Syncope in the Primary Care Setting. Ibrahim Hanna MD

Transcription

1 Syncope in the Primary Care Setting Ibrahim Hanna MD

2 Definitions SYNCOPE: Abrupt but transient loss of consciousness associated with the absence of postural tone, followed by a rapid and usually complete recovery without any intervention to stop the episode. A prodrome may be present. The underlying process is the transient (5-20sec) global interruption of cerebral blood flow, specifically to the reticular formation.

3 Limitations Syncope is a non-specific symptom rather than a specific diagnosis. It can be caused by a variety of conditions ranging from benign to malignant. Syncope and near-syncope are often confused with other vague symptoms such as transient confusion or weakness, intoxication, dizziness and vertigo, falling episodes, sleep disorders, seizures, or even coma.

4 Epidemiology Lifetime risk of syncope is ~30%. The risk is similar in men and women. Incidence of Syncope has a bi-modal distribution. It is most common in the young (20yrs) and the elderly (80yrs).

5 Implications of Syncope on Affected Patients Impairs QOL, on par with chronic back pain or RA. Patients can have a fear of recurrence or death. Patients often change their lifestyle such as limiting their driving or work attendance. Can cause injuries in 1/3 rd of patients, especially in the absence of a warning prodrome. Interestingly, 10% of falls in the elderly are due to syncope. Can be the premonitory sign of a serious cardiac problem. In fact, in some instances the difference between syncope and sudden death is that in the former the patient wakes up.

6 Implications of Syncope on Healthcare System ~1% of all ER visits are due to syncope % get admitted. On average a patient with syncope makes 10 visits/year to a physician and sees 3 different specialists. These admissions and evaluations are often redundant, expensive, low yield and unnecessary.

7 ANNUAL COST $2.4 billion according to MEDICARE database.

8 Causes of Syncope CARDIOVASCULAR NEUROLOGIC/PSYCH OTHER 1ry Arrhythmic: AV Block Sinus pause Long QT/Short QT Brugada syndrome CPVT Structural: HCM Anomalous coronaries VT with structural HD ARVC PE Cardiac tamponade AS Atrial myxoma Reflexive: Vasodepressor syndrome Orthostasis/Dysautonomia Carotid hypersensitivty Micturition/defecation/degl utition/ post-tussive Seizure Migraine Psychogenic: Hysteria Panic with hyperventilation Carcinoid Mastocytosis Hypoglycemia/hyp oxia Drugs: Alcohol Illicit drugs Prescription drugs especially in elderly with polypharmacy UNDIAGNOSED (30-40%)

9 Diagnostic Approach History and PE: May be the single most important part of the evaluation and may establish an etiology in 75% of diagnosed cases. Patient s age: Younger patients more likely to have NCS. Length of the episode: Long episodes (>5mns) not likely cardiovascular (seizure, metabolic, intoxication, psychogenic). Triggers: Emotional triggers, pain, sight of blood, post-exercise may indicate NCS. Abrupt rise from prone position point to orthostasis/dysautonomia. Cough, micturition, cold carbonated beverages indicate situational syncope. Exercise induced may indicate HCM (most commonly in the young), AS, LQTS or CPVT.

10 Diagnostic Approach Number of episodes and time since first episode: Numerous, and of many years duration: More likely benign. Prodromal symptoms: Nausea, pallor and diaphoresis: NCS or other increased vagal state (CHS, situational). Aura: seizure. Palpitations: possible tachy-arrhythmic cause, but not specific. Anginal chest pain: ischemic etiology. Impending doom, acral and perioral tingling and choking sensation: panic attack/hyperventilation. Associated findings: Tongue biting, violent jerking and loss of continence: seizure. (Myoclonus can be seen with NCS due to transient cerebral hypoxia. Also NCS can produce incontinence). Blue skin: cardiac arrhythmic.

