Angina and ACS PDF

Today we will be discussing chest pain, acute coronary syndromes, ST elevation myocardial infarctions, non-ST elevation myocardial infarctions, resuscitative measures with CPR and ACLS, and targeted temperature management. We will conclude this lecture with a case study and comprehensive questions....

Today we will be discussing chest pain, acute coronary syndromes, ST elevation myocardial infarctions, non-ST elevation myocardial infarctions, resuscitative measures with CPR and ACLS, and targeted temperature management. We will conclude this lecture with a case study and comprehensive questions. Chest pain Guideline: Here is the latest guideline for the evaluation and diagnosis of chest pain per the American Heart Association. Chest pain is the second most common reason for adults to present to the emergency department (ED) in the United States and accounts for over 6.5 million visits. Chest pain requires thorough clinical evaluation by providers. Although the cause of chest pain is often noncardiac, coronary artery disease (CAD) affects over 18.2 million adults in the United States and remains the leading cause of death for men and women which accounts for more than 365,000 deaths annually. The AGACNP needs to be able to distinguish between serious and benign causes of chest pain. Patient descriptions: Patients with chest pain often report pressure, tightness, squeezing, heaviness, or burning. They may also report a location other than the chest, including the shoulder, arm, neck, back, upper abdomen, or jaw. Despite individual variability, the discomfort induced by myocardial ischemia is often characteristic. Features more likely to be associated with ischemia have been described as typical versus atypical; how-ever, this can be confusing because it is frequently used to describe symptoms considered nonischemic as well as noncardiac. Although other nonclassic symptoms of ischemia, such as shortness of breath, nausea, radiating discomfort, or numbness, may be present, chest pain or chest discomfort remains the predominant symptom reported in men and women who are ultimately diagnosed with myocardial ischemia. Pain that is described as sharp, fleeting, related to inspiration or pleuritic or position, or shifting locations suggests a lower likelihood of ischemia. Differential Diagnoses for chest pain and exam findings: Patients presenting with nontraumatic chest pain are a frequent diagnostic challenge. The priorities are rapid initiation of optimal management in patients with life-threatening conditions such as ACS, aortic dissection, and pulmonary embolism, as well as nonvascular syndromes like esophageal rupture, and tension pneumothorax. The initial EKG is important to the evaluation, but history, examination, biomarkers, and other aids remain essential. A comprehensive history that captures all the characteristics of chest pain but not limited to its nature, onset, duration, location and radiation, precipitating factors, relieving factors; and associated symptoms can help better identify potential cardiac causes and should be obtained from all patients. Angina: Angina pectoris is perceived as a retrosternal chest discomfort that builds gradually in intensity over several minutes, is usually precipitated by physical or emotional stress or occurs at rest with characteristic radiation and its associated symptoms like dyspnea, nausea, and lightheadedness. When actively treated or spontaneously resolving, it dissipates over a few minutes. Increased age is a significant risk factor for Acute Coronary Syndrome. However, it is also a risk factor for comorbidities that are associated with alternative diagnoses associated with chest pain. In patients with chest pain who are >75 years of age, ACS should be considered when accompanying symptoms such as shortness of breath, syncope, or acute delirium are present, or when an unexplained fall has occurred. There are marked racial and ethnic disparities when triaging patients who present for the evaluation of chest pain. Despite a greater number of Black patients presenting with angina pectoris relative to other races, this population is less likely to be treated urgently and less likely to have an ECG performed, samples for cardiac biomarkers drawn, cardiac monitoring performed, or pulse oximetry measured. Similar treatment disparities are found with Hispanic patients and those who are covered by Medicaid or are uninsured. Such disparity in the management of chest pain among diverse population subgroups contributes to worse outcomes, including the greater incidence of AMI and fatal coronary events seen in these key population subgroups. There are also disparities in the management of patients of South Asian descent who present with ACS, with the diagnosis often missed or delayed, resulting in poor outcomes. Consideration of race and ethnicity in the evaluation of patients with suspected ACS and in the outpatient evaluation of symptomatic patients is paramount to improving outcomes. Cultural competency training of providers is recommended to address health disparities in the evaluation and management of diverse patient population subgroups with chest pain. Among patients of diverse race and ethnicity presenting with chest pain in whom English may not be their primary language, addressing language barriers with the use of formal translation services is recommended Chest pain flowsheet: The ACC/AHA STEMI and NSTE-ACS guidelines categorize chest pain cause into 4 types: STEMI, NSTE-ACS, stable angina, and non-cardiac. The 12-lead ECG, which should be acquired and interpreted within 10 minutes of arrival to a medical facility and is pivotal in the evaluation because of its capacity to identify and triage patients with STEMI to urgent coronary reperfusion. Other ST-T abnormalities consistent with possible ischemia also mandate prompt evaluation in a hospital setting. The ECG is central to the evaluation