diagnostic territorial distributions. For example, the left anterior descending coronary artery supplies blood flow to the interventricular septum, anterolateral wall, and ventricular apex. The left circumflex artery supplies blood to the posterolateral wall. The right coronary artery supplies the right ventricle. The inferior wall is supplied either by the left circumflex or right coronary artery. [8]

Histopathology

The histology of myocardial infarction changes over the time-course of the disease. At time 0, there are no microscopic histologic changes. Under light microscopy, within 0.5 to 4 hours, waviness of fibers at the periphery of the tissue is seen. Glycogen is depleted. At 4 to 12 hours, the myocardium undergoes coagulation necrosis and edema. At 12 to 24 hours, the gross specimen becomes dark and mottled. There are contraction band necrosis and neutrophil predominance on histopathology. At 1 to 3 days, there is a loss of nuclei, and at 3 to 7 days, macrophages appear to remove apoptosis cells. At 7 to10 days, granulation tissue appears. At 10 days and onward, there is collagen one deposition. After 2 months, the myocardium is scarred.

Toxicokinetics

Cardiac biomarkers are useful in the diagnosis of acute myocardial infarction, specifically non-ST-elevation MI. Troponin is the most specific lab test and has two isoforms, I and T. Troponins peak at 12 hours and persist for seven days. Creatinine Kinase, MB is also specific to the myocardium. It peaks at ten hours, however, normalizes within two to three days. LDH peaks over 72 hours and normalizes over ten to 14 hours. In clinical practice, LDH is not used to diagnose acute MI. Finally, MB has very low specificity for myocardium and is not used clinically; it quickly rises and normalizes. High-sensitivity troponin has recently been approved for use in the United States after having been heavily studied and utilized in Europe. Although it is more sensitive than conventional troponin, it is also less specific. Thus, potential challenges include numerous false-positive interpretations.[3]

History and Physical

The history of and physical exam is often inconsistent when evaluating for acute myocardial infarction. The history should focus on the onset, quality, and associated symptoms. Recent studies have found that diaphoresis and bilateral arm radiating pain most often are associated with myocardial infarction in men. Physical exam most importantly should note vital signs and patient’s appearance, including diaphoresis, as well as lung findings and cardiac auscultation.

Evaluation

Early and rapid ECG testing should be employed in all patients presenting with chest pain. Women often have atypical symptoms such as abdominal pain or dizziness and may present without chest pain at all. Elderly patients more often have shortness of breath as their presenting symptom for myocardial infarction. All of these presentations should prompt ECG testing, as well.[9][10][11]

The ECG is highly specific for MI (95% to 97%), yet not sensitive (approximately 30%). Right-sided, posterior lead placement, and repeat ECG testing can increase ECG sensitivity. For example, peaked T-waves on ECG, known as “hyperacute T waves,” often indicate early ischemia and will progress to ST elevation. When present, findings of  ST-elevations greater than 2 mm in two contiguous leads on ECG (Inferior: leads II, III, aVF; Septal equal V1, V2; Anterior: V3, V4; Lateral: I, aVL, V5, V6) are indicative of an ST-elevation myocardial infarction. Often, there are ST depressions that are visualized in opposite anatomical regions of the myocardium.

ECG diagnosis of STEMI can be difficult, particularly in patients with a left bundle branch block and pacemakers. Sgarbosa described criteria that can assist the physician or practitioner in diagnosing STEMI in these patients. Isolated ST-elevations in aVR are indicative of left main coronary artery occlusion in the appropriate clinical setting. Wellens noted deeply biphasic T waves in V2, V3, and found they are often predictive of an impending proximal left anterior descending artery occlusion which may lead to devastating anterior wall myocardial infarction.

Patients that present with myocardial infarction may not have diagnostic ST-elevation ECG abnormalities. Patients with typical chest pain should be investigated for NSTEMI with subtle abnormalities on ECG, including ST-depressions and T wave changes. Serial ECGs can be helpful here as well to look for dynamic changes. ECG without acute changes or any abnormalities is common in NSTEMI.

There are diagnostic guidelines that can assist the practitioner in determining whether further testing is useful in identifying patients with NSTEMI. Given the poor sensitivity of ECG for STEMI, troponins are almost universally used for patients with a suspicious clinical history. The HEART score has been validated and popularized. It utilizes clinician’s suspicion, patient risk factors, ECG diagnostics, and troponin level to determine the “risk level” of the patient. 

