EM 3- Cardiac/Chest
Identify what the following findings on physical exam may reveal about the patient with acute coronary syndrome:
- Bradycardia Bradycardic rhythms are more common with inferior wall myocardial ischemia. In the setting of an anterior wall infarction, a bradycardic rhythm or heart block is an extremely poor prognostic sign. - Hypertension Blood pressure can be normal, elevated (due to baseline hypertension, sympathetic stimulation, and anxiety), or decreased (due to pump failure or inadequate preload). Extremes of blood pressure are associated with a worse prognosis. - Hypotension = pump failure or inadequate preload - S3 - An S3 is present in 15% to 20% of patients with AMI. If an S3, if truly detected, may imply a failing myocardium - S4 - An S4 is common in patients with long-standing hypertension or myocardial dysfunction. - New systolic murmur The presence of a new systolic murmur is an ominous sign, because it may signify papillary muscle dysfunction, a flail leaflet of the mitral valve with resultant mitral regurgitation, or a ventricular septal defect. - Rales The presence of rales, with or without an S3 gallop, is associated with left ventricular dysfunction and left-sided CHF. - JVD Jugular venous distention, hepatojugular reflex, and peripheral edema suggest right-sided CHF.
Ttroponin I and troponin T may be detectable in serum as early as
2 hours after AMI but are not reliably elevated in all patients until 6 to 12 hours. Levels reach their peak at 12 hours and remain elevated for 7 to 10 days, making troponin a uniquely useful test for patients with delayed presentations.
Clinical value fo ECG for ACS
: Patients with chest pain or other symptoms suggestive of ACS should receive a 12-lead ECG upon ED presentation within the goal of ten minutes of ED arrival for all patients with chest discomfort or other symptoms suggestive of ACS
New-onset angina
Angina of at least CCSC III severity with onset within 2 mo of presentation
The "cardiac isoenzyme,"
CK-MB is found in greater proportion in cardiac muscle but accounts for only 14% to 42% of total cardiac muscle activity. Thus, the predominant enzyme in the heart is also CK-MM. CK levels become elevated within 4 to 8 hours after coronary artery occlusion, peak between 12 and 24 hours, and return to normal between 3 and 4 days
Symptoms of angina, their duration and what can trigger them.
Duration: Anginal pain (or other anginal symptoms) is typically described as lasting from 2 to 20 minutes Triggers: Anginal pain is often brought on by exertion and relieved by rest, although pain worsened by body movement or body position is suggestive (but certainly not diagnostic) of another etiology. Angina may also occur at rest, either due to destabilization of a preexisting coronary lesion or to coronary artery spasm with or without underlying atherosclerotic lesions
Cause of angina pectoris
If the demand for myocardial blood flow exceeds the capacity of the obstructed coronary arterial tree to supply it, the discomfort (angina pectoris) lasts until the excessive demand for coronary flow is reduced.
Identify the major risk factors according for cardiovascular disease.
Noncoronary atherosclerotic disease, Diabetes mellitus, Chronic, Age and gender, Family history, Hypertension, Hyperlipidemia, Lifestyle factors, Cigarette smoking , Exercise, Psychosocial factors
Describe what is considered a "silent AMI" and the patient who is more likely to present with one.
Presentations with atypical features or silent myocardial ischemia are common. Reportedly, • 37.5% of women present without chest pain • 27.4% of men present without chest pain. The prognosis for patients with atypical symptoms (fatigue, weakness, not feeling well, vague discomfort) at the time of infarction is worse than that of patients with more typical symptoms. Women and the elderly are more likely to have atypical presentations. Up to one half of patients with unstable angina present with atypical features.
Increasing angina
Previously diagnosed angina that is distinctly more frequent, longer in duration, or lower in threshold (increased by at least one CCSC class to at least CCSC III severity)
Clinical presentation of Esophageal rupture (Boerhaave syndrome)
S&S: A rare but potentially life-threatening cause of chest pain. Patients classically present with a history of substernal, sharp chest pain of sudden onset that occurs immediately after an episode of forceful vomiting. The patient is usually ill-appearing, dyspneic, and diaphoretic. The physical examination is often normal but may reveal evidence of pneumothorax or subcutaneous air. Chest radiography may be normal or may demonstrate pleural effusion (left more common than right), pneumothorax, pneumomediastinum, pneumoperitoneum, and/or subcutaneous air. The diagnosis can be confirmed by a study with water-soluble contrast
Clinical features and presentation of Pulmonary embolism
S&S: Can manifest with any combination of chest pain, dyspnea, syncope, shock, and/or hypoxia. In theory, the pain associated with a pulmonary embolism occurs when inflammation of the parietal pleura overlying the infarction causes chest pain that is generally sharp and related to respiration; however, most patients with pulmonary embolism and pleuritic chest pain have no radiographic evidence of pulmonary infarction. The discomfort of massive pulmonary embolism (such as saddle embolism) is described using more visceral terms such as a heaviness and tightness. Dyspnea, fever, cough, and/or hemoptysis also may be present, and the chest wall may be tender to palpation. Patients with massive pulmonary embolism often present with unstable vital signs and chest pain and dyspnea associated with tachypnea, tachycardia, and hypoxemia.
