Chapter 19 - Chest Discomfort Flashcards
How can one triage patients who present with chest discomfort?
“(1) myocardial ischemia (2) other cardiopulmonary causes (pericardial disease, aortic emergencies, and pulmonary conditions); and (3) non-cardiopulmonary causes.”
Summarize the epidemiology of chest discomfort in the United States.
“Chest dicomfort is the third most common reason for visits to the ED in the United States, resulting in 6 to 7 million emergency visits each year. More than 60% of patients with this presentation are hospitalized for further testing, and the rest undergo additional investigation in the ED. Fewer than 25% of evaluated patients are eventually diagnosed with acute coronary syndrome, with rates of 5-15% in most series of unselected populatios. In the remainder, the most common diagnoses are gastrointestinal causes, and fewer than 10% are other life-threatening cardiopulmonary conditions.”
How many patients are discharged from the emergency department with chest discomfort of presumed non-ischemic etiology who have had a missed myocardial infarction?
2-6%.
In a study with more than 350 000 patients with unspecified non-cardiopulmonary chest discomfort, what mortality would you expect after 1-year follow up?
Less than 2%, which is similar to the death rate in the general population, age-adjusted.
After excluding patients with ST-segment elevation or definite noncardiac chest pain, how many patients with chest discomfort stratified as low risk will have a major cardiovascular event through a 30-day follow-up?
2,5%.
What is the duration of myocardial cell hypoxia that leads to irreversible damage? Compare it to the usual duration of myocardial infarction.
20 minutes and ≥30 minutes, respectively.
Make the correlation between the type of angina pectoris and the EKG and cardiac biomarkers alterations. Also, explain the pathophysiology that is mostly associated with each type of these findings.
“Stable angina is characterized by ischemic episodes that are typically precipitated by a superimposed increase in oxygen demand during physical exertion and relieved upon resting. Ischemic heart disease becomes unstable most commonly when rupture or erosion of one or more atherosclerotic lesions triggers coronary thrombosis. Unstable ischemic heart disease is classified clinically by the presence or absence of detectable myocardial injury and the presence or absence of ST-segment elevation on the patient’s electrocardiogram (ECG). When acute coronary atherothrombosis occurs, the intracoronary thrombus may be partially obstructive, generally leading to myocardial ischemia in the absence of ST-segment elevation. Marked by ischemic symptoms at rest, with minimal activity, or in an accelerating pattern, unstable ischemic heart disease is classified as unstable angina when there is no detectable myocardial injury and as non-ST elevation MI (NSTEMI) when there is evidence of myocardial necrosis. When the coronary thrombus is acutely and completely occlusive, transmural myocardial ischemia usually ensues, with ST-segment elevation on the ECG and myocardial necrosis leading to a diagnosis of ST elevation MI (STEMI).”
Name causes for ischemia due to the following: (i) increased oxygen demand; (ii) decreased oxygen delievery.
(i) increases in heart rate, ventricular wall stress and myocardial contractility, as well as during intense psychological stress or fever);
(ii) anemia, hypoxia or hypotension.
Classify the acute coronary syndromes in different types.
Type 1: acute coronary thrombosis.
Type 2: imbalance of myocardial oxygen sypply and demand.
Name three examples of vascular dominant causes of cardiac ischemia without obvious arterious obstruction.
Endotelial dysfunction, microvascular disease and vasospasm.
Give examples of non-atherosclerotic processes that might lead to myocardial ischemia.
“non-atherosclerotic processes, including congenital abnormalities of the coronary vessels, myocardial bridging, coronary arteritis, and radiation-induced coronary disease, can lead to coronary obstruction. In addition, conditions associated with extreme myocardial oxygen demand and impaired endocardial blood flow, such as aortic valve disease, hypertrophic cardiomyopathy, or idiopathic dilated cardiomyopathy, can precipitate myocardial ischemia in patients with or without underlying ostructive atherosclerosis.”
Heberden initially described angina as a sense of “strangling and anxiety”.
True or False?
True.
How does one differentiate stable from unstable angina with clinical history information?
“Stable angina usually begins gradually and reaches its maximal intensity over a period of minutes before dissipating within several minutes with rest or with nitroglycerin. The discomfort typically occurs predictably at a characteristic level of exertion of psychological stress. By definition, unstable angina is manifest by self-limited anginal chest discomfort that is exertional but occurs at increased frequency with progressively lower intensity of physical activity or even at rest. Chest discomfort associated with MI is typically more severe, is prolonged (usually lasting ≥30 miin), and is not relieved by rest.”