Treatment / Management

All patients with STEMI and NSTEMI require immediately chewed aspirin 160 mg to 325 mg. Furthermore, the patient should have intravenous access and oxygen supplementation if hypoxic less than 91%. Opioids may be used for pain control in addition to sublingual nitroglycerin if the blood pressure is adequate.[12][13][14]

Treatment for STEMI includes immediate reperfusion. Preference is for emergent percutaneous coronary intervention (PCI). Before PCI, patients should receive dual antiplatelet agents, including intravenous heparin infusion as well as an adenosine diphosphate inhibitor receptor (P2Y2 inhibitor), most commonly ticagrelor. Furthermore, Glycoprotein IIb/IIIa inhibitor or direct thrombin inhibitor may be given at the time of percutaneous intervention.

If percutaneous intervention is unavailable within 90 minutes of diagnosis of STEMI, reperfusion should be attempted with an intravenous thrombolytic agent.

NSTEMI in a stable asymptomatic patient may not benefit from emergent percutaneous coronary intervention and should be managed medically with antiplatelet agents. Percutaneous coronary intervention can be done within 48 hours of admission and may lead to improved in-hospital mortality and decreased the length of stay. In NSTEMI patients with refractory ischemia or ischemia with hemodynamic or electrical instability, PCI should be performed emergently

Before discharge for acute MI, patients may routinely be given aspirin, high-dose statin, beta-blocker, and/or ACE-inhibitor.

Differential Diagnosis

  • Aortic dissection
  • Pericarditis
  • Acute gastritis
  • Acute cholecystitis
  • Asthma
  • Esophagitis
  • Myocarditis
  • Pneumothorax
  • Pulmonary embolism

Enhancing Healthcare Team Outcomes

Acute myocardial infarction in the US is managed by a health team that is solely dedicated to heart disease. Besides the cardiologist, the team usually consists of a cardiac surgeon, an interventional cardiologist, intensivist, cardiac rehabilitation specialist, critical care nurses and physical therapists. Because many patients die before even reaching the hospital, the key is to educate the patient on symptoms and early arrival to the emergency department. Patients should be educated on how to take nitroglycerin, and if there is no relief after three doses, then 911 should be called. After discharge, the patient needs to enter a cardiac rehabilitation program, eat a healthy diet, discontinue smoking, abstain from alcohol, reduce body weight and lower cholesterol and blood glucose levels. The patient should be educated on the importance of compliance with medications to lower blood pressure and blood cholesterol. [15][16][17](Level II)

Outcomes

Acute myocardial infarction continues to have a high mortality out of the hospital. Data indicate that at least one-third of patients die before coming to the hospital and another 40-50% are dead upon arrival. Another 5-10% of patients will die within the first 12 months after their myocardial infarction. Readmission is common in about 50% of patients within the first 12 months after the initial MI. The overall prognosis depends on the ejection fraction, age, and other associated comorbidity. Those who do not undergo any type of revascularization will have a poorer outcome compared to patients who undergo revascularization. The best prognosis is in patients with early and successful reperfusion and preserved left the ventricular function.[18][19][20] (Level II)

 

 


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Acute Myocardial Infarction - Questions

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An 11-month-old child suddenly dies and an autopsy is done. A primary acute myocardial infarction is suspected. Which of the following will most likely be seen on autopsy?



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A 61-year-old patient presents with a two-hour history of crushing chest pain associated with diaphoresis and dyspnea. Triage in the emergency department reveals that he has ECG changes in lead I, AVF, and AVL and slightly elevated troponin levels. What is the most likely diagnosis?



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What is the best indicator of an acute myocardial infarction after a coronary artery bypass graft?



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What is the best medication to perfuse the heart 6 hours after a myocardial infarction?



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After a myocardial infarction, cardiac enzymes are increased. When is the peak elevation of CK-MB fraction seen?



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A 71-year-old patient with a history of chronic obstructive pulmonary disease suffers a myocardial infarction and recovers without any incidence. Prior to his discharge, it is found that he has an elevated blood pressure and a chronic cough. What is the drug of choice to treat his hypertension?



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What is the drug of choice in patients post myocardial infarction?



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In a patient with chest pain of a few hours duration, which set of cardiac enzymes will have the most significance on the diagnosis?



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In a patient that expired 24-48 hours following occlusion of the coronary artery, what will a microscopic examination of the myocardial infarction reveal?



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A 60-year-old obese man is admitted to the hospital with substernal chest pain and diaphoresis. Blood work at 6 hours will show an elevation of which of the following enzymes?



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A patient dies of a massive myocardial infarction. An autopsy performed 7 days after death will reveal which of the following?



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A lateral, left ventricular myocardial infarction is due to the occlusion of which of the following arteries?



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How long should air travel be postponed after a patient experiences an uncomplicated myocardial infarction?



