Chapter 19 - Chest Discomfort Flashcards Preview

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Flashcards in Chapter 19 - Chest Discomfort Deck (59)
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1
Q

How can one triage patients who present with chest discomfort?

A

“(1) myocardial ischemia (2) other cardiopulmonary causes (pericardial disease, aortic emergencies, and pulmonary conditions); and (3) non-cardiopulmonary causes.”

2
Q

Summarize the epidemiology of chest discomfort in the United States.

A

“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.”

3
Q

How many patients are discharged from the emergency department with chest discomfort of presumed non-ischemic etiology who have had a missed myocardial infarction?

A

2-6%.

4
Q

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?

A

Less than 2%, which is similar to the death rate in the general population, age-adjusted.

5
Q

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?

A

2,5%.

6
Q

What is the duration of myocardial cell hypoxia that leads to irreversible damage? Compare it to the usual duration of myocardial infarction.

A

20 minutes and ≥30 minutes, respectively.

7
Q

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.

A

“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).”

8
Q

Name causes for ischemia due to the following: (i) increased oxygen demand; (ii) decreased oxygen delievery.

A

(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.

9
Q

Classify the acute coronary syndromes in different types.

A

Type 1: acute coronary thrombosis.

Type 2: imbalance of myocardial oxygen sypply and demand.

10
Q

Name three examples of vascular dominant causes of cardiac ischemia without obvious arterious obstruction.

A

Endotelial dysfunction, microvascular disease and vasospasm.

11
Q

Give examples of non-atherosclerotic processes that might lead to myocardial ischemia.

A

“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.”

12
Q

Heberden initially described angina as a sense of “strangling and anxiety”.
True or False?

A

True.

13
Q

How does one differentiate stable from unstable angina with clinical history information?

A

“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.”

14
Q

How would you describe the chest discomfort due to ischemic cardiac disease?

A

“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.”

15
Q

Summarize the mechanisms of cardiac pain, referred pain and irradiated pain.

A

“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.”

16
Q

The visceral surface and most of the parietal surface of the pericardium are insensitive to pain.
True or False?

A

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.”

17
Q

How does one explain the shoulder and neck pain, as well as upper abdominal pain that might occur in those with pericarditis?

A

“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.”

18
Q

Summarize the features of Takotsubo cardiomypathy.

A

“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.”

19
Q

How does one explain the pathophysiology of pain due to myocarditis?

A

Myocardial inflammation or severe inscrease in wall stress related to poor ventricular performance.

20
Q

Name the conditions that might lead to acute aortic disease and their definitions.

A

“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.”

21
Q

What is the typical pain due to an acute aortic syndrome?

A

“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.”

22
Q

Which type of aortic dissection has a greater risk of complications? Why is it so?

A

“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.”

23
Q

Compare the incidence of acute aortic syndromes to that of pulmonary embolism.

A

3 cases per 100 000 versus ~1 per 1000 persons, respectively.

24
Q

Name the major risk factors for aortic dissection.

A

“Nontraumatic aortic disssections are very rare in the absence of hypertension or conditions associated with deterioration of the elastic or muscular components of the aortic media, including pregnancy, bicuspid aortic disease, or inherited connective tissue diseases, such as Marfan and Ehlers-Danlos syndromes.”

25
Q

How does one explain pathophysiologically the chest pain due to pulmonary embolism?

A

“Typically pleuritic in pattern, the chest discomfort is associated with pulmonary embolism may result from (1) involvement of the pleural surface of the lung adjacent to a resultant pulmonary infarction; (2) distension of the pulmonary artery; or (3) possibly, right ventricular wall stress and/or subendocardial ischemia related to acute pulmonary hypetsnion. The pain associated with small pulmonary emboli is often lateral and pleuritic and is believed to be related to the first of these three possible mechanisms. In contrast, massive pulmonary emboli is often lateral and pleuritic and is believed to be related to the first of these three possible mechanisms. In contrast, massive pulmonary emboli may cause severe substernal pain that may mimic an MI and that is plausibly attributed to the second and third of these potential mechansims.”

26
Q

What is the incidence of primary spontaneous pneumothorax?

A

7 per 100 000 among men and less than 2 per 100 000 among women.

27
Q

Name the risk factors for primary spontaneous pneumothorax.

A

Male sex, smoking, family history, and Marfan syndrome.

28
Q

What type of esophageal disease closely mimics myocardial infarction?

A

“The pain of esophageal spasm, in contrast, is commonly an intense, squeezing discomfort that is retrosternal in location and, like angina, may be relieved by nitroglycerin or dihydropyridine calcium channel antagonists.”

29
Q

Why should one consider hepatobiliary disorders in the differential diagnosis of chest discomfort?