How would you describe the chest discomfort due to ischemic cardiac disease?
“Chest discomfort characteristic of myocardial ischemia is typically described as aching, heavy, squeezing, crushing, or constricting. However, in a substantial minority of patients, the quality of discomfort is extremely vague and may be described as a mild tightness, or merely an uncomrfortable feeling, that sometimes is experienced as numbness or a burning sensation. The site of the discomfort is usually retrosternal, but radiation is common and generally occurs down the ulnar surface of the left arm; the right arm, both arms, neck, jaw, or shoulders may also be involved.”
Summarize the mechanisms of cardiac pain, referred pain and irradiated pain.
“Ischemic episodes are thought to excite local chemosensitive and mechanoreceptive receptors that, in turn, stimulate release of adenosine, bradykinin, and other substances that activate the sensory ends of sympathetic and vagal afferent fibers. The afferent fibers transverse the nerves that connect to the upper five thoracic sympathetic ganglia and upper five distal thoracic roots of the spinal cord. From there, impulses are transmitted to the thalamus. Within the spinal cord, cardiac sympathetic afferent impulses may converge with impulses from somatic thoracic structures, and this convergence may be the basis for referred cardiac pain. In addition, cardiac vagal afferent fibers synapse in the nucleus tractus solitarius of the medulla and then descend to the upper cervical spinothalamic tract, and this route may contribute to anginal pain experienced in the neck and jaw.”
The visceral surface and most of the parietal surface of the pericardium are insensitive to pain.
True or False?
True.
“the pain of pericarditis is thought to arise principally from associated pleural inflammation and is more common with infectious causes of pericarditis, which typically involve the pleura.”
How does one explain the shoulder and neck pain, as well as upper abdominal pain that might occur in those with pericarditis?
“owing to the overlapping sensory supply of the central diaphragm via the phrenic nerve with somatic sensory fibers originating in the third to fifth cervical segments, the pain of pleural pericarditis is often referred to the shoulder and neck. Involvement of the pleural surface of the lateral diaphragm can lead to pain in the upper abdomen.”
Summarize the features of Takotsubo cardiomypathy.
“The symptoms of Takotsubo (stress-related) cardiomyopathy often start abruptly with chest pain and shortness of breath. This form of cardiomyopathy, in its most recognizable form, is triggered by an emotionally or physically stressful event and may mimic acute MI because of its commonly associated ECG abnormalities, including ST-segment elevation, and elevated biomarkers of myocardial injury. Observational studies support a predilection for women >50 years of age.”
How does one explain the pathophysiology of pain due to myocarditis?
Myocardial inflammation or severe inscrease in wall stress related to poor ventricular performance.
Name the conditions that might lead to acute aortic disease and their definitions.
“Acute aortic dissection is a less common cause of chest discomfort but is important because of the catastrophic natural history of certain subsets of cases when recognized late or left untreated. Acute aortic syndromes encompass a spectrum of acute aortic diseases related to disruption of the media of the aortic wall. Aortic dissection involves a tear in the aortic intima, resulting in separation of the media and creation of a separate “false” lumen. A penetrating ulcer has been described as ulceration of an aortic atheromatous plaque that extends through the intima and into the aortic media, with the potential to initiate an intramedial dissection or ruptute into the adventitia. Intramural hematoma is an aortic wall hematoma with no demonstrable intimal flap, no radiologically apparent intimal tear, and no false lumen. Intraluminal hematoma can occur due to either rupture of the vasa vasorum or, less commonly, a penetrating ulcer.”
What is the typical pain due to an acute aortic syndrome?
“acute aortic syndrome typicaly presents with chest discomfort that is often severe, sudden in onset, and sometimes described as “tearing” in quality. Acute aortic syndromes involving the ascending aorta tend to cause pain in the midline of the anterior chest, whereas descending aortic syndromes most often present with pain in the back. Therefore, dissections that begin in the ascending aorta and extend to the descending aorta tend to cause pain in the fron of the chest that extends toward the back, between the shoulder blades.”
Which type of aortic dissection has a greater risk of complications? Why is it so?
“Proximal aortic dissections that involve the ascending aorta (type A in the Stanford nomenclature) are at high risk for major complications that may influence the clinical presentation, including (1) compromise of the aortic ostia of the coronary arteries, resulting in MI; (2) disruption of the aortic valve, causing acute aortic insufficiency; and (3) rupture of the hematoma into the pericardial space, leading to pericardial tamponade.”
Compare the incidence of acute aortic syndromes to that of pulmonary embolism.
3 cases per 100 000 versus ~1 per 1000 persons, respectively.