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Which of the following describes the histological alteration that occurs in a heart after a myocardial infarction?



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A 65-year-old patient with diabetes mellitus develops a myocardial infarction (MI). He also has a history of hypertension and premature ventricular contractions. What is the drug of choice for this patient post-MI?



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In a patient who has an acute myocardial infarction, when should the first dose of aspirin be administered, assuming there are no contraindications?



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A patient who is suspected of having an acute myocardial infarction is prescribed two chewable aspirin STAT. What is the purpose of this drug in this situation?



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After a myocardial infarction, cardiac enzymes are increased. When does the peak elevation of the creatine kinase (CK)-MB fraction occur?



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During recovery from myocardial infarction, which of the following explains why patients commonly develop infarcts in other organs?



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Which of the following is true of ventricular septal rupture following a myocardial infarction?



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A 65-year-old presents with chest pain that started a few hours ago. Blood work is quickly drawn and it is observed that his enzymes peaked at 24-48 hours and lasted for several days. Which of the following enzymes were measured?



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Based on an ECG, which of the following is an indication that there is a high probability of a myocardial infarction?

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What is the most important next step in the management of a patient having an acute myocardial infarction who has a BP of 165/80 mmHg, a pulse of 75 bpm, elevated troponin, T wave inversions on ECG and has been given heparin, morphine, aspirin, and an oxygen mask?



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A 59-year-old male comes in with retrosternal pain, jaw pain, mild left shoulder pain, and chest pain with exertion. EKG shows acute changes and troponins are elevated. Which of the following is not considered part of the treatment for this patient?



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Which of the following is the first to show a raise in blood levels after myocardial infarction?



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Which medication should the majority of patients be started on right after an acute myocardial infarction?



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Painless myocardial infarction rarely occurs in which population?



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A patient presents with an acute myocardial infarction and has a blood pressure of 165/80 mmHg, a pulse of 75 bpm, elevated troponin, T wave inversions on ECG and has been given heparin, morphine, aspirin, and an oxygen mask. What is the most important next step in the management of this patient?



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When is myoglobin normally detected after an acute myocardial infarction?



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Which of the following statements is true regarding reperfusion therapy for acute myocardial infarction (MI)?



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Which of the following steps in working up a patient with suspected myocardial infarction should be completed first?



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Which of the following best explains the reason that a person experiences chest pain during a myocardial infarction?



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What is the most appropriate diet for a 67-year-old following an acute myocardial infarction?



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Autopsy on a patient after a heart attack shows thrombosis of the left anterior descending artery with coagulation necrosis and neutrophilic infiltration. There are few lymphocytes or histiocytes. How long after the myocardial infarction did the patient die?



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Which of the following medications has been shown to decrease long-term survival in patients with acute myocardial infarction?



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Which of the following is a component of the emergent management of acute myocardial infarction?



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A 58 year old female with a history of hypertension and diabetes mellitus type 2 complains of substernal chest pain, nausea, and vomiting. She has no cardiac history. She is on metformin and lisinopril. She smokes one and a half packs a day. Her ECG shows intermittent ST elevation of 1 mm in II, III, and aVF but no other abnormalities. Select the most likely diagnosis.



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A 62-year-old patient has an acute anterior myocardial infarction and develops a new holosystolic murmur and dyspnea. Vital signs are blood pressure 90/52 mmHg, heart rate 120 beats/min, and respiratory rate 20. Exam shows jugular venous distention, rales at the lung bases, and cool extremities with edema. What is the best initial test?



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A patient with cocaine use disorder has a heart attack and dies. The biopsy of the affected myocardium would show elevated levels of which enzyme if taken right before he died?



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What is the best route of administration of beta blocker during acute myocardial infarction?



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What time period after acute myocardial infarction carries the worst prognosis with ventricular fibrillation?



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What is the most common cause of myocardial infarction?



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Select the correct statement about myocardial infarction (MI) in those greater than 70 years.



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Which is true regarding diabetes mellitus (DM) and myocardial infarction (MI)?



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Which of the following is the most common cause of death in those hospitalized with acute myocardial infarction?



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Which section of the myocardium is most susceptible to ischemic damage?



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Which of the following was the least significant factor influencing 30-day mortality in the Global Utilization of Streptokinase and tissue plasminogen activator for Occluded Arteries-I trial?



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What antiplatelet regimen does the American College of Cardiology/American Heart Association recommend for high-risk, troponin-positive patients prior to angiography?



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Which of the following stenotic lesions has the highest survival rate post myocardial infarction?



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In a patient with acute myocardial infarction, thrombolytic door-to-drug administration should occur in less than what time period?