of stable angina in the office setting to ensure that ACS is not missed. Early recognition of STEMI improves outcomes. Therefore, regardless of the setting, an ECG should be obtained and interpreted within 10 minutes of arrival. Patients with chest pain and new ST-elevation, ST depression, or new left bundle branch block on ECG should be treated according to STEMI and NSTE-ACS guidelines. An initial normal ECG does not exclude ACS. Patients with an initial normal ECG should have a repeat ECG, if symptoms are ongoing, until other diagnostic testing rules out ACS. An ECG may identify other nonischemic causes of chest pain like pericarditis, myocarditis, arrhythmia, electrolyte abnormalities, paced rhythm, hypertrophic cardiomyopathy, pulmonary hyper-tension, congenital long QT, or normal variant. When ST- elevation is present on the initial ECG, management should follow the prescribed STEMI treatment algorithms in associated guidelines. Furthermore, if ST depression is identified on the initial ECG, management should follow the NSTE-ACS guidelines. A normal ECG may be associated with left circum-flex or right coronary artery occlusions and posterior wall ischemia, which is often “electrically silent”; therefore, right-sided ECG leads should be considered when such lesions are suspected Patients with acute chest pain: Cardiovascular biomarkers can be useful for the diagnostic and prognostic assessment of patients with chest pain. Their most important application in clinical practice is for the rapid identification or exclusion of myocardial injury. The preferred biomarker to detect or exclude myocardial injury is cardiac. Coronary Computed Tomography Angiography can visualize and help to diagnose the extent and severity of nonobstructive and obstructive CAD, as well as atherosclerotic plaque. Invasive coronary angiography defines the presence and severity of a luminal obstruction of an coronary artery, including its location, length, and diameter, as well as coronary blood flow. The primary goal is the characterization and detection of a high-grade obstructive stenosis to define feasibility and necessity of percutaneous or surgical revascularization Symptom-limited exercise ECG involves graded exercise until physical fatigue, limiting chest pain, marked ischemia, or a drop in blood pressure occurs. Transthoracic echocardiography can visualize and aid in the differential diagnosis among the numerous causes of acute chest pain such as acute aortic dissection, pericardial effusion, stress cardiomyopathy, and hypertrophic cardiomyopathy. Although TTE does provide information, for patients with acute chest pain, visualization of left and right ventricular function and regional wall motion abnormalities allows for the assessment of CAD risk and may help to guide clinical decision-making. STEMI: Here are the latest STEMI clinical practice guidelines you should become familiar with. The first one is the 2013 American Cardiology Foundation and American Heart Association’s STEMI guidelines, and the other is the 2015 update on percutaneous coronary intervention for patients with STEMI. Patients with severe and acute myocardial infarction or ST-elevation myocardial infarction or STEMI require rapid diagnosis and treatment to reduce the risk of death and permanent myocardial injury. The primary goal of STEMI management is to reduce the risk of death and the extent of permanent cardiac injury associated with MI. Therapy for patients with STEMI becomes less effective with each minute its delivery is delayed. Initial assessment: The rapid diagnosis of STEMI only requires the presence of symptoms suspicious for an acute coronary syndrome or ACS like chest discomfort, dyspnea, sudden death and a confirmatory electrocardiogram. It does not require evidence of elevated cardiac biomarkers such as troponin. Thus, patients with suspected ACS should undergo a focused history and ECG within ten minutes of hospital arrival to identify the key findings of STEMI. The AGACNP needs to assess for the signs and symptoms that suggest the presence of STEMI to include chest pain or chest discomfort, dyspnea, ventricular arrhythmias, cardiac arrest, or syncope, and atypical symptoms such as malaise and weakness. The AGACNP also needs to review EKG for findings suggestive of STEMI to include ST segment elevation, newly identified Left bundle branch block, as well as other high risk EKG findings to include Winter sign and transient ST segment elevation. Diagnosis: The AGACNP should review the EKG strip and assess for any ST elevation with 1 mm of ST elevation in 2 contiguous leads which is required to diagnose STEMI. Below is an image which shows each EKG lead, and the area of the heart that is affected. The AGACNP should know that the lateral leads include I, avL, v5, and v6 and the left circumflex or the diagonal of the left anterior distending coronary arteries are affected by the ischemia or occlusion. The inferior leads include II, III, avF and the right coronary artery and/or the left circumflex coronary artery is affected. The anterior septal leads include v1 through v4, and any ST elevation in these leads are concerning for left anterior descending coronary artery ischemia or occlusion. Posterior MI: Posterior infarction accompanies 15-20% of STEMIs, usually occurring in the context of an inferior or lateral infarction. Posterior extension of an inferior or lateral infarct implies a much larger area of myocardial damage, with an increased risk of left ventricular dysfunction and death. Isolated posterior infarction is an indication for emergent coronary reperfusion. However, the lack of obvious ST elevation in this condition means that the diagnosis is often missed. The posterior myocardium is not directly visualized by the standard 12-lead ECG, so the AGACNP needs to be mindful to look for reciprocal changes of STEMI in the anteroseptal leads V1-3. EKG findings suggestive of a posterior MI