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Facilitator Version Module # 7– Syncope Created by Dr. Merideth Prevost 3/2014 Objectives: 1. Identify the important aspects of the patient history in order to differentiate the causes of syncope 2. Develop a strategy for initial diagnostic evaluation of syncope 3. Determine the appropriate management for specific kinds of syncope References: Guidelines for the Diagnosis and Management of Syncope, The Task Force for the Diagnosis and Management of Syncope of the European Society of Cardiology (ESC), European Heart Journal (2009) 30, 2631-2671. AHA/ACCF Scientific Statement on the Evaluation of Syncope, Journal of the American College of Cardiology, Circulation, 2006;113:316-327. “Medical Management of Symptomatic Aortic Stenosis,” Catherine M Otto, MD and Stephanie Cooper, MD, UpToDate. “Indications for Valve Replacement in Aortic Stenosis in Adults,” William H Gaasch, MD, UpToDate. “Evaluation and Management of Patients With Aortic Stenosis,” Blase A. Carabello, MD, Journal of the American College of Cardiology, Circulation, 2002; 105: 1746-1750. MKSAP 16 Case A 71 yo male with history of CAD, hypertension, hyperlipidemia, diabetes, BPH, chronic back pain and PTSD presents after a fall while walking his dog. He complains of maxillary and nose pain. He has no chest pain or shortness of breath. He cannot remember any symptoms leading up to the fall. He simply woke up on the ground. A neighbor saw him fall, then called 911 and he was brought to the hospital via ambulance. Outpatient medications include: ASA, Clopidogrel, Isosorbide Mononitrate, Metoprolol, Lisinopril, Simvastatin, Furosemide, Terazosin, Glargine, Metformin, Gabapentin, Oxycodone, and Fluoxetine What other information would you like to obtain in the history? Important historical features to address when interviewing a patient about syncope: What were the circumstances just prior to the event? Position (supine, standing, sitting) Activity (at rest, with exertion, during urination, coughing, defecation) Predisposing factors (prolonged standing, in crowd, fear, intense pain, neck movements, shortly after a meal) What happened at the beginning of the event? N/V, diaphoresis, cold, aura, pain, blurred vision, dizziness, lightheadedness Palpitations, chest pain Describe the event itself (including eye witness accounts) Duration of loss of consciousness, way of falling (slumping, kneeling or keeling), skin color (cyanotic, pale, flushed), breathing patterns (fast, slow, labored), abnormal movements, tongue biting What happened at the end of the event? Confusion, muscle aches, N/V, diaphoresis, chest pain, palpitations, incontinence Background questions Family history of sudden death and arrhythmia Past Medical History-- Cardiac disease, arrhythmia, neurologic disorder, seizures, diabetes Medications/Medication changes—Antihypertensives, antianginals, diuretics, QT prolonging agents, antidepressants, alpha blockers What are the general categories of syncope and how does the history help you to narrow the differential diagnosis? Syncope is defined as a sudden cessation of cerebral blood flow that causes a loss of consciousness. It generally only takes 6-8 sec of blood flow cessation to cause syncope. Cerebral blood flow is affected by both cardiac output and peripheral vascular resistance, so a decrease in either of these can lead to syncope. These two mechanisms are behind all true syncopal episodes. Other etiologies of loss of consciousness, including epilepsy, hypoxemia, hypoglycemia, hyperventilation, intoxication and vertebrobasilar TIA, are not true syncope because they are not caused by global cerebral hypoperfusion. Other things that may be confused with syncope are drop attacks, psychogenic pseudosyncope, falls, cataplexy. There are three classifications of syncope-- reflex syncope, orthostatic hypotension and cardiac syncope. Reflex syncope refers to a neurally mediated process such as vasovagal, situational, carotid sinus hypersensitivity, as well as unexplained syncope. Orthostatic hypotension can be caused by primary autonomic failure (multiple system atrophy, Parkinson’s, Lewy Body dementia), secondary autonomic failure (diabetes, amyloidosis, uremia, spinal cord injury), medications/drugs or volume depletion. Cardiac syncope encompasses bradycardia, tachyarrhythmias and structural heart disease such as valvular disease, hypertrophic