A 48-year-old man presents to the hospital with swelling of the abdomen and legs. He first noticed shortness of breath with exertion several months ago, and has had a few episodes where he momentarily became lightheaded and lost consciousness. Now the symptoms have been progressing with increased dyspnea and edema. He reports that he has always lived a healthy lifestyle and has no past medical history. There is no family history of any cardiac or pulmonary disease, or any cancer. He was born in Brazil and moved to the United States at the age of 43. He does not smoke or drink alcohol. On cardiac examination, the apex is displaced laterally with an S3 on auscultation. Estimated central venous pressure is 15 mmHg, and there are faint crackles at the base of his lungs. He has hepatomegaly with shifting dullness and bilateral pitting edema of the lower extremities. An ECG is normal, with no visible Q waves.
Which infectious etiology is most likely responsible for this patient’s disease?
Trypanosoma cruzi. The most common cause of nonischemic cardiomyopathy in Latin America is Chagas disease. This patient has evidence of dilated cardiomyopathy and is in heart failure based on the symptoms and physical examination. In addition, he has had several episodes of syncope that are likely the result of arrhythmias. Trypanosoma cruzi is a parasite transmitted in the feces of the reduviid bug. The initial infection is commonly asymptomatic, but if untreated it can result in chronic Chagas heart disease, which may include chest pain, arrhythmias, heart failure, and thromboembolic disease. Once the disease has reached the chronic phase, it is irreversible. Treatment of the acute infection is with either benznidazole or nifurtimox, but treatment for chronic Chagas heart disease is the same as for other causes of heart failure. In a younger patient from Latin America with no atherosclerotic risk factors who presents with heart failure, consider Chagas heart disease as a potential diagnosis.
A 62-year-old man presents to the hospital with chest pain and shortness of breath. The symptoms started suddenly 2 hours ago, when he experienced a squeezing sensation in his chest and began to get short of breath. He has a history of hypertension and diabetes. On examination, the patient has a blood pressure of 104/63 mmHg with a heart rate of 105 beats per minute and a respiratory rate of 22 breaths per minute. He appears diaphoretic with a 2/6 blowing systolic murmur at the apex that radiates to his axilla. Rales are heard bilaterally over the lung bases. An ECG is performed and is shown in Figure below.
The hospital is not equipped to perform PCI, and the nearest hospital with a catheterization laboratory is 15 minutes away. Which of the following is the best next step in management?
Transfer the patient for PCI. This patient is presenting with STEMI and requires urgent reperfusion of his coronary arteries. The earlier the intervention, the more amount of myocardium that is saved. There are two options for reperfusion: mechanical reperfusion with PCI and stent placement, or chemical reperfusion with fibrinolytics. For most patients, PCI is the treatment of choice; however, not all hospitals have a catheterization laboratory with dedicated cardiologists on call all the time. If PCI is to be most effective, the door-to-balloon time (the time from which the patient presents to the time they undergo catheterization) should be less than 90 minutes, although up to 120 minutes is still acceptable. If this time limit cannot be achieved, the fibrinolytics should be given within 30 minutes after contraindications are assessed (such as previous intracerebral hemorrhage, intracranial tumor/ aneurysm, active internal bleeding). (C) This patient should be transferred to the hospital 15 minutes away for PCI rather than fibrinolytics.
(D) The patient has a murmur of mitral regurgitation, which can be seen in acute myocardial infarctions; however, emergency valvular surgery is not treating the underlying problem of coronary artery occlusion. (B) Ibuprofen and colchicine would be appropriate therapies for acute pericarditis; however, the patient does not have a suggestive history and the ECG does not show diffuse ST elevations in all leads.
the past few days, her symptoms have worsened and she experiences severe chest pain with each inspiration; she has been bedridden over this time. A review of systems is significant for an unintentional weight loss of 6.8 kg (15 lb) over the past few months. She has no past medical history and has not been to a doctor since she was a child. She takes no medications. The patient’s vitals show a blood pressure of 138/88 mmHg with a heart rate of 112 beats per minute and respiratory rate of 28 breaths per minute. Cardiovascular examination reveals distended neck veins, and her lungs are clear to auscultation bilaterally. There is hepatomegaly with lower-extremity edema. She is admitted, and a CT with contrast shows a large thrombus in the inferior vena cava with thrombi in multiple small pulmonary vessels. She is eventually diagnosed with ovarian cancer and receives anticoagulation, with subsequent CT imaging showing pulmonary vasculature without any thromboemboli; however, she continues to have distended neck veins and episodes of hypotension.
A pulmonary artery catheter is advanced through the internal jugular vein to record pressures within the heart. Which of the following recordings most accurately reflect the pressures found by Pulmonary artery in this patient? (Note: SVC is superior vena cava, RA is right atrium, RV is right ventricle, PA is pulmonary artery, and PCWP is pulmonary capillary wedge pressure.)