include changes in v1-v3 to include horizontal ST depression, tall, broad R waves, upright T waves, and a dominant R wave as pictured in the powerpoint slide. Posterior MI: To better assess for a posterior MI, the AGACNP should order a posterior lead or right sided EKG. Leads V7-9 are placed on the posterior chest wall in the following positions as you can see in the diagram pictured. V7 is placed to the left posterior axillary line, in the same horizontal plane as V6, V8 is placed at the tip of the left scapula, in the same horizontal plane as V6, and V9 is placed to the left paraspinal region, in the same horizontal plane as V6. The EKG should be reviewed for marked ST elevation in V7 through 9 with Q-wave formation which confirms involvement of the posterior wall. The EKG pictured shows these changes and reveals this to be an inferior-lateral-posterior STEMI which is a big territory infarct for this patient. Monitoring and testing: For patients with STEMI, initial monitoring and testing typically include the following vital signs, lab data, and imaging. Patients with STEMI require frequent blood pressure measurements, continuous heart rhythm monitoring with telemetry, and continuous pulse oximetry. All patients with STEMI should have laboratory studies to evaluate for metabolic abnormalities, acute kidney injury, anemia, thrombocytopenia, and coagulopathy. Troponin levels should be obtained, but the acute management of STEMI does not require elevated troponin levels. Patients with STEMI should have a chest radiograph to evaluate for other causes of chest discomfort and to assess for the complications of MI like pulmonary edema. Echo, CTA, and other imaging studies are not routinely obtained unless a specific diagnosis is suspected like aortic dissection or pericardial tamponade. Evaluation for life threatening conditions: The initial assessment of patients with STEMI includes a brief evaluation for conditions that require additional treatment or that alter the approach to STEMI therapy. These conditions include shock, heart failure, aortic dissection, and coagulopathy and/ or thrombocytopenia. Patients with STEMI should be assessed for evidence of shock and, if present, for signs or symptoms like cool extremities and jugular venous distension that help to characterize the type of shock as cardiogenic or distributive. Patients with shock require specific management of shock as well as appropriate and timely reperfusion. All patients with STEMI should be assessed for signs and symptoms of heart failure which include orthopnea, jugular venous distension, or pulmonary edema. Aortic dissection is a rare cause of STEMI but should be considered in all patients with STEMI. The signs and symptoms of aortic dissection include severe pain or tearing located in the chest or back, asymmetric upper extremity pulses or pulse deficits, and widening of the mediastinum on chest radiograph. Patients with STEMI caused by aortic dissection require management that is different from the typical management of STEMI. The management of patients with STEMI typically requires treatments that increase the risk of bleeding. Thus, all patients with STEMI should be assessed for chronic use of anticoagulant or antiplatelet medications, history of bleeding or coagulation disorders like uremia, or heparin-induced thrombocytopenia, and the presence of abnormal coagulation studies or thrombocytopenia. Initial management: The initial management of patients with STEMI requires rapid selection and administration of reperfusion therapy. Patients with STEMI should also receive treatments that prevent further coronary artery thrombosis, minimize myocardial injury, and treat the symptoms of MI. For patients diagnosed with STEMI, the primary goal of acute management is to rapidly restore blood flow to the acutely occluded coronary artery with a reperfusion therapy to include percutaneous coronary intervention or fibrinolysis. Thus, a reperfusion strategy should be chosen within minutes of arrival. After a reperfusion strategy is chosen, local STEMI protocols should be initiated without delay. These protocols mobilize the key multidisciplinary personnel like the interventional cardiologist, pharmacist, cardiac nurses, and resources like interhospital transfer that is required to deliver reperfusion therapy as quickly as possible. PCI: The PCI procedure consists of arterial access via the radial or femoral artery, diagnostic angiography, and interventional procedures like stenting and thrombectomy that open the acutely obstructed coronary artery. Additional treatments or managements may be necessary depending on the patient’s condition and angiography findings. Diagnostic angiography may reveal acute lesions that are causing the myocardial infarction but also may reveal lesions that are more chronic in nature. In patients whose angiography demonstrates multivessel coronary artery disease or left main coronary artery disease, the culprit lesions are typically treated with immediate PCI. In some patients with residual three vessel disease or left main coronary artery disease, a coronary artery bypass grafting may be performed later. Fibrinolysis: If PCI is not possible within the first 120 minutes of first medical contact, fibrinolytic therapy should be initiated within 30 minutes of patient arrival at the hospital. P2Y inhibiting antiplatelet medication choice depends on whether the patient underwent PCI or fibrinolytic therapy. Ticagrelor and prasugrel are preferred to clopidogrel in patients who undergo PCI due to recent trials showing superiority. Patients undergoing fibrinolytic therapy should be started on clopidogrel. It is important to be careful about relative contraindications of P2Y12 inhibitors. Prasugrel is contraindicated in patients with history of transient ischemic attack and stroke. Anticoagulation should also be started alongside with unfractionated heparin, low-molecular-weight