11 Diagnostic Evaluation Post-syncopal symptoms: Headache, protracted confusion: seizure. Feeling drained and tired for hours post event: NCS. Medication history: Assess changes in medications preceding syncope onset. Check for medication interactions, dosages and patient s compliance/confusion with dosages: Antihypertensives (diuretics) Alpha blockers (coreg and flomax) Psychotropic medications Anti-arrhythmics (Class Ic drugs in patients with CAD) QT prolonging drugs (sotalol and levaquin) FMHX of SCD

12 Physical Exam Check VS at rest. Perform an orthostatic challenge: If SBP drops (>20mmHg) or DBP (>10mmHg) and HR increases (10bpm): INTACT ANS If BP drops and HR does not change: ANS FAILURE If BP changes little but HR increases by >30bpm: POTS Examine pulses: Subclavian steal, AS, HOCM, aortic dissection. Examine the heart (gallop, murmurs, lift, etc ) Complete a neurological exam (Parkinson s disease, focal neurological deficits, Todd s paralysis).

13 Diagnostic Testing Always perform an EKG: leads to the diagnosis in 10% of cases. Otherwise, no specific battery of tests is always indicated. The choice should be individualized. TTE r/o structural heart disease if high suspicion based on PE and EKG ECG monitoring most direct proof of presence/absence of arrhythmia Cardiac cath r/o CAD or anomalous coronaries causing ischemia Exercise test if exertional syncope (CPVT, long QT ) Carotid U/S not useful as focal stenosis unlikely to cause global ischemia CT scan of brain -low yield. Indicated if suspicion of neuro process EEG low yield. Indicated if suspicion of seizures

14 Tilt Table Test

15 Tilt Table Testing TTT has a sensitivity of 30-80% and a specificity of 90% if the patient s prodrome is reproduced. If the history is clearly compatible with NCS, a TTT may not be necessary and may be falsely negative. TTT is most useful when NCS is suspected or the patient has an otherwise undiagnosed syncope. TTT can be falsely positive and the results have to be interpreted with caution. e.g. Reggie Lewis had syncope and +ve TTT but died of VF due to HCM.

16 EPS Can be very useful in assessing the inducibility of monomorphic VT or hemodynamically unstable SVT. Performs poorly in assessing sinus node and AV node functions. Not useful in patients with Long QTc, HCM or the Brugada syndrome.

17 Prognostic Implications ES Soteriades et al. N Engl J Med 2002;347:878-85

18 Case 1 A 46 yo male OBGYN suffered a syncopal episode at the dinner table. The patient had no prodrome and passed out for a few seconds before regaining full consciousness without sequelae. His wife insisted that he gets checked out. He is seen by his Cardiology colleague. The patient has no PMHx and until the syncopal episode was very active. The PE exam is unremarkable. He is not orthostatic. His TTE shows no structural abnormalities with a normal LVEF. The patient has no FMHx of SCA. On further questioning, the patient s wife insists that the patient s face turned blue during the episode of LOC. What is the next diagnostic step?

19 BRUGADA

20 Patient receives an ICD due to increased risk of VF

21 Case 2 A 29 yo nursing student is sent by her supervisor because she sustained a syncopal episode while donating blood at the local hospital. The patient reportedly turned pale before passing out. She experienced nausea and diaphoresis. She was attended to by other nursing students who noted that she had an absent radial pulse for 1-2minutes. She was observed to have some upper extremity jerking. She did not lose continence and had no tongue biting. When she regained consciousness, the patient displayed no confusion but reported that she felt tired and sleepy for the rest of the day. She was sent home to rest. PE and EKG are unremarkable. What is the next diagnostic step?

22 No Further Testing Diagnosis established based on already available information: NEURO-CARDIOGENIC SYNCOPE

23 Case 3 A 39 yo woman presented to an OSH with recurrent episodes of syncope ongoing for 2 years, without significant trauma. She was prescribed an event monitor and was noted to have 3-4sec sinus pauses. The pauses were preceded by progressive slowing of the sinus rate and the development of a 1 st degree AV block. She was admitted urgently and underwent a dual chamber pacemaker implant. Do you agree with the management?