Clinical presentation of Panic disorder
S&S: Ccharacterized by recurrent unexpected panic attacks (discrete periods of intense fear or discomfort) with at least four of the following symptoms: palpitations, diaphoresis, tremor, dyspnea, choking, chest pain or discomfort, nausea, dizziness, derealization or depersonalization, fear of losing control or dying, paresthesias, chills, or hot flushes. The diagnosis can be made only in the absence of direct physiologic effects of a substance disorder, a general medical condition, or symptoms better accounted for by another mental disorder. Many patients with panic disorder and other anxiety disorders have elevated baseline sympathetic tone that may be an independent risk factor for coronary artery disease
Clinical presentation of Mitral valve prolapse
S&S: The most frequently diagnosed cardiac valvular abnormality and is more commonly diagnosed in women than in men. The discomfort of mitral valve prolapse often occurs at rest, is atypical for myocardial ischemia, and can be associated with dizziness, hyperventilation, anxiety, depression, palpitations, and fatigue. Discomfort may be related to papillary muscle tension, and many patients benefit from the administration of beta-adrenergic blocking agents. Two-dimensional echocardiography is the diagnostic tool of choice and, with physical examination findings. Palpitations and every type of supraventricular or ventricular dysrhythmia have been associated with mitral valve prolapse.
Clinical presentation of Aortic dissection
S&S: The pain (i.e., midline substernal chest pain) is classically described as tearing, ripping, or searing and radiating to the interscapular area of the back. Typically, the pain is at its worst at symptom onset and is often felt above and below the diaphragm. Secondary symptoms resulting from arterial branch occlusions include stroke, AMI, or limb ischemia, and may overshadow the clinical presentation. No combination of clinical factors or chest radiography findings are adequate to exclude the diagnosis of aortic dissection, and specific imaging studies are usually required
Clinical presentation of Chest wall pain syndrome (e.g. Costochondritis, Tietze syndrome, etc.)
S&S: characterized by highly localized, sharp, positional chest pain. Pain that is completely reproducible by light to moderate palpation of a discrete area of the chest wall often represents pain of musculoskeletal origin, although chest wall tenderness occurs in some patients with pulmonary embolism and myocardial ischemia.
Clinical repsentation of Pneumonia
S&S: chest pain or discomfort that is usually sharp and pleuritic. It is usually associated with fever, cough, and, possibly, hypoxia. Physical examination may reveal rales over the affected lobes, decreased breath sounds, and signs of consolidation (i.e., bronchial breath sounds). A chest radiograph confirms the diagnosis.
Clnical presentation of Acute pericarditis
S&S: is typically acute, sharp, severe, and constant. It is usually described as substernal, with radiation to the back, neck, or shoulders, and is exacerbated by lying down and by inspiration. It is classically described as being relieved by leaning forward. A pericardial friction rub is the most important diagnostic finding. The ECG may show diffuse ST-segment elevation and T-wave inversion. In addition, depression of the PR segment is a highly specific ECG finding for pericarditis.
Clinical prensentation of Spontaneous pneumothroax
S&S: may occur due to sudden changes in barometric pressure, in smokers or patients with chronic obstructive pulmonary disease or idiopathic pleural bleb disease, or in those with another pulmonary pathology. Patients usually complain of a sudden, sharp, lancinating, pleuritic chest pain and dyspnea. Auscultation of the lungs may reveal absence of breath sounds on the ipsilateral side and hyper-resonance to percussion, but clinical impression alone is unreliable. Diagnosis of a simple pneumothorax is made by chest radiography.
N-STEMI - The diagnosis of non-ST-segment elevation myocardial infarction (NSTEMI) depends on abnormal elevation of biologic markers but may include ECG changes not meeting criteria for STEMI.
The identification of NSTEMI as a trigger for recommended therapies is usually accompanied by positive biomarkers, which often occurs after the ED course. Patients with unstable angina or NSTEMI should be treated with antiplatelet agents and antithrombins as well as beta-antagonists, and, possibly, nitrates.
Describe the initial approach to the patient with chest pain
The recommended initial approach to acute chest pain takes into account that some causes are serious and life-threatening, and prompt medical attention may prevent death and limit morbidity. Therefore, all patients should be triaged promptly. Patients with visceral-type chest pain, abnormal vital signs, significant vascular disease risks, and those with dyspnea should be placed into a treatment bed, a cardiac monitor initiated, an IV line established, oxygen administered, and an ECG performed.
Tietze syndrome is
a particular cause of costochondral pain related to fusiform swelling in one or more upper costal cartilages and has a pain pattern similar to that of other costochondral syndromes.