heparin, bivalirudin, or fondaparinux. Routine therapy: Regardless of the chosen reperfusion strategy, the following therapies are routinely given to patients with STEMI to slow the progression of coronary artery thrombus formation, minimize the extent of myocardial injury, and treat the patient’s symptoms All patients with STEMI should receive aspirin as soon as possible. In patients with STEMI, nitrates can reduce the symptoms of chest discomfort and Heart failure as well as treat hypertension. Patients with resistant chest symptoms may be sequentially treated with higher doses of nitrates and opioids. Patients with STEMI who do not have shock, Heart failure, bradycardia, or heart block typically receive an oral beta blocker as part of the initial therapy for STEMI. Most patients with STEMI receive treatment with an anticoagulant and a P2Y12 inhibitor, like Plavix. However, the approach to the use and selection of these agents is determined by the reperfusion strategy and other patient characteristics. In patients with STEMI who do not already take a statin, a statin is typically started soon after presentation to the hospital. The routine use of morphine and oxygen can alleviate cardiac discomfort in patients. The use of Morphine is to treat chest symptoms refractory to nitrates and other medical therapy, guidelines suggest not to routinely administer morphine to all patients with STEMI Patients with STEMI and Heart failure may require therapy for volume overload with diuretics and supportive care for their respiratory distress with supplemental oxygen and positive pressure ventilation. NSTEMI: Now we will be moving onto the diagnosis and management of Non- ST elevation myocardial infarctions or NSTEMI. Here are the 2014 American Heart Association’s latest clinical practice guidelines for you to review. Again, a diagnosis of NSTEMI requires prompt recognition, diagnosis, and treatment from providers. It is estimated that 60 to 65 percent of myocardial infarctions occur in patients over the age of 65 years, and 33 percent occur in patients over the age of 75 years. Unfortunately, around 80 percent of all deaths related to myocardial infarctions occur in people of the age of 65 years. Elderly patients are more likely to have an NSTEMI rather than a STEMI. Elderly patients also present with atypical symptoms to include syncope, weakness, and confusion which can delay diagnosis and therapy. Patients can also present with cocaine induced ischemic symptoms, and the provider should avoid betablockers due to the possibility of exacerbating coronary artery vasoconstriction in the setting of an acute myocardial infarction. Definitions: Among patients considered to have angina, there are three common clinical presentations of angina that suggest acute coronary syndrome. These would include angina at rest which is usually more than 20 minutes in duration, new onset angina that markedly limits the patient’s activities, and increasing angina that is more frequent, longer in duration, and or occurs with less exertion than previous angina. Unstable angina is considered to be present in patients with ischemic symptoms suggestive of acute coronary syndrome and no elevation in troponins, with or without EKG changes indicative of ischemia. NSTEMI is considered to be present in patients having the same manifestations as patients with unstable angina, but they will have an elevation in troponins. The elevations of troponins may not be detectable for hours after presentation, unstable angina and NSTEMI are frequently indistinguishable at initial presentation. For this reason initial management for these syndromes are treated the same. Diagnosis: Unstable angina, acute non-ST elevation myocardial infarction, and acute ST elevation myocardial infarction are the three presentations of acute coronary syndromes. The first step in the management of patients with acute coronary syndrome is prompt recognition and testing with an EKG and serial cardiac enzymes. Once the diagnosis of either unstable angina or acute NSTEMI, the acute management of the patient involves relief of ischemic pain, assessment of the patient’s hemodynamics like hypertension and tachycardia. History, ECG, and cardiac biomarkers are the mainstays in the evaluation. An ECG should be performed as soon as possible in patients presenting with chest pain or those with a concern for ACS. A normal ECG does not exclude ACS and NSTEMI. ST-elevation or anterior ST depression should be considered a STEMI until proven otherwise and treated as such. Findings suggestive of NSTEMI include transient ST elevation, ST depression, or new T wave inversions. ECG should be repeated at predetermined intervals or if symptoms return. Cardiac troponin is the cardiac biomarker of choice. Troponin is more specific and more sensitive than other biomarkers and becomes elevated relatively early in the disease process. While contemporary cardiac troponin may not be elevated within the first 2 to 4 hours after symptom onset, newer high sensitivity troponin assays have detectable elevations much earlier. It is also true that the amount of troponin released, and therefore the time to elevation, is proportional with infarct size, so it is unlikely to have a negative initial troponin with larger infarcts. Regardless of infarct size, most patients with true ischemia will have elevations in troponin within 6 hours, and negative troponins at this point effectively rule out infarct in most patients. Most assays use a cutoff value of greater than a 99th percentile as a positive test. In older, contemporary troponin assays, no detectable troponin is reported in most healthy individuals without the disease. Newer high sensitivity troponin assays often will report a normal detectable range in healthy individuals without the disease. NSTEMI is diagnosed in patients determined to have symptoms consistent with ACS and troponin elevation but without ECG changes