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Which of the following is an atypical sign or symptom of myocardial infarction (MI) in the elderly?



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What is the mortality rate of acute myocardial infarctions (AMI)?



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During an acute myocardial infarction, which measure helps limit the infarct size?



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If a patient had a myocardial infarction several days ago and experiences nausea during assessment of bathing skills, what should be done?



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A patient is being assessed by an OT after a myocardial infarction. The patient's endurance level during self-care is to be done. What should be done first?



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Which of the following are signs of a myocardial infarction?



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For which diagnosis is providing adequate rest is a priority in the care of a patient?



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A patient with chest pain and possible myocardial infarction presents to the ER. Which of the following should be performed first in the care of this patient?



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Which of the following descriptions of chest pain is most consistent with myocardial infarction?



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A 78-year-old female with a history of coronary artery disease and is found to have an ST segment myocardial infarction with classic symptoms. Within 3 hours, the patient is stable and pain-free. Which complication would be of greatest concern over the next 24 hours?



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With 100 patients admitted for acute myocardial infarction, how many are expected to have diagnostic changes on ECG?



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A patient presents with acute onset of chest pain. Which ECG finding is most suggestive of an acute myocardial infarction, AMI?



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When is there marked neutrophilic infiltrate present at the site of an acute myocardial infarct?



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The earliest macroscopic change in an acute myocardial infarct is:



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A 62-year-old woman with diabetes mellitus presents to the emergency department with a 50-minute history of crushing substernal chest discomfort that radiates to her left arm. ECG shows ST depression in leads V1-V4. She is not currently taking any medications. The correct diagnosis is made, she is treated and subsequently discharged from the hospital. From the following choices, what medication could have reduced this patient's risk of developing the underlying condition responsible for her hospital visit?



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Which of the following is consistent with acute myocardial infarction? Select all that apply.



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Which of the following are consistent with acute myocardial infarction on a 12-lead ECG? Select all that apply.

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Attributed To: Contributed by Wikimedia Commons, Displaced (Public Domain-Self)



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A nurse is making morning rounds and enters the room of a client with hypertension and hyperlipidemia who is taking lisinopril and simvastatin. The client admits to 9/10 chest pain. The pain is mid-sternal, radiating down the left arm, and the client complains of nausea. The client is ashen in color, short of breath, and sweat is dripping off their forehead and chest. The client's blood pressure is 80/50 mmHg, heart rate 48 beats/min, respiratory rate 26, and pulse oximetry 89% on room air. How should the nurse proceed in the management of care for this client? Select all that apply.



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Acute Myocardial Infarction - References