Peptic ulcer disease is classically characterized as
a postprandial, dull, boring pain in the midepigastric region Patients often describe being awakened from sleep by discomfort. Duodenal ulcer pain is usually relieved after eating food, in contrast to gastric ulcer symptoms, which are often exacerbated by eating. Symptomatic relief is usually provided by antacid medications.
Esophageal spasm is often associated with reflux disease and is characterized by
a sudden onset of dull, tight, or gripping substernal chest pain, frequently precipitated by the consumption of hot or cold liquids or a large food bolus and often lasting for hours. The pain may disappear with the administration of sublingual nitroglycerin, typically with a slight delay.
Costochondritis is
an inflammation of the costal cartilages and/or their sternal articulations and causes chest pain that is variably sharp, dull, and/or increased with respirations.
Xiphodynia is
another inflammatory process that causes sharp, pleuritic chest pain reproduced by light palpation over the xiphoid process.
Reciprocal ST-segment changes (such as ST-segment depressions in the
anterior precordial leads in the setting of an inferior wall AMI) predict a larger infarct distribution, an increased severity of underlying CAD, more severe pump failure, a higher likelihood of cardiovascular complications, and increased mortality. In general, the more elevated the ST segments and the more ST segments that are elevated, the more extensive the injury.
Anginal symptoms include
chest pressure, heaviness, tightness, fullness, or squeezing. Exercise, stress, or a cold environment classically precipitate angina pectoris. Angina typically has a duration of symptoms of <10 minutes, occasionally lasting up to 10 to 20 minutes, and usually improves within 2 to 5 minutes after rest or nitroglycerin. Ask about the frequency of anginal episodes and any change in frequency of episodes over the past months. Determine if there is any increase in severity or duration of symptoms, or whether less effort is required to precipitate symptoms.
Texidor twinge or precordial catch syndrome is
described as a short, lancinating chest discomfort that occurs in episodic bunches lasting 1 to 2 minutes near the cardiac apex associated with inspiration and poor posture and inactivity
classic presentation of angina pectoris
is a retrosternal left anterior chest or epigastric discomfort described as crushing, tightening, squeezing, or a pressurelike sensation
Clinical value of X-ray: chest radiograph for evaluation of ACS
is of limited value in the evaluation of ACS, but aids in detection and exclusion of a variety of other serious diagnoses.
The standard 12-lead ECG
is the single best test to identify patients with AMI upon ED presentation. The initial 12-lead ECG should be obtained and interpreted within 10 minutes of presentation for patients with symptoms suggestive of myocardial ischemia. The ECG can also be used to predict the infarct-related vessel.
Rest angina
occurring at rest and usually prolonged >20 min occurring within 1 wk of presentation
AMI Symptoms
often will be described as discomfort rather than as pain. patients will sometimes describe their symptoms as knife-like, sharp, or stabbing. The classic location is substernal or in the left chest. Radiation to the arm, neck, or jaw may occur. Reproducible chest wall tenderness is not uncommon, possibly because the pericardium may become inflamed, and it sits beneath the chest wall. AMI is usually accompanied by more prolonged and severe chest discomfort, more prominent associated symptoms (nausea, diaphoresis, shortness of breath, etc.), and little, if any, response to initial sublingual nitroglycerin. fatigability may be a prominent symptom of ACS, especially in women
Symptoms that may be indicateACS
patients whose pain is described as stabbing, positional, or pleuritic do have a reduced likelihood of ACS as a cause of chest pain. The presence of certain associated symptoms during chest pain—dyspnea, diaphoresis, nausea, and/or vomiting—is common and does indicate a twofold higher risk of ischemia. Discomfort radiating from the chest to either shoulder, arm, hand, or jaw also indicates a significantly increased probability of ACS. However, lack of such radiation does not exclude ischemia.
STEMI The diagnosis of ST-segment elevation myocardial infarction (STEMI) depends on the ECG in the setting of symptoms suggestive of MI. Patients with persistent symptoms and STEMI should receive
reperfusion with either percutaneous coronary intervention (PCI) or fibrinolytic therapy in <90 minutes. Treatment with antiplatelet agents, antithrombins, beta-antagonists, and nitrates are recommended for most STEMI patients. Angiotensin-converting enzyme (ACE) inhibitors should be considered, based on symptoms, vital signs, and the presence or absence of heart failure; however, these medications are rarely initiated in the early treatment period.
After AMI, serum myoglobin levels
rise within 3 hours of symptoms and are elevated in 80% to 100% of patients at 6 to 8 hours, peak at 4 to 9 hours and, with normal kidney function, return to baseline within 24 hours
CK-MB had been universally adopted as
the gold standard for diagnosis of AMI. However, 37 conditions other than AMI have been associated with elevated CK-MB levels, and it has now been largely replaced for routine use by the more sensitive and specific cardiac troponins.
Acute pancreatitis and biliary tract disease present
with right upper quadrant or epigastric pain and tenderness but also can cause chest pain.
