A 68-year-old woman is admitted for shortness of breath and is found to be in heart failure. Her blood pressure is 140/60 mmHg, with a heart rate of 102 beats per minute. When you examine her, you notice that her carotid arteries have a noticeably brisk rise and fall. When you apply pressure to her fingernails, you see subungual pulsations.
Which of the following findings on cardiac examination is most likely?
Diastolic decrescendo murmur at the left upper sternal border. This represents the murmur of aortic regurgitation (aortic insufficiency), which is the cause of this patient’s acute heart failure. Hints to the diagnosis come from the widened pulse pressure (>40 mmHg), the brisk rise and fall of her pulse (“water hammer” pulse, A.K.A. Corrigan pulse), and the subungual pulsations (Quincke sign). Though these are not all sensitive and specific signs, together they make the likely diagnosis of aortic regurgitation.
(A) This is the murmur of aortic stenosis, which radiates to the carotid arteries. Other examination findings would be parvus et tardus (delayed carotid upstroke), and a left ventricular heave with an S4 in advanced disease. (C) Mitral regurgitation presents with this murmur, which radiates to the axilla. There can also be a split S2 (aortic valve closing early) and atrial fibrillation from left atrial enlargement. An S3 might be heard in advanced disease. (D) Mitral stenosis presents as a diastolic murmur with an opening snap. Like mitral regurgitation, it can cause left atrial enlargement and atrial fibrillation.
A 68-year-old woman with chronic obstructive pulmonary disease (COPD) comes to the hospital because of 3 days of fatigue and worsening dyspnea. She has no history of hypertension or heart disease. Her blood pressure is 102/58 mmHg with a heart rate of 142 beats per minute. The jugular venous waveform is monophasic. An ECG is taken and shown below (Figure below).
Which of the following is the first step in management of this condition?
Start diltiazem. The ECG above shows an irregularly irregular rhythm with no distinct P waves, confirming the diagnosis of atrial fibrillation. It also shows a fast rate, which is called atrial fibrillation with rapid ventricular response. The venous waveform will be monophasic due to loss of the atrial kick (a wave), leaving only the v wave. Many patients are asymptomatic from atrial fibrillation, since two-thirds of left ventricular filling occurs during diastole with the atrial kick only contributing one-third of the preload to the left ventricle. Older patients or those with underlying cardiac disease will often be symptomatic.
(C) This is the patient’s first known episode of atrial fibrillation; she is currently stable and therefore does not require immediate cardioversion. The first step in stable patients is rate control with a β-blocker or calcium channel blocker (another option is digoxin). A calcium channel blocker such as diltiazem is preferred over a β-blocker given the patient’s COPD; propranolol is a nonselective β-blocker and therefore would cause bron-chospasm due to blockade of β2 receptors. (E) Amiodarone is another option for rate control, but would be a bad idea in this patient since it can cause chemical cardioversion and cause embolization of a thrombus if one is present.
After rate control is achieved (goal resting heart rate <110 beats per minute according to the RACE II trial), the patient should be anticoagulated since there is a risk of thrombus formation in the left atrium (usually in the atrial appendage) that can embolize to the brain and cause a stroke. Patients with new onset atrial fibrillation less than 48 hours can undergo cardioversion (low risk of stroke), but in patients with onset greater than 48 hours ago (this patient) there are two options: either the patient can have a transesophageal echocardiogram to rule out a left atrial thrombus before cardioversion, or they can start empiric anticoagulation for at least 3 weeks before cardioversion is attempted. After cardioversion is completed, all patients must have at least 4 weeks of anticoagulation unless there are serious contraindications.
(A) Aspirin should be given in chronic atrial fibrillation when the CHADS2 score is 0 or 1. (B) Anticoagulation will be given to this patient, but it is not the first step in management. (Note: the CHA2DS2-VASc score is a newer model for estimating the risk of stroke in patients with atrial fibrillation; however, the CHADS2 score is sufficient for the shelf examination.)
A 52-year-old woman presents to the hospital with a severe headache and nausea. She has no history of headaches and is concerned that she is having a stroke. Her medical history is significant for longstanding hypertension, diabetes, and GERD. She admits that she is not always compliant with her medications, and recently ran out of them. Her blood pressure is 193/124 mmHg, and fundoscopic examination reveals papilledema. The rest of her physical examination, including a neurologic examination, is normal.
Which of the following is the correct diagnosis and treatment?
Hypertensive emergency; rapid lowering of blood pressure with IV agents. Hypertensive urgency is defined as a systolic blood pressure >180 mmHg and/or a diastolic blood pressure >120 mmHg with no end-organ damage. Hypertensive emergency is the same definition with the addition of end-organ damage. Many organs are acutely affected by high blood pressure, including the brain (stroke), eyes (papilledema), heart (aortic dissection), lungs (pulmonary edema), and kidneys (renal failure). Within the umbrella term of hypertensive emergency, there are additional terms for specific end-organ involvement: malignant hypertension refers to hypertensive emergency in the presence of papilledema (other ophthalmologic findings include retinal exudates and hemorrhage), and malignant nephrosclerosis refers to renal damage. This patient has a hypertensive emergency with end-organ involvement including the brain (headache) and the eyes (papilledema).
