Week 32: Cardio Pt III Chest Pain and CHF

This patient presents with symptoms of acute decompensated heart failure and should be started on nitroglycerin therapy immediately. Patients present with shortness of breath, increased work of breathing, tachycardia, hypoxia, crackles on lung examination and jugular venous distension. These patients experience acute worsening of left ventricular function and output secondary to a number of mechanisms including increased systemic vascular resistance. Therapy focuses on reduction of preload to decrease the flow of blood into the lungs and afterload reduction to increased the effectiveness of the left ventricle. Both of these goals can be accomplished through the administration of nitroglycerin. At lower doses, nitroglycerin acts as a peripheral vasodilator and increases venous capacitance leading to decreased preload. At higher doses, nitroglycerin causes arterial vasodilation leading to decreased afterload. Because of its rapid onset of action, nitroglycerin is the first line medication in patients with ADHF.

Furosemide (A) may be useful in patients with volume overload and ADHF but this represents less than half of patients with ADHF. Additionally, the effects are delayed. Heparin (B) can be given in cases of ischemia induced ADHF but will not yield any immediate benefits. Morphine (C) was historically used as a preload reducer but has been associated with increased morbidity in patients with ADHF and is no longer recommended.

A typical feature of acute coronary syndrome is crushing retrosternal chest pain or pressure. Often this is lacking, and patients present with atypical features of the pain or the presence of angina equivalent symptoms (e.g., dyspnea, nausea, vomiting, dizziness). Many patients with a diagnosis of ACS have pain that is pleuritic, positional, or reproduced by palpation. One large study showed that up to 33% of patients diagnosed with acute myocardial infarction did not have chest pain on presentation. Atypical complaints include dyspnea; nausea; diaphoresis; syncope; and pain in the arms, epigastrium, shoulder, or neck.

Atypical features of ACS are present with increasing frequency in older populations. In patients older than 85 years (A), atypical symptoms are more common than typical chest pain, with dyspnea being the most common. Isolated physical exam findings are rarely diagnostic of the origin of chest pain. Palpation of the chest wall (B) may reveal localized tenderness, but 5%–10% of patients with ACS have chest pain and associated palpable chest wall tenderness. Being female (D) is a risk factor for an atypical presentation of ACS.

Noninvasive ventilation is a useful and powerful tool in treating acute decompensated heart failure. It has been shown to simultaneously decrease preload and afterload and therefore ameliorate the symptoms of heart failure. It also improves lung mechanics by recruiting atelectatic alveoli, increasing intrathoracic pressure, improving pulmonary compliance, and reducing the work of breathing. Noninvasive ventilation has also been shown to decrease endotracheal intubation rates, decrease the need for ICU admissions, and decrease mortality.

Distal esophageal spasm (formerly diffuse esophageal spasm) presents with sudden and severe chest pain and can present similarly to a myocardial infarction. The underlying pathophysiology is not well elucidated, however, it is believed to be associated with an overactivity of excitatory innervation or increased smooth muscle response to excitatory nerves. Patients with risk factors for coronary artery disease or an unclear presentation should have a cardiac etiology ruled out with an ECG and cardiac troponins. Specific historical factors that can point toward esophageal pathology include findings such as inability to swallow solids or liquids during these episodes. The diagnosis of diffuse esophageal spasm can be confirmed with manometry. Treatment includes management of GERD symptoms (if present), a calcium channel blocker such as diltiazem, or tricyclic antidepressants.