24 Case 3 (continued) The patient is now presenting to you 6 months after pacemaker implant with persistent symptoms. Interrogation of the device shows <2% Atrial pacing and no RV pacing. On further questioning, she works at a call center with prolonged periods of sitting down. In fact, she further mentions that most of the episodes have occurred at her desk, while the rest have occurred while standing up. Her prodrome consists of a warm sensation followed by lightheadedness. On occasion, she has been able to abort the progression into LOC by lying down. The rest of the history, PE and EKG are unremarkable. She undergoes a TTT.

25 TTT with Cardio-inhibitory response reproduces her symptoms. She is started on appropriate therapy with good response.

26 Case 4 A 74 yo female with AF on sotalol presents to the ER with 4 back to back episodes of syncope over a 24hr period without prodrome. Her husband witnessed the last 2. He reports that the patient starts out screaming. He saw her put her hand up to her left chest just before passing out. She sustained a hematoma to the scalp after falling against the kitchen table with the last event. The patient has no known CAD or LV dysfunction. She had recently lost her son in a car accident and was started on Celexa for depression. Otherwise, She takes HCTZ for hypertension. On PE exam, she is lucid but has poor recollection of the events. She denies syncope and only reports unexplained falls. Her HR and BP are within normal. CT scan of the head shows no acute IC process. TTE shows normal LVEF, mild LVH and mild MR. What is the next step

27 An EKG is obtained: QT RR

28 Labs Na: 139 K: 3.4 Bun: 16 Cr: 0.7

29 Acquired Long QTc 3 HITS: HypoK on HCTZ: QT prolongation Sotalol: Class III AAD: QT prolonging Celexa: SNRI: Black box warning about QT prolongation and TdP

30 Case 5 A 29 yo male collapses while running on the treadmill at the gym. He receives brief CPR before regaining full consciousness and is taken to a near-by hospital for evaluation. There, he is hemodynamically stable and upon further investigation is dismissed home with the advice of maintaining adequate hydration and avoiding over exertion. Do you agree with the recommendation?

31 Case 5 (continued) The patient is in his first year of medical residency, and is very fit. He has a rigorous training program and was not exerting at an unusually high level. Because he is concerned about his disposition, he refuses to have his IV catheter removed, obtains a copy of his EKG and presents to your office.

32 EKG

33 ARVC Suspected Fibro-fatty infiltration of the RV leads to a substrate for reentrant VT. TTE showed normal LVEF, mild RV enlargement and suspicion for focal apical akinesis.

34 Diagnosis EPS produced a hemodynamically unstable monomorphic VT. Cardiac MR confirmed the diagnosis of ARVC. ICD was implanted.

35 Case 6 A 74 yo male with dementia fell at home and was brought by his wife to the ER. She did not witness the event but heard a thump upstairs that prompted her to attend to him. She found him on the floor unconscious. He came back to within seconds and recovered very quickly. She noted him to be pale. He has known HTN on coreg and recently had worsening BPH symptoms that responded well to a new agent started 1 week prior by his urologist. Since starting the new regimen the patient appeared to have an unsteady gait, especially when rising from bed in the morning.

36 Case 6 (continued) Medications: Coreg 12.5mg PO BID Lisinopril 2.5mg PO QD Aricept 5mg PO QD Flomax 0.8mg PO QD PE: BP 160/78, HR 58bpm. o/w S4. EKG: Sinus bradycardia. What is the next step

37 Check orthostatic BP VS obtained with the patient lying down on a stretcher. Orthostatic challenge undertaken: SBP drops to 60mmHg and HR increases to 112bpm. Patient gets weak and has to be supported to stand.

38 Diagnosis ORTHOSTATIC HYPOTENSION exacerbated by combination of 2 alpha blockers (Coreg and flomax). Stop flomax. Consider changing coreg to metoprolol or atenolol. Institute conservative measures.

39 Conclusion Identifying the cause of syncope can be a frustrating undertaking. 40% of all syncope events remain undiagnosed. History, PE and other tools deployed in a thoughtful manner can help establish the diagnosis. Reflexive and haphazard testing is not useful, and can be very expensive. PCPs are often the first contact for patients with syncope and play an important role in guiding the work up and therapy.