cardiomyopathy, acute myocardial infarction, cardiac masses, pericardial disease, congenital coronary anomalies. Pulmonary emboli, pulmonary hypertension and aortic dissection are also considered cardiac etiologies. You talk to the patient more about the events surrounding his fall. You also interview the neighbor. The patient states that 2 weeks ago he saw his PCP for increased swelling in his legs and some shortness of breath with exertion. His PCP prescribed furosemide for him. He was also having to get up a lot at night to urinate, so his terazosin dose was increased. His swelling and urination got better with these medication changes. The patient reports he had no chest pain or palpitations when he was walking his dog, but he felt very fatigued and a little lightheaded before the event. He had no diaphoresis, N/V. The neighbor reports that the patient was just walking along, then paused slightly and fell forward onto his knees, then his face. He had no incontinence and no jerking movements. He was pale and his nose was bleeding. His LOC lasted about 30 seconds and when he woke up, the patient behaved normally. He was confused about how he got to the ground, but was otherwise oriented. On physical examination, his temperature is 36.5 °C, blood pressure is 116/68 mm Hg, heart rate is 64/min, and respiratory rate is 16/min. The patient is alert and oriented. He has bilateral periorbital ecchymosis and facial abrasions, with edematous nose and blood crusted at nares. RRR, 3/6 late peaking systolic murmur best heard at the right upper sternal border with radiation to carotids and delayed upstroke of carotid pulse. He has JVD, scant bibasilar crackles, 1-2+ pitting edema to mid-calf. Neuro exam is normal. Labs: CBC: WBC 4.9, Hgb 12, Hct 36, Plt 231. Chem 10: Na 137, K 3.4, Cl 98, HCO3 29, BUN 31, Cr 1.5, Glc 163, Ca 8.3, PO4 2.8, Mg 1.7 LFTs: Normal What are the leading diagnoses on your differential for this man’s syncope? Aortic stenosis, orthostatic hypotension due to dehydration or medication effect, arrhythmia. What physical exam findings suggest aortic stenosis as a possible cause? Late peaking systolic crescendo-decrescendo murmur and delayed carotid upstroke are indicative of severe aortic stenosis, which may be symptomatic. As aortic stenosis becomes more severe, you may also find loss of the aortic component of the second heart sound as well as decreased intensity of the carotid pulse. What are some of the medications that may have contributed to this episode of syncope? The new furosemide and the increased dose terazosin are the most likely culprits since they were just changed. However, metoprolol, lisinopril, isosorbide mononitrate and fluoxetine could have played a role as well. You order an ECG. What are you looking for? Arrhythmias, blocks, ischemic changes and QTc prolongation What other studies do you want to get? Orthostatic vitals, CXR, TTE, troponin, BNP For this patient, the most likely causes of syncope are cardiac in origin or orthostatic hypotension. Therefore, the workup should focus on differentiating between cardiac causes of syncope and determining if orthostasis is playing a role. This patient has a history of coronary disease and he has evidence of heart failure on exam. MIs are often associated with arrhythmias due to decreased perfusion and irritability of the electrical system. Heart failure with reduced ejection fraction confers increased risk of ventricular arrhythmias and sudden death. He also has clinical evidence of valvular disease, specifically aortic stenosis. A TTE will be important to ascertain the severity of the aortic stenosis, though clinically it is likely severe. Orthostatic vitals will help determine which medications should be held and if this is a contributing factor. You get the test results: Orthostatics: Supine—BP 116/68 HR 64 Sitting—BP 110/62 HR 68 Standing—BP 94/56 HR 74 ECG: NSR, old Q waves in inferior leads, T wave flattening anterolateral leads, QTc 435 ms Trop: 0.018 NT-ProBNP: 2348 TTE: EF 35-40%, LV dilation, inferior akinesis, anterolateral and septal hypokinesis, mild MR and TR, severe AS with AVA 0.9 cm2, aortic jet velocity 5.1 m/sec, mean gradient 43 mmHg. CXR: Cardiomegaly, increased vascular congestion with cephalization and Kerley B lines, small bilateral effusions What are his diagnoses? Severe aortic stenosis, coronary artery disease, decompensated heart failure with reduced