This patient has an ECG consistent with an anterior ST segment elevation myocardial infarction. Myocardial infarction occurs due to insufficient blood supply and lack of oxygen delivery most often secondary to ruptured coronary artery plaque and thrombus formation. Classic signs and symptoms of acute MI include chest pain radiating to either arm or the neck, nausea, dyspnea, and diaphoresis. The anterior wall is supplied by the left anterior descending artery. ST segment elevation in leads V3 and V4 is suggestive of an anterior wall infarct. Cardiac enzymes should be drawn and troponin I would characteristically be elevated in ST segment elevation myocardial infarction two to six hours after symptom onset. Lack of positive troponin should not delay treatment. ST segment elevation in two contiguous anatomic leads should prompt immediate initiation of therapy. Aspirin 324 mg PO chewable should be administered immediately to prevent further platelet aggregation. Clopidogrel and heparin are also indicated. Nitroglycerin may be given improve myocardial oxygen supply by dilating the coronary arteries; however, it is contraindicated in right ventricular infarct due to risk for profound hypotension. Definitive treatment for ST segment elevation myocardial infarction is cardiac catheterization and revascularization. If time from medical contact to balloon time is going to be greater than 120 minutes, thrombolytics are recommended. While there is improvement in mortality with time to first medical contact to balloon time of less than 90 minutes compared to 120 minutes, the 2013 American College of Cardiology Foundation/American Heart Association recommends 120 minutes as an acceptable cut off for administering thrombolytics. This cut off is reasonable as presentation to a center without PCI available is a leading cause for delay in door to balloon time. The appropriate dosing of alteplase in ST segment elevation myocardial infarction is administration of alteplase 15 mg IV push followed by two subsequent alteplase infusions (0.75 mg/kg over 30 minutes and 0.5 mg/kg over 60 minutes). Arrangements for transfer should be made concurrently. Contraindications to alteplase should be reviewed before administration.

Administer intravenous atenolol and arrange for transfer (B) is incorrect. While beta-blockers are part of the management of coronary ischemia, the patient requires immediate thrombolysis. Transfer the patient via ground transport with alteplase available if patient deteriorates (C) is incorrect given that the patient is four hours away from the nearest cardiac catheterization lab by ground and alteplase should be given without delay. Transfer the patient via helicopter to the nearest cardiac catheterization lab (D) is correct if you can transfer the patient and have them in the cardiac catheterization lab within 120 minutes of first medical contact; however, your center is over two hours away by air, thus alteplase should be given.

contraindications to thrombolysis include (1) acute aortic dissection (confirmed or suspected), (2) active internal bleeding (excluding menses), (3) intracranial tumor, hemorrhage or arteriovenous malformation, (4) ischemic stroke within 3 months, (5) significant head or facial trauma within 3 months, or (6) a known allergy to the thrombolytic agent. Relative contraindications include (1) chronic or poorly controlled hypertension, (2) blood pressure > 180/110 mm Hg, (3) major surgery within 3 weeks, (4) internal bleeding within 2 to 4 weeks, (5) noncompressible vascular punctures, (6) pregnancy, (7) active peptic ulcer disease, and (8) current anticoagulation use.

This patient is presenting with symptoms and an ECG consistent with Wellen’s syndrome which is highly specific for critical stenosis of the left anterior descending artery. Patients are at high risk for extensive anterior myocardial infarction within weeks to months. It is thought that patients have sudden occlusion of the LAD resulting in anginal symptoms and transient STEMI. Spontaneous reperfusion of the LAD results in resolution of symptoms and the classic findings on ECG. Patients are often asymptomatic when evaluated in the Emergency Department. The most common finding on ECG (found in 75% of cases) is deeply and symmetrically inverted T waves in the anterior precordial leads. Alternatively, biphasic T waves (initial positivity and terminal negativity) are seen in 25% of cases. The ECG findings are present when the patient is pain free. Cardiac markers are normal or mildly elevated. Patients should be admitted for cardiac catheterization given their high risk of infarction.

Wellen Syndrome

Highly specific for critical stenosis of the left anterior descending artery

ECG: deeply inverted or biphasic T waves in V2-3

May be pain free

Normal or minimally elevated troponin

Rx: urgent or emergent percutaneous coronary intervention

The circumflex artery (A) supplies the anterolateral portions of the heart. The left main coronary artery (C) gives rise to the left anterior descending artery and the circumflex artery. The right coronary artery (D) supplies the right ventricle and inferior portions of the heart. These arteries are not involved in Wellen’s syndrome.