A

“Hepatobiliary disorders, including cholecystitis and biliary colic, may mimic acute cardiopulmonary diseases. Although the pain arising from these disorders usually localizes to the right upper quadrant of the abdomen, it is variable and may be felt in the epigastrium and radiate to the back and lower chest. This discomfort is sometimes referred to the scapula or may in rare cases be felt in the shoulder, suggesting diaphragmatic irritation. The pain is teady, usually lasts several hours, and subsides spontaneouly, without symptoms between attacks. Pain resulting from pancreatitis is typically aching epigastric pain that radiates to the back.”

30
Q

Name three syndromes that might be associated with chest discomfort.

A

Mallory-Weiss, Booerhave and Tietze.

31
Q

How many patients with chest discomfort that present to the emergency room have a panic disorder or related condition as the cause of this symptom?

A

10%

32
Q

Name five conditions which need prompt interventions due to its high-risk and related to chest discomfort leading to emergency department visit.

A

“The high-risk conditions of principal concern are acute cardiopulmonary processes, including ACS, acute aortic syndrome, pulmonary embolism, tension pneumothorax, and pericarditis with tamponade. Among non-cardiopulmonary causes of chest pain, esophageal rupture likely holds the greatest urgency for diagnosis.”

33
Q

Patients sometimes use the word “sharp” to convey the intensity of discomfort rather than the quality of chest pain.
True or False?

A

True.

34
Q

Regading the quality of pain give examples of unusual quality of the following: (i) miochardial ischemia; (i) pulmonary embolism and pericarditis; (iii) acute aortic syndromes.

A

(i) any;
(ii) “Less frequently, the pain of pericarditis or massive pulmonary embolism is a steady severe pressure or aching that can be difficult to discriminate from myocardial ischemia.”
(iii) “However, acute aortic emergencies also present commonly with severe, knifelike pain.”

35
Q

Pain that occurs solely above the mandible or below the epigastrium is rarely angina. Also, the irradiating pain to the trapezius ridge is characteristic of pericardial pain and does not usually occur with angina.
True or False?

A

True.

36
Q

Pain that is fleeting (lasting only a few seconds) is rarely ischemic in origin. Similarly, pain that is constant in intensity for a prolonged period (many hours to days) is unlikely to represent myocardial ischemia if it occurs in the absence of other clinical consequences, such as abnomalities of the ECG, elevation of cardiac biomarkers, or clinical sequelae (e.g., heart failure or hypotension).
True or False?

A

True.

37
Q

Gastroesophageal reflux might be associated with morning pain.
True or False?

A

True.
“Both myocardial ischemia and acid reflux may have their onset in the morning, the latter because of the absence of food to absorb gastric acid.”

38
Q

How would you describe “warm-up angina”?

A

“clinicans should be aware of the phenomenon of “warm-up angina” in which some patients experience relief of angina as they continue at the same or even a greater level of exertion without symptoms.”

39
Q

How long afer a meal does one patient with peptic ulcer disease have chest discomfort complains?

A

60 to 90 minutes.

40
Q

What is the meaning of a delay in >10 minutes after nitroglycerin for chest discomfort?

A

“A delay of >10 min before relief is obtained after nitroglycerin suggests that the symptoms either are not caused by ischemia or are caused by severe ischemia, such as during acute MI.”

41
Q

What is the pathophysiology of nausea and vomiting in myocardial infarction?

A

“Alghough nausea and vomiting suggest a gastroitnestinal disorder, these symptoms may occur in the setting of MI (more commonly inferior MI), presumably because of activation of the vagal reflex or stimulation of left ventricular receptors as part of the Bezold-Jarisch reflex.”

42
Q

Give examples of chest discomfort accompanied with either hypotension or hypertension. Also, explain why acute aortic emergencies might be associated with either hypertension or hypotension.

A

“Significant tachycardia and hypotension are indicative of important hemodynamic consequences of the underlying cause of chest discomfort and should prompt a rapid survery for the most severe conditions, such as acute MI with cardiogenic shock, massive pulmonary embolism, pericarditis with tamponade, or tension pneumothorax. Acute aortic emergencies usually present with severe hypertension but may be associated with profound hypotension when there is coronary arterial compromise or dissection into the pericardium.”

43
Q

The presence of low-grade fever is specific because it may occur with MI and with thromboembolism in addition to infection.
True or False?

A

False.

It is nonspecific.

44
Q

Which ECG findings are suggestive of myocardial ischemia in the absence of STEMI?

A

“ST-segment depression and symmetric T-wave inversions at least 0,2mV in depth are useful for detecting myocardial ischemia in the absence of STEMI and are also indicative of higher risk of death or recurrent ischemia.”

45
Q

What is the ECG sensitivity for myocardial ischemia?

A

It is as low as 20% in some studies.

46
Q

Hyperventilation associated with panic disorder can lead to nonspecific ST and T-wave abnormalities.
True or False?

A

True.

47
Q

Rapid rule-out protocols that use serial testing an changes in troponin concentration over as short a period as 1-2 h appear promising and remain under investigation.
True or False?

A

True.

48
Q

Explain the utility of serial troponin measurement when one suspects myocardial ischemia.