: Increased SVC, increased RA, increased RV, increased PA, normal PCWP. This patient is suffering from pulmonary hypertension from chronic thromboembolic events (WHO classification group 4). Although she is presenting with acute decompensation likely from an increase in clot burden, her symptoms started several months ago, suggesting a chronic process. Her underlying ovarian cancer is causing a hypercoagulable state, and she has been bedridden for the past few days, both of which contribute to further clot formation. Chronic thromboemboli to the lungs cause obstruction in blood flow, which increases the pressure in the right side of the heart. Over time, pulmonary hypertension will lead to right heart failure, which is manifested by distended neck veins, hepatomegaly, and peripheral edema. Pulmonary artery catheterization is a method for measuring pressures within the right side of the heart. In addition, it can accurately estimate left atrial pressure by the PCWP, which should be normal given that the left atrium is distal to the disease process.
A 57-year-old woman with hypertension and end-stage renal disease presents to the hospital with worsening confusion and hypotension. According to her husband, she has been compliant with her medications and diet. She receives dialysis 2 times weekly, with her last session occurring 2 days ago. On examination, she is hypotensive with distant heart sounds and distended neck veins. An echocardiogram is performed which shows a moderate amount of pericardial fluid with collapse of the right atrium during diastole. A blood pressure cuff is placed on the patient and she is asked to take a deep breath.
Which of the following changes will take place during inspiration? (Note: RV is right ventricle, LV is left ventricle, PVC is pulmonary vascular compliance.)
Decreased blood pressure, increased RV volume, decreased LV volume, increased PVC. This patient is presenting with Beck’s triad of cardiac tamponade: distant heart sounds, elevated jugular venous pressure, and hypotension. Patients with a history of advanced renal disease are at risk for uremic pericarditis, which may or may not present with chest pain. Effusions are typically present and may develop into tamponade. In cardiac tamponade, the surrounding pericardial fluid causes equalization of pressure within the four heart chambers and leads to obstruction of blood flow without pulmonary edema. During inspiration, the negative intrathoracic pressure draws blood into the right ventricle, increasing the volume of the right ventricle and causing the interventricular septum to shift and decrease the volume of the left ventricle. In addition, pulmonary vascular compliance is increased during inspiration (increased volume of the lung parenchyma and vasculature), which also decreases preload to the left ventricle. This results in a reduced stroke volume of the left ventricle and a decrease in blood pressure. Although a small decrease in systolic blood pressure occurs in healthy patients during inspiration, a decrease ≥10 mmHg is defined as pulsus paradoxus and is commonly seen with cardiac tamponade.
Treatment of uremic pericarditis involves increasing the frequency or duration of hemodialysis. Because she is currently having tamponade physiology, she will require pericardiocentesis to remove the pericardial fluid.
A 65-year-old woman presents to the hospital complaining of difficulty breathing. She reports that the symptoms have developed over the past few weeks, starting with leg swelling. She was previously eating well and exercising several times weekly, but admits that the past month has been extremely busy so her diet and exercise has suffered. She now cannot walk to her mailbox without becoming short of breath. She has a history of hypertension but admits that she does not regularly take her medication. Her blood pressure is currently 158/104 mmHg. She has an S4 on cardiac examination, with an elevated estimated central venous pressure. On examination of her lungs, she has dullness to percussion at the bases with wet rales halfway up the lung fields. She has pitting edema around her ankles. An echocardiogram shows a normal ejection fraction.
Based on this patient’s likely diagnosis, which of the following treatments have been shown to reduce mortality?
None of the above. This patient is presenting in CHF with evidence of diastolic dysfunction. Heart failure can generally be divided into two categories: systolic dysfunction (reduced ejection fraction) and diastolic dysfunction (preserved ejection function). Causes of diastolic dysfunction include hypertension, ischemia, hypertrophic and restrictive types of cardiomyopathies, and aortic stenosis. In hypertension, the increased afterload experienced by the left ventricle leads to increased pressure work, and the heart responds by remodeling with concentric hypertrophy. The myocardial wall thickens and becomes stiff, losing its ability to relax (loss of compliance) and allow a sufficient volume of blood to be pumped out during systole (although the proportion of blood volume ejected during systole remains the same). This patient has a history of hypertension with findings of CHF on examination, as well as an S4 which make the likely diagnostic category diastolic dysfunction.
Heart failure with systolic dysfunction often leads to a dilated cardiomyopathy with eccentric hypertrophy (dilation) as a response to increased volume work. This type of heart failure will present with findings of CHF on examination and an S3. Many trials have shown that certain medications reduce the mortality in patients with systolic dysfunction: ACE inhibitors, angiotensin receptor blockers, β-blockers, aldosterone antagonists, omega-3 fatty acids, cardiac resynchronization therapy, implantable cardiac defibrillator, and hydralazine with nitrates (especially in African Americans). Unfortunately, these medications have not been shown to reduce mortality in patients with diastolic dysfunction.
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