consistent with STEMI. Unstable angina and NSTEMI differ primarily in the presence or absence of detectable troponin leak. Initial therapy: Patients with unstable angina or acute NSTEMI should be treated with an early medical regimen similar to that used in an acute STEMI with one exception which includes no benefit with fibrinolysis and actually an increased risk of harm for the patient. Oxygen is only recommended in patients with oxygen saturations less than 94% and with no signs of respiratory distress. The theory is that hyperoxia has been shown to have direct vasoconstrictor effect on the coronary arteries. Ultimately, stop placing routine oxygen on your patients, especially the ones who are having chest pain. Sublingual nitro is administered to patients with ischemic chest pain, followed by intravenous nitroglycerin in patients with persistent pain after 3 sublingual nitroglycerin tablets were give, for hypertension, or for heart failure. The provider needs to be mindful with nitrates, as the complication with severe hypotension can have detrimental effects due to serious hemodynamic decompensation as seen with right ventricular infarction or severe aortic stenosis. Also nitrates are contraindicated in patients who have taken a phosphodiesterase inhibitor for erectile dysfunction within the previous 24 hours. In the setting of acute myocardial infarction, intravenous morphine should be avoided if possible and reserved for patients with an unacceptable level of pain. Betablocker therapy is initiated in all patients without contraindications within 24 hours. Patients should also be started on high intensity statin therapy with Atorvastatin or rosuvastatin. This therapy should be started regardless of low density lipoprotein cholesterol level. The provider will also need to obtain baseline and follow up liver function tests, and monitor patient for muscle pain. Antiplatelet therapy with aspirin and a platelet P2Y12 receptor blocker is indicated in all patients with a NSTEMI. This therapy should be started as soon as diagnosis is made. The provider will need to monitor for excessive dosing of antithrombotic and antiplatelet agents as these can increase the patient’s bleeding risk. There is limited evidence to suggest that treating a patient’s electrolyte abnormalities by maintaining potassium levels greater than 4 and magnesium levels greater than 2 may have a benefit to the patient. For this reason, it is suggested to monitor and treat patients as needed with electrolyte repletion. Patients with NSTEMI are at a higher risk for atrial and ventricular arrythmias which can cause hypoperfusion and death. The provider will need to proactively manage arrythmias.. Risk stratification: Early risk stratification in patients with acute coronary syndromes is essential to identify patients at highest risk for further cardiac events who may benefit from a more aggressive therapeutic approach. Several tools and scores have been developed to assist in the workup of ACS. The HEART score was specifically developed for emergency department patients and has gained popularity in this setting. NSTEMI Treatment and Management: Initial management strategies aim to reduce cardiac ischemia and prevent death. Oxygen, aspirin, and nitrates are administered based on initial concern for ACS and prior to a definitive diagnosis. Subsequent treatment depends on confirmation of diagnosis or a high index of suspicion with or without a definitive diagnosis. Oxygen was previously recommended for all patients presenting with concern for ACS, but newer data suggests this strategy may be harmful in patients who otherwise do not warrant supplemental oxygen. Supplemental oxygen is now recommended in patients with oxygen saturation less than 90%, those with respiratory distress, or when high-risk features of hypoxemia are present. Chewable aspirin should be given to all patients who present with concern for ACS unless otherwise contraindicated. Patients with ongoing symptoms should receive sublingual nitroglycerin every 5 minutes for up to three doses or until the pain is relieved, unless otherwise contraindicated. Contraindications include the recent use of phosphodiesterase inhibitors and hypotension. Nitrates should be used with extreme caution in patients with concerns for right-sided infarction. Continuous intravenous nitroglycerin should be considered in patients with persistent signs of heart failure or hypertension. Many patients will present with concern for ACS but will not have positive findings of ischemic ECG changes or positive troponin on initial workup. These patients may be observed with serial ECG and troponin measurements every 3 to 6 hours. Patients also may undergo testing such as the treadmill stress test or myocardial perfusion imaging. Low-risk patients often may be discharged with a referral for further outpatient testing after initial ACS is ruled out. In patients where NSTEMI has been definitively diagnosed or is highly likely, anticoagulation should be initiated. Cardiology consultation should be obtained. This is especially true when there is the possibility of percutaneous intervention, as this may change anticoagulation strategies. Unfractionated heparin with bolus dosing and a continuous infusion is commonly used. Other strategies may include the use of enoxaparin, bivalirudin, fondaparinux, and dual antiplatelet therapies. Fibrinolytic therapies should not be used in NSTEMI. When NSTEMI has been diagnosed, patients should be admitted to cardiac care units for further management. Beta-blocker therapy should be started within 24 hours after the presentation in patients who do not have a contraindication. Contraindications include signs of heart failure, hypotension, heart conduction block, or reactive airway disease. Unless otherwise contraindicated, ACE Inhibitors should be initiated in patients with an ejection fraction less than 40%, hypertension, diabetes, or chronic