A

“Because of superior cardiac tissue-specificity compared with creatine kinase MB, cardiac troponin is the preferred biomarker for the diagnosis of MI and should be measured in all patients with suspected ACS at presentation and repeated in 3-6 h. testing after 6 h is required only when there is uncertainty regarding the onset of pain or when stuttering symptoms have ocurred. It is not necessary or advisable to measure troponin in patients without suspicion of ACS unless this test is being used specifically for risk tratification (e.g., in pulmonary embolism or heart failure).”

“In addition, observation of a change in cardiac troponin concentration between serial samples is useful in discriminating acute causes of myocardial injury from chronic elevation due to underlying structural heart disease, end-stage renal disease, or interfering antibodies.”

49
Q

Myeloperoxidase and other putative biomarkers of acute myocardial ischemia or acute coronary syndromes have not been adopted in routine use.
True or False?

A

True.

50
Q

What is the clinical utility of integrative decision-aids algorithms? Specifiy the factors used for each of the available tools and their common features.

A

“decisionaids have been derived on the basis of their capacity to estimate either of two two closely related but not identical probabilities: (1) the probability of a final diagnosis of ACS and (2) the probability of major cardiac events during short-term follow-up. Such decision-aids are used most commonly to identify patients with a low clinical probability of ACS who are candidates either for early provocative testing for ischemia or for discharge from the ED. Goldman and Lee developed one of the first such decision-aids, using only the ECG and risk indicators - hypotension, pulmonary rales, and known ischemic heart disease - to categorize patients into four risk categories ranging from a less than 1% to a >16% probability of a major cardiovascular complication. The Acute Cardiac Ischemia Time-Insensitive Predictive Instrument (ACI-TIPI) combines age, sex, chest pain presence, and ST-segment abnormalities to define a probability of ACS. (…) Elements common to each of these tools are (1) symptoms typical for ACS; (2) older age; (3) risk factor or known atherosclerosis; (4) ischemic ECG abnormalities; and (5) elevated cardiac troponin levels. Although, because of very low specificity, the overall diagnostic performance of such decision-aids is poor (area under the receiver operating curve, 0,55-0,65), they can help identify patients with a very low probability of ACS (e.g., less than 1%). Nevertheless, no such decision-aid (or single clinical factor) is sufficiently sensitive and well validated to use as a sole tool for clinical decision-making.”

51
Q

TIMI and GRACE are examples of integrative decision-aids algorithms.
True or False?

A

False.
These tool are used after a an established diagnosis of acute coronary syndrome and are used to stratify the patient’s risk.

52
Q

When should one use a “stress test” for chest discomfort investigation?

A

“Early exercise testing is safe in patients without high-risk findings after 8-12 h of observation and can assist in refining their prognostic assessment.”

“Professional soeciety guidelines identify ongoing chest pain as a contraindicaion to stress testing.”

53
Q

How high is the rate of cardiac events in those with no ischemia and those with ischemia or equivocal results on “stress testing”?

A

2% and 15%, respectively.

54
Q

Summarize the utility of CT angiography in evaluating chest discomfort.

A

“CT angiography is emerging as a modality for the evaluation of patients with acute chest discomfort. Coronary CT angiography is a sensitive technique for detection of obstructive coronary disease, particularly in the proximal third of the major epicardial coronary arteries. CT appears to enchance the speed to disposition of patients with a low-intermediate probability for ACS; its major strenght being the negative predictive value of a finding of no significant disease. In addition, contrast-enchanced CT can detect focal areas of myocardial injury in the acute setting as decreased areas of enchancement. At the same time, CT angiography can exclude aortic dissection, pericardial effusion, and pulmonary embolism. Balancing factors in the consideration of the emerging role of coronary CT angiography in low-risk patients are radiation exposure and additional testing prompted by nondiagnostic abnormal results.”

55
Q

Which tests are there available for aortic dissection study?

A

CT and transeophageal echocardiogaphy are usually more pratical in the emergency department.

56
Q

Name the reasons why some hospitals have organized critical pathways for chest discomfort assessment and chest pain units.

A

“(1) rapid identification, triage, and treatment of high-risk cardiopulmonary conditions (e.g., STEMI); (2) accurate identification of low-risk patients who can be safely observed in units with less intensive monitoring, undergo early exercise testing, or be discharged home; and (3) through more efficient and systematic accelerated diagnostic protocols, safe reduction in costs associated with overuse of testing and unnecessary hospitalizations. In some studies, provision of protocol-driven care in chest pain units has decreased costs and overall duration of hospital evaluation with no detectable excess of adverse clinical outcomes.”

57
Q

How high is the prevalence of chest pain in outpatient practice?

A

20-40% lifetime prevalence in the general population.

58
Q

How many patients have had a primary care physician visit in the previous month of a myocardial infarction?

A

> 25%.

59
Q

Diagnostic-aids developed for settings with a high prevalence of significant cardiopulmonary disease have a lower positive predictive value when applied to outpatient practice.
True or False?

A

True.