Download Module # 7– Syncope - UNM Hospitalist Wiki

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:
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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
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