ejection fraction, orthostatic hypotension. What medications do you order? Fluids? Continue ASA, clopidogrel, statin for CAD. Switch terazosin to tamsulosin to continue treating BPH but minimize BP effects. May continue fluoxetine as QTc normal. Patient is already fluid overloaded, so although adding fluid may help mild orthostasis, it would worsen CHF and should be avoided. The decision to continue the rest of the cardiac medications is more difficult. For AS: Patient is preload dependent. Nitrates and diuretics will cause decrease in preload, and therefore decrease stroke volume and therefore cardiac output. They should be avoided if possible. Beta blockers should be avoided in patients with symptomatic AS and heart failure due to its effect of decreasing myocardial contractility. Vasodilators should also be avoided if possible due their ability to decrease systemic blood pressure and reduce coronary artery perfusion pressure. For CHF: Beta blocker dose should remain the same or lower given decompensation. ACEI should be continued and diuretics used for fluid overload. For CAD: Patient should be on ASA, clopidogrel (depending on when last stent was placed), statin, beta blocker and ACEI. Long acting nitrate is helpful for angina ssx and microvascular involvement Overall: This patient’s main problem is his severe AS with CHF. He does not have ischemic symptoms now, and no signs ischemia on labs or EKG. Therefore, it is probably safe to stop nitrate and beta blocker, and stopping these medications may improve AS symptoms. Given his decompensated CHF, may consider lower dose furosemide to maintain even to 500mL negative fluid balance. Continue ACEI, but consider lowering the dose of this as well given orthostasis. Does the patient qualify for Aortic Valve Replacement? Yes The main criterion for AVR is symptomatic AS, usually manifesting as with syncope, heart failure or angina. Average survival after the onset of these symptoms is only two to three years, with a high risk of sudden death, and mortality decreases with AVR. Age is not a large risk factor for AVR, so surgery should be pursued even in those patients >80yo with symptomatic AS. The 2006 American College of Cardiology/American Heart Association (ACC/AHA) guidelines on the management of valvular heart disease concluded that valve replacement should not be routinely performed for isolated severe AS in asymptomatic patients. The most notable exception is in the case of patients undergoing coronary artery bypass graft surgery or surgery on the aorta or other heart valves, who also have AS. What other tests does this patient require prior to surgery? Cardiology should be consulted and patient should undergo catheterization to assess coronary vasculature and need for coronary artery bypass grafting at the same time as the aortic valve replacement. CT Surgery also usually requests that all age appropriate cancer screening is done prior to surgery to ensure that 5 yr mortality is low from other causes. MKSAP 16 Questions Gen IM Question 21- diagnose the cause of syncope. Answer B Gen IM Question 86- evaluate vasovagal syncope. Answer E Gen IM Question 31- evaluate a patient with recurrent syncope. Answer D Gen IM Question 156- manage syncope in elderly patient. Answer C CV Med Question 90- evaluate need for AVR. Answer D CV Med Question 35- treat AS with LV dysfunction. Answer C Post Module Evaluation Please place completed evaluation in an interdepartmental mail envelope and address to Dr. Wendy Gerstein, Department of Medicine, VAMC (111) or give to Dr. Patrick Rendon at UNM Hospital. 1) Topic of module:__________________________ 2) On a scale of 1-5, how effective was this module for learning this topic? _________ (1= not effective at all, 5 = extremely effective) 3) Were there any obvious errors, confusing data, or omissions? Please list/comment below: _____________________________________________________________________________________ _____________________________________________________________________________________ _____________________________________________________________________________________ _________________________________ 4) Was the attending involved in the teaching of this module? Yes/no (please circle). 5) Please provide any further comments/feedback about this module, or the inpatient curriculum in general: 6) Please circle one: Attending Resident (R2/R3) Intern Medical student