While rounding with the team, a nurse asks you to come see a patient recovering from pneumonia who has developed an unusual rhythm on his monitor (Figure below). The patient reports that he does not feel weak or have any palpitations, and his vitals are normal. His medical history is only significant for hypertension, for which he takes diltiazem. He has no family history of heart disease and does not smoke. You attempt a carotid sinus massage, and you see that there are more dropped beats on the monitor.
Which of the following is the most appropriate next step in management?
The rhythm shown in the ECG is second-degree atrioventricular (AV) block, Mobitz type I (also known as Wenckebach). This is a benign rhythm disturbance caused by abnormal conduction through the AV node that causes a gradual prolongation of the PR interval with each beat until a beat is dropped. Vagal stimulation (e.g., carotid sinus massage) can increase the parasympathetic tone in the AV node and worsen the condition, causing more dropped beats. This is in contrast to Mobitz II, another type of second-degree AV block that shows a fixed PR interval with occasional dropped beats that improves with vagal stimulation.
First-degree AV block presents with a prolonged PR interval (>200 ms) without any dropped beats. Third-degree AV block presents with complete AV dissociation, in which there is no conduction through the AV node. Pacemaking cells beyond the AV node, which have a slower inherent rate and are normally suppressed by proximal pacemaking cells (overdrive suppression), now fire independently from the atrial impulse as an escape rhythm. First-degree and second-degree Mobitz I are relatively harmless and generally do not require treatment. Mobitz II can progress to third-degree AV block, and therefore both of these conditions require a pacemaker.
(B) Increasing the dose of his calcium channel blocker would slow conduction through the AV node further and exacerbate the condition. (E) Giving atropine would improve AV conduction, but no treatment is required in this case. (C, D, E) This is a harmless rhythm that does not require cardioversion, anti-arrhythmics, or anticoagulation.
A 53-year-old man is hospitalized with pneumonia and is placed on a cardiac monitor. While in the room, you notice that he is in normal sinus rhythm but has occasional wide complexes without any pattern or relationship to the cardiac cycle. They occur several times per minute. The patient states that every once in awhile he feels like his heart skips a beat. He has no history of heart disease or sudden death in the family, and his vitals are normal.
Avoidance of caffeine and other stimulants. Premature ventricular contractions (PVCs), also known as ventricular premature beats, are very common electrical disturbances that are usually benign. They are concerning if they occur frequently, are symptomatic, or occur in a patient with structural heart disease (e.g., previous myocardial infarction). The presence of occasional PVCs in a structurally normal heart may be associated with an increased mortality; however, the use of prophylactic medications or procedures has not been shown to affect mortality. For the shelf examination, the right answer for a “next step in management” question is often the least invasive option (e.g., lifestyle modification), and therefore the patient should avoid any triggers of PVCs. (A, B, C) Occurrence of PVCs is extremely common (occur in about 80% of healthy patients); catheter ablation, β-blockers, and anti-arrhythmics are not likely to be helpful or cost effective. These options may be pursued in the setting of frequent or symptomatic PVCs if trigger avoidance fails to resolve the symptoms.
A 48-year-old man presents to the hospital after passing out during a basketball game with his friends. He was running toward the basket when he “blacked out.” He does not remember how long he was out, but he does remember waking up. On examination, his vitals are normal. Cardiac examination reveals a 3/6 midsystolic crescendo– decrescendo murmur heard best over the right upper sternal border, which radiates to the carotid arteries. The rest of the examination, including a neurologic examination, is normal. An ECG suggests left ventricular hypertrophy.
Which of the following symptoms carries the worst prognosis in this condition?
Dyspnea from pulmonary edema. This patient presents after an episode of syncope, with the murmur of aortic stenosis on examination. Because he is relatively young, he likely has aortic stenosis as a result of a congenital bicuspid valve. Once patients develop symptoms, they require surgical aortic valve replacement or else the prognosis is poor. (B, C) The typical symptoms of aortic stenosis can be remembered using the mnemonic ASD, which also relates to the mean survival once symptoms develop: Angina (mean survival 5 years), Syncope (mean survival 3 years), and Dyspnea from heart failure (mean survival 2 years). This patient experienced syncope as a result of decreased cerebral perfusion, which occurs due to an inability of the heart to increase cardiac output (fixed obstruction) in the setting of peripheral vasodilation during exercise. (D) Though patients with aortic stenosis often develop atrial fibrillation, the development of palpitations would not necessarily qualify a patient as having “symptomatic aortic stenosis” and does not correlate with mortality.
