Week 6: Cardiology Part 2/5: Chest Pain, ACS, Heart Failure, Cardiomyopathy

This patient presents with symptoms of acute decompensated heart failure and should be started on nitroglycerintherapy 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.

Endpoints of death, nonfatal reinfarction, and stroke have been used in comparisons of thrombolytics and PCI. Each of these measured parameters is less in the PCI comparison group. Cumulatively endpoints were present for 8% of PCI patients versus 14% for the thrombolytic group. These groups were broken down into less short-term mortality at 30 days (4.4% vs. 6.5%), less nonfatal reinfarction (3% vs. 7%), and less hemorrhagic stroke (0.1% vs. 1.1%). PCI is especially indicated in patients that have cardiogenic shock, severe congestive heart failure and/or pulmonary edema, and hemodynamically compromising ventricular arrhythmias. These patients should proceed to primary PCI as the reperfusion strategy of choice. The addition of both thrombolytic therapy and PCI as a primary reperfusion strategy has been investigated as a therapy for STEMI. Full-dose fibrinolytic therapy followed by immediate PCI may be harmful and should not be utilized. Facilitated PCI, the term for this strategy, has been shown to have higher mortality rates as well as bleeding rates. These patients also had higher rates of recurrent infarction and needs for subsequent PCI. Rescue PCI has resulted in higher rates of early infarct arterial patency, improved regional infarct-zone wall motion, and greater freedom from adverse in-hospital events than with a deferred PCI strategy or medical therapy.

Preload and afterload reduction is your first priority in this patient. The patient’s sudden decompensation, profound hypertension, and relative lack of peripheral edema suggest this patient has acute decompensated heart failure from the “vascular pathway”. In these patients, rapid preload and afterload reduction will dramatically decrease the symptoms of acute decompensated heart failure by decreasing venous return and lowering the systolic blood pressure. The lower systolic blood pressure allows the left ventricle to empty its contents more easily. Diuresis should be delayed until afterload is reduced or not done at all. Diuresis is reserved for patients with gradual fluid accumulation and significant peripheral edema. Agents to increase inotropy are used for hypotensive patients and patients resistant to first-line therapies. Morphine is no longer a first-line agent for acute decompensated heart failure and is associated with increased rates of intubation.

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.

Furosemide exerts its positive effects in treating acute decompensated heart failure by decreasing total body water and therefore preload. Furosemide does activate the renin–angiotensin system; however this is a deleterious effect as this often leads to increased blood pressure. There is no convincing evidence that furosemide has significant venous vasodilatory effects or causes afterload reduction.

See AHA recommendations (http://www.heart.org/HEARTORG/Professional/MissionLifelineHomePage/EMS/Recommendations-for-Criteria-for-STEMI-Systems-of-Care_UCM_312070_Article.jsp).

Transfer if door-to-balloon is <90 (total, including transfer). Typically need rapid transfer protocol set up.

These are deWinters complexes, indicative of LAD occlusion and generally regarded as a cath lab activating EKG. Classically depressions in V2-4 with acute t waves. Don’t need ST elevation here.

Sgarbossa criteria here met in V2 and V5, V6. Use Sgarbossa because of LBBB.

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. Cardiac catheterization (B) is mandatory in this patient who has symptoms consistent with myocardial ischemia and an ECG suggestive of an anterior wall myocardial infarction. As noted above, the catheterization is unlikely to reveal an acute thrombus, but the emergency physician and cardiologist must exclude an acute myocardial infarction as the etiology of the signs and symptoms. 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 concerning for a right ventricular infarct. In this situation, the patient becomes preload dependent (essentially the right ventricle is impaired to there is “passive” flow into the left ventricle). When these patients become hypotensive, the immediate treatment is intravenous hydration to increase preload. Right ventricular infarction is represented on an ECG by noting ST elevation in right-sided leads (V3R and V4R). Because the right coronary artery often supplies the right side of the heart and the inferior wall of the heart, any ECG with ST elevations in leads II, III, and aVF (inferior leads) should have another ECG performed with right-sided lead placement. Aggressive volume loading with normal saline boluses is used to restore blood flow to the right ventricle and inotropic support is indicated if hypotension persists. Early percutaneous coronary intervention or thrombolytic therapy should be initiated as soon as possible. In general, patients’ with right ventricular myocardial infarction are treated in a manner similar to those with acute ST-elevation myocardial infarction. This includes the early use of dual antiplatelet therapy, statin therapy, and an anticoagulant.

Medications that lower preload such as nitroglycerin (C) and morphine (B) or drugs that slow heart rate such as beta blockers (A) should be avoided or used with extreme caution.