References

Nascimento BR,Brant LCC,Marino BCA,Passaglia LG,Ribeiro ALP, Implementing myocardial infarction systems of care in low/middle-income countries. Heart (British Cardiac Society). 2018 Sep 29     [PubMed]
Barberi C,van den Hondel KE, The use of cardiac troponin T (cTnT) in the postmortem diagnosis of acute myocardial infarction and sudden cardiac death: A systematic review. Forensic science international. 2018 Sep 17     [PubMed]
Alaour B,Liew F,Kaier TE, Cardiac Troponin - Diagnostic Problems and Impact on Cardiovascular Disease. Annals of medicine. 2018 Sep 28     [PubMed]
Massberg S,Polzin A, [Update ESC-Guideline 2017: Dual Antiplatelet Therapy]. Deutsche medizinische Wochenschrift (1946). 2018 Aug     [PubMed]
Scheen AJ, [From atherosclerosis to atherothrombosis : from a silent chronic pathology to an acute critical event]. Revue medicale de Liege. 2018 May     [PubMed]
Berg DD,Wiviott SD,Braunwald E,Guo J,Im K,Kashani A,Gibson CM,Cannon CP,Morrow DA,Bhatt DL,Mega JL,O'Donoghue ML,Antman EM,Newby LK,Sabatine MS,Giugliano RP, Modes and timing of death in 66 252 patients with non-ST-segment elevation acute coronary syndromes enrolled in 14 TIMI trials. European heart journal. 2018 Sep 20     [PubMed]
Deng D,Liu L,Xu G,Gan J,Shen Y,Shi Y,Zhu R,Lin Y, Epidemiology and Serum Metabolic Characteristics of Acute Myocardial Infarction Patients in Chest Pain Centers. Iranian journal of public health. 2018 Jul     [PubMed]
Haig C,Carrick D,Carberry J,Mangion K,Maznyczka A,Wetherall K,McEntegart M,Petrie MC,Eteiba H,Lindsay M,Hood S,Watkins S,Davie A,Mahrous A,Mordi I,Ahmed N,Teng Yue May V,Ford I,Radjenovic A,Welsh P,Sattar N,Oldroyd KG,Berry C, Current Smoking and Prognosis After Acute ST-Segment Elevation Myocardial Infarction: New Pathophysiological Insights. JACC. Cardiovascular imaging. 2018 Jul 13     [PubMed]
Alquézar-Arbé A,Sanchís J,Guillén E,Bardají A,Miró Ò,Ordóñez-Llanos J, Cardiac troponin measurement and interpretation in the diagnosis of acute myocardial infarction in the emergency department: a consensus statement. Emergencias : revista de la Sociedad Espanola de Medicina de Emergencias. 2018 Oct     [PubMed]
Perera M,Aggarwal L,Scott IA,Logan B, Received care compared to ADP-guided care of patients admitted to hospital with chest pain of possible cardiac origin. International journal of general medicine. 2018     [PubMed]
Riley RF,Miller CD,Russell GB,Soliman EZ,Hiestand BC,Herrington DM,Mahler SA, Usefulness of Serial 12-Lead Electrocardiograms in Predicting 30-Day Outcomes in Patients With Undifferentiated Chest Pain (the ASAP CATH Study). The American journal of cardiology. 2018 Aug 1     [PubMed]
Larson E,German DM,Shatzel J,DeLoughery TG, Anticoagulation in the Cardiac Patient: A Concise Review. European journal of haematology. 2018 Sep 10     [PubMed]
Bath PM,Woodhouse LJ,Appleton JP,Beridze M,Christensen H,Dineen RA,Flaherty K,Duley L,England TJ,Havard D,Heptinstall S,James M,Kasonde C,Krishnan K,Markus HS,Montgomery AA,Pocock S,Randall M,Ranta A,Robinson TG,Scutt P,Venables GS,Sprigg N, Triple versus guideline antiplatelet therapy to prevent recurrence after acute ischaemic stroke or transient ischaemic attack: the TARDIS RCT. Health technology assessment (Winchester, England). 2018 Aug     [PubMed]
Adamski P,Adamska U,Ostrowska M,Navarese EP,Kubica J, Evaluating current and emerging antithrombotic therapy currently available for the treatment of acute coronary syndrome in geriatric populations. Expert opinion on pharmacotherapy. 2018 Sep     [PubMed]
Aeyels D,Seys D,Sinnaeve PR,Claeys MJ,Gevaert S,Schoors D,Sermeus W,Panella M,Bruyneel L,Vanhaecht K, Managing in-hospital quality improvement: An importance-performance analysis to set priorities for ST-elevation myocardial infarction care. European journal of cardiovascular nursing : journal of the Working Group on Cardiovascular Nursing of the European Society of Cardiology. 2018 Aug     [PubMed]
Schwaab B, [Cardiac Rehabilitation]. Die Rehabilitation. 2018 Apr     [PubMed]
El Hajj MS,Jaam MJ,Awaisu A, Effect of pharmacist care on medication adherence and cardiovascular outcomes among patients post-acute coronary syndrome: A systematic review. Research in social     [PubMed]
Stone GW,Ellis SG,Gori T,Metzger DC,Stein B,Erickson M,Torzewski J,Williams J Jr,Lawson W,Broderick TM,Kabour A,Piegari G,Cavendish J,Bertolet B,Choi JW,Marx SO,Généreux P,Kereiakes DJ, Blinded outcomes and angina assessment of coronary bioresorbable scaffolds: 30-day and 1-year results from the ABSORB IV randomised trial. Lancet (London, England). 2018 Sep 24     [PubMed]
Lopes RD,de Barros E Silva PGM,de Andrade Jesuíno I,Santucci EV,Barbosa LM,Damiani LP,Nakagawa Santos RH,Laranjeira LN,Dall Orto FTC,Beraldo de Andrade P,de Castro Bienert IR,Alexander JH,Granger CB,Berwanger O, Timing of Loading Dose of Atorvastatin in Patients Undergoing Percutaneous Coronary Intervention for Acute Coronary Syndromes: Insights From the SECURE-PCI Randomized Clinical Trial. JAMA cardiology. 2018 Sep 24     [PubMed]
Choi AR,Jeong MH,Hong YJ,Sohn SJ,Kook HY,Sim DS,Ahn YK,Lee KH,Cho JY,Kim YJ,Cho MC,Kim CJ, Clinical characteristics and outcomes in acute myocardial infarction patients with versus without any cardiovascular risk factors. The Korean journal of internal medicine. 2018 Sep 1     [PubMed]

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