kidney disease. High-dose statins should be initiated for cholesterol management. Prognosis and complications: Patients who present with NSTEMI have a lower 6-month mortality rate than those who present with unstable angina. Morbidity and mortality further depend on the degree of troponin elevation as well as comorbid conditions such as the severity of diabetes, presence of peripheral vascular disease, presence of renal dysfunction, and dementia. Complications of NSTEMI are secondary to the systemic effects of the disease rather than structural complications of STEMI. Cardiomyopathy with diffuse hypokinesis may be seen but left ventricular aneurysms or papillary muscle dysfunction is rare. Pulmonary edema due to poor cardiac output may be seen in severe cases. Other complications of poor cardiac output such as renal dysfunction may be seen as well. CPR/ ACLS: Now, we're going to move on to cardiopulmonary resuscitation. The focus here is not the ACLS guidelines, but to focus more on discussion of withholding or terminating CPR. Here, you will see four conditions in, which withholding resuscitation efforts are acceptable. Those are conditions not compatible with life. If a patient has a clearly documented DNR status, if the patient has obvious signs of death and then unsafe conditions for which the rescuer would have to perform CPR. Terminating resuscitative efforts. Situations vary greatly during a code and the amount of time is spent resuscitating a patient. Terminating efforts are not set in stone and, in many cases, as a judgement call. Practitioners should consider whether their arrest was witnessed, the initial arrest rhythm and the time elapsed between arrest and CPR. A return of spontaneous circulation at some point during the resuscitative efforts should also be considered. When it comes to adults in a hospital setting, stopping resuscitative efforts may depend on duration of CPR, the cause of the cardiac arrest, and the patient's overall health condition or status. Unfortunately, literature is lacking or fails to be definitive in regards to termination of resuscitative efforts. Literature has varied widely on the time whereas some report 15 to 20 minutes resuscitative efforts as having good outcomes and others stating once on a higher end of time such as 20 to 30 minutes as having a poor prognosis. As mentioned above, the patient's overall health status and reason for arrest may play a large part into how the patient responds or does post-arrest. Factors that are shown to improve survivability include witnessed cardiac arrest with immediate CPR and utilization of defibrillation when indicated. Young and healthy patients are more likely to obtain ROSC compared to the elderly and those who have more co-morbidities. Those who are a victim of penetrating trauma have an increased chance of survival than blunt traumatic arrest. Studies have not shown proven benefit for advanced life support level of care in cardiac arrest, including endotracheal intubation and intravenous medication administration. Additional considerations include that healthcare workers understand the legal and ethical considerations for making the decision to withhold or terminate resuscitation. Keep in mind that you may not always know the patient's code status particularly outside of the hospital. If you have any doubt regarding code status, err on the side of caution and start resuscitation. Life- saving measures can be terminated once you have determined the patient is a DNR. Family support is essential. Regardless at the age or condition of the patient, the loss of the loved one is difficult to deal with even if expected. Family members may have different needs based on their spiritual beliefs and cultural background. Provide support from social workers and hospital chaplains when resuscitation is terminated. Then, debriefing may be an effective tool to discuss what went well during the resuscitation and what can be improved. It provides an opportunity to express negative feelings, which can be beneficial for team members after a difficult code. Targeted temperature management: If ROSC is obtained, the determination to provide targeted temperature management will be made. Targeted temperature management aims to reduce mortality and improve neurological outcomes in unresponsive patients who achieve ROSC after cardiac arrest. Candidates for targeted temperature management include those who have a medical etiology, are unresponsive and are stable. The goal is to achieve a core temperature of 32 to 34 degrees Celsius as soon as possible, maintain this temperature for 12 to 24 hours, and then rewarm at a controlled rate of 0.2 to 0.5 C/hour. Targeted temperature management has shown to improve mortality and neurological outcomes in patients who have survived a medical cardiac arrest. Every hospital institution should have protocols for induction, cooling, and rewarming. The 2015 recommendations for post-cardiac arrest care from the American Heart Association include using targeted temperature management to treat patients who are comatose after out of hospital cardiac arrest with initial rhythms of pulseless ventricular tachycardia or ventricular fibrillation which is Class 1 with strong evidence, as well as using targeted temperature management to treat patients who are comatose after in-hospital cardiac arrest and patients with non-shockable rhythms. The 2015 International Consensus on CPR and Emergency Cardiovascular Care Science with Treatment Recommendations from the International Committee on Resuscitation recommends hypothermia for patients who are comatose after out of hospital cardiac arrest with initial shockable or non-shockable rhythm and for patients who are comatose after in-hospital cardiac arrest with an initial rhythm. Case Study: A 55-year-old man presents to the ED with sudden onset of chest pain described as crushing pressure, shortness of breath, and diaphoresis. He