Sgarbossa criteria here is positive and activation of cath lab is indicated:

-Concardant ST depression: V2

-Concordant ST elevation: V5, V6

-Discordant ST elevation of over 25% of QRS complex: lead III, avF

Takotsubo cardiomyopathy is also known as left apical ballooning or broken heart syndrome. Most commonly, patients are postmenopausal women who have just experienced significant emotional distress although there are numerous case reports from myriad other causes. It is unclear exactly why this occurs, but a sudden weakness in the myocardium develops after emotional distress possibly related to stress hormones, vascular spasm, focal myocarditis or other cellular changes. Patients develop symptoms consistent with acute coronary ischemia which most commonly include chest pain and dyspnea on exertion. The ECG is abnormal with ST segment elevations or deep T wave inversions usually on the anterior wall. Cardiac biomarkers are often positive. On cardiac catheterization, the coronary arteries do not have obstructive disease. If ventriculography or echocardiography is performed, the apex of the left ventricle is seen ballooning with an impaired ejection fraction. Prognosis is typically very good with recovery to normal wall motion and ejection fraction within a month.

Beta-blockers (A) do not change mortality in this condition. Almost all patients with takotsubo regain completely normal ejection fraction with no long term effects of the episode. Although beta-blockers and angiotensin converting enzyme inhibitors are considered mainstay therapy they do not impact mortality in these patients. AICD placement (B) is not indicated in this patient, as reduced EF is expected to naturally improve. Nitroglycerin (D) is not contraindicated in this patient. Nitroglycerin is unlikely to have any effect given the absence of coronary obstruction. In patients with hypertrophic cardiomyopathy and preload dependence for ventricular filling, agents that decrease preload like nitroglycerin should be avoided.

This patient has an ECG consistent with an inferior ST segment elevation myocardial infarction. Inferior wall myocardial infarction may be accompanied by bradycardia due to involvement of the AV node or hypotension due to total right ventricular involvement. The inferior wall and right ventricle are supplied by the right coronary artery. ST segment elevation in leads II, III, and aVF is suggestive of an inferior wall infarct. This patient is suffering from hypotension and bradycardia as well, which suggest a potential right ventricular infarct. ECG findings suggestive of this include ST segment elevation in leads II, III, and aVF with the elevation in lead III greater than that of lead II or associated elevation in lead V1. Any ST segment elevation in the inferior leads should prompt a right-sided electrocardiogram. ST segment elevation in leads V4R, V5R and V6R is diagnostic of a right ventricular infarct. Cardiac enzymes should also be drawn and troponin I would characteristically be elevated in ST segment elevation myocardial infarction 2-6 hours after symptom onset. Lack of positive troponin should not delay treatment. ST segment elevation in two contiguous anatomic leads should prompt immediate initiation of therapy. Aspirin 325 mg PO chewable should be administered immediately to prevent further platelet aggregation. Clopidogrel and heparin are also indicated. Nitroglycerin may be given to improve myocardial oxygen supply by dilating the coronary arteries; however, it is contraindicated in right ventricular infarct due to risk for profound hypotension. This patient’s hypotension should be treated with IVF. Definitive treatment for ST segment elevation myocardial infarction is cardiac catheterization and revascularization. If the patient is going to be greater than 90 minutes from medical contact to balloon time from the nearest cardiac catheterization center, thrombolytics are recommended.

A chest radiograph (A) would be appropriate if you were concerned for occult pneumothorax or as an initial study to evaluate for widened mediastinum in aortic dissection. CT angiogram of the chest/abd (B) would be appropriate as a definitive study if you were concerned for aortic dissection, AAA, or pulmonary embolism. Posterior electrocardiogram (C) would be appropriate to evaluate for posterior ST segment elevation if you saw deep depression in leads V1 and V2 with prominent R waves.