A 56-year-old man was recently hospitalized for an acute myocardial infarction. He was treated appropriately and had no complications during his hospitalization. After discharge, he follows up regularly in your clinic. Several months after his hospitalization, he comes to clinic for a regular visit with no complaints, stating that he is tolerating his new medications well. As he begins to leave, he mentions problems during intercourse with his wife and asks if he could have a prescription for sildenafil. A further history is obtained, and he reports that he no longer has morning erections.
Which of the following is most likely responsible for this complaint?
Metoprolol. β-blockers have a high incidence of erectile dysfunction as a side effect. Since he just recently suffered a myocardial infarction, it is assumed that he is now taking the standard discharge medications (dual antiplatelet therapy, β-blocker, ACE inhibitor, statin). (A) ACE inhibitors may cause cough and hyperkalemia, and they are teratogenic. They should be avoided in patients with hereditary angioedema (C1 esterase inhibitor deficiency) since there will be rapid accumulation of bradykinin causing angioedema. (C) β-blockers are preferred to calcium channel blockers after myocardial infarction. (D) Statins may cause myopathies and elevation of transaminases, but not erectile dysfunction. (E) Psychosocial stressors are a common cause of erectile dysfunction; however, this patient just started a medication that commonly causes erectile dysfunction and so this is the more likely answer. In addition, the lack of morning erections indicates an organic etiology rather than psychosocial problems.
A 72-year-old man presents to the Emergency Department complaining of chest pain. The patient is afebrile with a blood pressure of 104/68 mmHg, heart rate of 112 beats per minute, respiratory rate 14 breaths per minute, and oxygen saturation of 97% on room air. The patient has jugular venous distention and his lungs are clear to auscultation bilaterally. An ECG shows ST elevation in leads V1 and V2, and a right-sided ECG shows ST elevation in V4R.
Which therapy should NOT be given at this time?
Nitroglycerin. Nitroglycerin is a nitrate medication that is used to relieve anginal pain. It works by causing the release of nitric oxide in smooth muscle, which increases intracellular cGMP leading to vascular relaxation. Its effect is more pronounced on veins than arteries, especially at low doses, so the major effect will be venodilation that reduces preload to the heart and thus decreases myocardial oxygen demand. This is thought to be the mechanism of relieving anginal pain, and not coronary artery dilatation (since the coronary arteries are maximally dilated in response to ischemia during angina).
In the situation described above, nitroglycerin is not recommended for two reasons: first, it may lead to hypotension (by causing peripheral vasodilation), and second, it is dangerous in a patient with a right ventricular infarct. Although rare, a right ventricular infarct can cause poor functioning of the right ventricle with a relatively normal left ventricle that can sustain cardiac output as long as there is sufficient preload coming from the right ventricle. It is important to maintain adequate filling pressures (preload) to the right ventricle to ensure that enough blood is getting to the left ventricle. Right ventricular infarcts are therefore preload dependent, and intravenous (IV) normal saline can be provided if the patient is hypotensive. Nitroglycerin would decrease preload through its action as a venodilator, reducing cardiac output and exacerbating the patient’s hypotension. Likewise, morphine should be avoided since it also causes venodilation and decreases preload.
The right ventricular infarct is suggested by the patient’s jugular venous distention with clear lung fields, implying that the “obstruction” is proximal to the lungs. On ECG, ST elevation in leads V1–V2 can be seen in a right ventricular infarct; however, ST elevation in V4R (right-sided chest leads) is the most sensitive finding. (A, B, D, E) The other answer choices are appropriate in patients presenting with ACS, although IV fluids are not usually given in the setting of left ventricular dysfunction since the excess preload can worsen cardiac output. Although lisinopril is an ACE inhibitor and acts as a diuretic, it is usually safe to give in patients with a systolic blood pressure over 100 mmHg.
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