was shoveling snow from his driveway two hours ago. The ECG shows a heart rate of 65 beats/min and ST-segment elevations of 3 mm in leads II, III, and aVF. Troponin levels are elevated, and blood pressure is 134/86 mm Hg. He continued to have chest pain after three doses of sublingual nitroglycerin and has required nitroglycerin 10 mcg/min IV to keep him free of chest pain. The patient was immediately transferred to the ICU. The patient was given aspirin 325 mg and plavix, and lovenox was started. ECG changes persist after one hour but are now only 1-mm elevations of the ST segments. Mild Jugular venous distention is noted on physical examination. The lungs have minimal rales at both lung bases. The heart sounds are normal without murmurs, and there are no S3 and S4 sounds heard. There is no lower extremity edema. The patient is breathing at 18 breaths/min without labor. He states he smokes 1 pack per day for the last 20 years. He has a history of dyslipidemia but is not compliant with statin therapy. ▪ What is the most likely diagnosis? ▪ What immediate therapeutic steps are indicated? ▪ What is the preferred treatment option for his condition? Answer: A 55-year-old man presents with an acute ST-elevation myocardial infarction (STEMI). Most likely diagnosis: Inferior wall ST-segment elevation MI (STEMI). ST elevations present in II, III, and aVF with elevated cardiac biomarkers confirm diagnosis of STEMI. Immediate steps in treatment: Administer aspirin 325 mg, clopidrogel, pain control with itroglycerin and morphine, low flow oxygen via nasal cannula, beta-blockade if not in heart failure, prepare patient for percutaneous coronary intervention and activate the cardiology and catheterization team. Treatment option: Differs depending upon whether the MI is a STEMI or a non-STEMI with PCI being the preferred treatment for STEMI and thrombolytic therapy with TPA an option when PCI is not possible. Bypass surgery backup should be available. Question: A 73-year-old woman is evaluated in the ED and transferred to the ICU because of chest pain of 4 hours’ duration. Her medical history includes a 20-year history of hypertension and Type II diabetes mellitus. Her medications include metformin, atenolol, and ASA. On physical examination, her blood pressure is 130/84 mm Hg, and her heart rate is 87 beats/min and regular. Her jugular vein is distended to 5 cm while the patient is upright. She has a faint left carotid bruit and bibasilar crackles to one quarter up from the lung bases. A normal S1 and S2 is heard, with a grade II/VI holosystolic murmur heard best at the apex to the axilla. An electrocardiogram from six months ago was normal. The ECG was seen during the chest pain. The initial serum troponin measurement is elevated. She is now admitted to the ICU for an MI. She is free of chest pain while on IV nitroglycerin, and her vital signs are stable. Which of the following is the most likely ECG diagnosis? A. Left bundle branch block with normal sinus rhythm B Idioventricular tachycardia C Right bundle branch block D Third-degree atrioventricular block (complete heart block) E Mobitztype II second-degree atrioventricular block Answer: The correct answer is A. The chest pain, elevated cardiac biomarkers, and new-onset left bundle branch block are considered equivalent to having an ST-elevation myocardial infarction (STEMI. The presentation of ACS with new left bundle branch block should be considered equivalent to a STEMI and true posterior wall MI, with management including early coronary intervention. Question: A 55-year-old man in the ICU has ACS, with 2 mm of ST elevation on the leads II, III, and aVF. The troponins are positive. The blood pressure is 130/70 mm Hg on a nitroglycerin drip at 5 μg/kg/min keeping the patient chest pain free, but ECG changes persist and only 1 mm of ST elevation is seen. There is no lower extremity edema. The patient was given ASA upon entry into the ED. What is/are the next best steps in the management of this patient? ▪ A Anticoagulation, IV β-blocker, ACE inhibitor, nitroglycerin, and alert catheterization lab ▪ B Give tissue plasminogen activator (TPA) ▪ C Increase nitroglycerin to 10 μg/kg/min ▪ D Get β-natriuretic peptide (BNP) level ▪ E Call cardiac surgeon for stat CABG post-PCI Answer: The correct answer is A. This patient is having a STEMI. Antithrombotic therapy is indicated. The combination of heparin and ASA reduces the incidence of MI. When administered immediately, ASA reduces mortality in patients with unstable angina or acute infarction by diminishing platelet aggregation. β-Blockers diminish myocardial oxygen demand by reducing heart rate, systemic arterial pressure, and myocardial contractility. An ACE inhibitor should be administered early in the course of ACS in most patients. ACE inhibitor therapy may also reduce the risk of recurrent infarction. In patients who cannot tolerate an ACE inhibitor, an ARB is an alternative. Statin therapy appears to improve endothelial function and reduce the risk of future ACS. Question: A 65-year-old man with history of diabetes presents to the Emergency Department stating he has had substernal chest pain and diaphoresis for 45 minutes. Which is the most important next step in management? ▪ A Sublingual nitroglycerin ▪ B Oxygen ▪ C Placement of defibrillator pads ▪ D Aspirin to chew ▪ E Morphine sulfate Answer: The most appropriate answer is D. While all of these interventions may be useful, aspirin significantly decreases mortality, with almost no downside in non-allergic patients, and it should be given immediately. Thus, aspirin is the first intervention. Question: In the initial evaluation of a patient with chest pain, which is the most important diagnostic test? ▪ A Treadmill stress test ▪ B PT ▪ C Chest x-ray ▪ D Troponin ▪ E ECG Answer: The correct answer is E. The history of chest pain is important to obtain. The ECG is the crucial first diagnostic test in the evaluation