(A, B, D) The management of hypertensive urgencies and emergencies is slightly different. In hypertensive urgency, the goal is to gradually lower the blood pressure to achieve a normal value within a couple of days. Oral antihypertensive agents are given while monitoring the reduction in blood pressure over hours. Some options for oral medications include labetalol, captopril, clonidine, furosemide, and hydralazine. In hypertensive emergency, there is ongoing end-organ damage and therefore blood pressure needs to be lowered quickly. The goal in this setting is to immediately lower blood pressure using IV agents, targeting a decrease in mean arterial pressure by 25% within minutes to hours. Some options for IV medications include nitroprusside, nitroglycerin, calcium channel blockers (e.g., nicardipine), labetalol, hydralazine, fenoldopam, and phentolamine. Because adaptive mechanisms occur with chronically elevated blood pressure, rapid lowering of blood pressure is not always tolerated and can cause cerebral hypoperfusion. If this happens, the blood pressure must be lowered more gradually.
A 68-year-old woman presents with progressive dyspnea. She has a history of longstanding hypertension, previous myocardial infarction, and several episodes of ventricular tachycardia that required cardioversion. She is now maintained on prophylactic medication with good cardiac function and no further arrhythmias. On examination, she is afebrile with a respiratory rate of 28 breaths per minute and oxygen saturation of 92% on room air. Cardiac examination is normal, but she has dry rales throughout her lung fields. A CT scan of the chest shows diffuse ground-glass opacities.
Which medication is most likely responsible for the patient’s symptoms?
Amiodarone. Amiodarone is an anti-arrhythmic medication that may be used for prophylaxis or treatment of serious arrhythmias, especially ventricular arrhythmias. This patient has a history of ventricular tachycardia, and therefore has an indication to be taking amiodarone. This drug has much toxicity, and therefore when started the patient must have baseline pulmonary function tests, thyroid function tests, and liver function tests due to the toxicity involving each of these organs. Other notable side effects include blue-gray discoloration of the skin, corneal deposits, and peripheral neuropathy. This patient developed pulmonary fibrosis as a result of chronic amiodarone use. (A, B) Digoxin and lisinopril are not associated with pulmonary fibrosis. (D) Bleomycin can cause pulmonary fibrosis, but it is an antineoplastic drug and the patient has no reason to be taking this medication.
A 41-year-old woman presents to the hospital with shortness of breath that developed over the last 2 weeks. She has also noticed progressive swelling in her legs. She sleeps with four pillows at night and sometimes wakes up in the middle of the night gasping for air. On review of systems, she mentions that over the past year she has been increasingly anxious with frequent perspiration and diarrhea. She has no significant medical history and takes no medications. The patient is afebrile with a blood pressure of 143/88 mmHg, heart rate of 107 beats per minute, and respirations of 30 breaths per minute with an oxygen saturation of 93% on room air. She appears anxious and is mildly diaphoretic. Her cardiac examination shows a regular rhythm, a 2/6 systolic murmur heard at best at the left upper sternal border, and an estimated central venous pressure of 14 mmHg. In addition, she has wet rales heard along the lung bases and 2+ pitting edema bilaterally to the level of her knees. Laboratory values are shown below:
Which of the following represents another disease process that can lead to this same presentation?
: Thiamine deficiency. This patient is presenting with CHF, which is indicated by her symptoms of dyspnea, orthopnea, and paroxysmal nocturnal dyspnea as well as the signs of jugular venous distention, pulmonary edema, and lower-extremity edema. The underlying process leading to this diagnosis is indicated by the review of systems, which suggests hyperthyroidism. Patients with prolonged hyperthyroidism may develop high output cardiac failure, and the question asks for another disease process that can cause this. One answer is thiamine deficiency with the manifestation of wet beriberi. Other causes of high output cardiac failure include anemia, sepsis, large arteriovenous fistulas, and Paget disease. This patient will require treatment for her heart failure as well as treatment of the underlying process of hyperthyroidism.
(A) Asbestos exposure causes pulmonary fibrosis of the lower lobes and increases the risk for squamous cell carcinoma and mesothelioma; it does not commonly cause heart failure. (B) Pulmonary hypertension can lead to heart failure, but this will cause right heart failure without the manifestations of left heart failure (dyspnea from pulmonary edema). (D) α1-antitrypsin deficiency causes panacinar emphysema (with physical examination findings of wheezes, not rales) and may also cause liver disease, depending on the genotype. (E) Sarcoidosis can cause a restrictive cardiomyopathy, but does not cause high output cardiac failure.
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