of chest pain. Presence versus absence of ST elevation represents a major branch point in deciding treatment. Serum cardiac levels take time and sometimes are not elevated at the time of patient encounter. Question: A 54-year-old man is seen at a rural ED with 1 hour of nausea and substernal chest pain radiating to his jaw. The ECG shows STEMI. PCI is not performed at this hospital and only performed at a hospital 2 1/2 hours away. Which of the following statements is most accurate? ▪ A Obtain a repeat ECG to assess if the patient truly has a STEMI. ▪ B Transfer the patient now for emergent PCI. ▪ C Administer thrombolytics, then transfer to PCI center. ▪ D Give aspirin, start heparin, and obtain a thallium stress test. Answer: The correct answer is C. PCI is the treatment of choice when it can be performed rapidly by an experienced cardiologist. However, if a patient presents to a hospital that does not offer PCI and cannot be transferred to one within 120 minutes, administration of thrombolytics, preferably within 30 minutes of arrival, is indicated. The patient should then be transferred to the nearest PCI center. Question: Which of the following is NOT an accurate description of hypothermia therapy for post-cardiac arrest patients? ▪ A Rapid cooling to reduce core temperature to 32-34°C for 24-48 hours ▪ B Therapeutic hypothermia has a proven effect in reducing the rate of recurrent ventricular fibrillation ▪ C Therapeutic hypothermia is associated with increased infections and bleeding complications ▪ D Therapeutic hypothermia is associated with some improved recovery of myocardial functions ▪ E The primary benefit of therapeutic hypothermia in the post-arrest patient is improved neurologic recovery Answer: The correct answer is B. Therapeutic hypothermia describes the practice of rapid cooling of patients to core temperatures of 32-42°C for 24-48 hours. This treatment approach has been shown to reduce the neurologic sequelae in the post-arrest patients. The treatment has also been suggested to improve the myocardial dysfunction associated with post-cardiac arrest patients. Therapeutic hypothermia has not been shown to reduce the recurrence of ventricular arrhythmia in post-arrest patients. Early coronary angiography and percutaneous coronary interventions have been demonstrated to prevent recurrent cardiac arrhythmias and sudden cardiac death. Question: A 64-year-old man who was being treated in the hospital for acute cholecystitis is found to be unresponsive. He was noted to be in VF and underwent chest compressions for several minutes in addition to cardioversion. The patient has return of spontaneous rhythm and vital signs. Which of the following is an important treatment for this patient? A Target oxygen saturation of 91% B Target serum glucose level at 110 mg/dL C Percutaneous coronary angiography D Target core body temperature of 35°C to 36°C E Continue fluid resuscitation for 12 hours Answer: The correct answer is C. Acute coronary syndrome is a likely cause for the VF arrest. Early cardiac intervention has been shown to improve prognosis in post-VF arrest patients. TH to target core temperatures of 32°C to 34°C and maintenance of serum glucose in the 144 to 180 mg/dL range are practices that have been reported to improve outcome. Resuscitation to achieve early hemodynamic goals (first 6 hours) has been shown to improve survival in septic patients; however, prolongation of resuscitation has not been shown to improve outcome. Intolerance of feeding, decreased pulmonary compliance, decreased oxygenation, and the development of abdominal compartment syndrome are associated with excess initial fluid administration and failure to reduce fluid administration following initial resuscitation from septic shock. Question: Which of the following statements regarding out-of-hospital sudden cardiac arrest (SCA) is true? ▪ A Bystander CPR is associated with reduced survival in SCA. ▪ B An initial rhythm of VT/VF is associated with reduced survival in SCA. ▪ C Interruption of CPR does not impact outcome in SCA. ▪ D The provision of AEDs in public places is associated with reduced survival in SCA. ▪ E Therapeutic hypothermia improves neurological outcome after SCA in patients with depressed mental status after resuscitation. Answer: The correct answer is E. Therapeutic hypothermia for 24–36 hours following revival after cardiac arrest in patients with altered mental status. Survival following out-of-hospital cardiac arrest has improved in recent years in part because of better awareness of heart disease in the general population and the availability of AED therapy in public places. Immediate, uninterrupted bystander CPR also improves outcome, as does presenting initially with a “shockable” rhythm such as VT or VF. Question: What type of MI is pictured? ▪ A. Septal ▪ B. Posterior ▪ C. Inferior ▪ D. Anterolateral Answer: The correct answer is C. As you can see the ST elevation is seen in leads II, III, and avF indicating the right coronary artery is occluded. the patient should be sent for emergency cardiac angiography to the catheterization lab with a goal door-to-vessel open time of under 90 minutes. Thrombolysis should be considered, depending on facility capability or anticipated long transport time to an interventional catheterization lab. If there is evidence of right ventricular infarction, avoid nitrates and provide volume to assure adequate preload. The right ventricle contains less myocardium than the left and is dependent on adequate preload to assure adequate cardiac function. If there is damage to the right ventricle, preload reduction from nitrates could result in significant hypotension. If this occurs, resuscitation with intravenous crystalloids and possible vasopressors are needed. Other treatment includes aspirin load with 162 to 325 mg, unfractionated heparin, GP IIb/IIIa antagonist, and additional P2Y12 anti-platelets such as clopidogrel.