Teaching Clinic - Three Cases with Syncope Flashcards
- Mr. YSM, M/54
- C/O: Sudden onset of palpitation associated with syncope
- Sudden onset of rapid palpitation for 1-2 minutes, associated with mild dyspnea and then LOC
- ? Mild twitching of all 4 limbs during the episode as noted by his wife
- Lasting for 30 seconds and patient spontaneous regain conscious
- No head injury or neurological abnormality after recovery
Hx:
- Head injury-related? Before or after passing out?
- Frequency (with previous recovery = better prognosis, means that patient has survived before vs. first episode may have worse prognosis)
- Previous heart attack
- Exertional angina / dyspnea ?
- Palpitatoins?
- Dizziness?
- LOC? Twitching/tongue-biting/post-ictal drowsiness? Up-rolling eyeballs? Cyanosis?
- Exercise capacity?
- Orthopnea? PND?
- Past history: heart disease? long-term medical therapy?
- Medication causing syncope? (ACEi S/E: first-dose hypotension, hyperkalemia, cough, angioedema, vascular leakage)
- Social history: Smoker? Drinker?
- Family history
- Drug history
- Age (young = vasovagal, inherited conditions [HOCM, Brugada) vs. middle age = structural heart disease)
What does it mean if a patient is twitching but we cannot open their eyes?
This is malingering. Eyes should roll backwards in true syncope.
Eye opening muscles are voluntary muscles.
What happens to blood pressure and breathing pattern during seizure?
- Blood pressure very high (sympathetic tone)
- Patient is not apneic (hypoxemic causing increased sympathetic tone)
Where may cardioembolism lead to syncope?
Brainstem (vertebral circulation) = unusual
When may Afib lead to syncope?
- Slow AF
- Poor ventricular function
- Brainstem stroke
- Sick sinus syndrome (long-pause)
- Wolff-Parkinson-White
How much cardiac output is contributed by atrial contraction?
10%, unless there is problem during filling phase (i.e. HOCM, ventricular dysfunction)
What are fatal conditions which must not be missed in a patient with syncope?
4 conditions that you cannot miss
- Myocardial infarction (1/8 will present with syncope) =60% get to hospital in time, 40% die at home
– Ischaemic-related ventricular fibrillation (can be due to transient ischaemia due to occlusion of arteries) - Pulmonary embolism (1/8 will present with syncope=saddle PE) = haemodynamic collapse. Increased pulmonary arterial pressure causes increased myocardial contraction which breaks up the clot. Syncope is a bad prognostic factor as it indicates a large clot.
- Aortic dissection
- Rhythem problem (slow heart beat or fatal arrhythmia: ventricular arrhythmia, TdP) = ventricular scar [re-entrant related tachycardia = 1-2 years after event]
Relative importance of diagnosis, frequency of disorder, presentation
4 highly fatal conditions that you cannot miss
Rhythm problem (heart block, bradycardia, ventricular rhythm issues), aortic dissection, pulmonary embolism, myocardial inafarction
Patient with MI wakes up. How come?
Spontaneous reperfusion (blood clot resolves) = Regain consciousness (not the entire artery is occluded)
Aortic dissection = Transient dissection (compress on false lumen)
What medication cannot be given with ACEi?
ACEi releases bradykinin
ARNI releases bradykinin (Sacubitril/valsartan)
High risk of angioedema
What 4 drugs are in the heart failure treatment regimen?
ARNI, a beta-blocker, an MRA, and an SGLT2 inhibitor
Drugs that prolong QT
Antibiotics (episodic drug):
- Macrolides
- Quinolones
- Septrin
Anti-psychotics:
Anti-emetic
Anti-depressant
Anti-arrhythmic
- class IA [quinidine]
- class IC [sodium channel blocker, i.e. flecainide]
- class III [i.e. amiodarone],
Drug abuse = methadone, analgesics (prolong QT = sudden death)
Anti-histamine
Anti-spasmodic drugs (GI upset)
TCM (acrolein)
What drug shorten QT?
Class II (B) = propanolol (shorten QT)
class IB [i.e. shorten QT = lidocaine, mexlitine = shorten QT]
Physical examination: conscious and alert
– BP: 110/65, pulse regular 70 bpm, all pulse equal and normal
– Heart sound normal with pansystolic murmur over apex, no carotid bruit
– Chest: mild bilateral basal crepitation
– Neurological examination: NAD
- Pansystolic murmur: malignant MVP syndrome [99% benign,1% malignant] = ventricular premature beat + ventricular arrhythmia
Rate: 85 bpm
Axis: Normal
Rhythm: Regular
Interval: QT 2.2, not prolonged
Chamber enlargement: Left atrial enlargement (mitral regurgitation), no ventricular enlargement
QRS complex: amplitude change & progression, widening of QRS:, L or R bundle, Q wave [V5, V6] = anterolateral , [II, III, aVF] = inferior)
Dx: inferior and anterolateral MI
Rate: 200 bpm
Axis: Extreme axis deviation
Rhyhtm:
Wide complex tachycardia: VT, SVT +/- WPW, BBB, pre-existing wide complex
Anterolateral myocardial infarction
RBBB, so it’s coming from the L-side
RBBB = left VT
7 criteria for VT
- Absence of typical RBBB or LBBB morphology
- Extreme axis deviation (“northwest axis”): QRS positive in aVR and negative in I and aVF
- Very broad complexes > 160ms
- AV dissociation: P and QRS complexes at different rates. P waves are often superimposed on QRS complexes and may be difficult to discern
- Capture beats: Occur when the sinoatrial node transiently “captures” the ventricles in the midst of AV dissociation, producing a QRS complex of normal duration (see 3)
- Fusion beats: Occur when a sinus and ventricular beat coincide to produce a hybrid complex
- Positive or negative concordance throughout the precordial leads, i.e. lead V1-6 show entirely positive (R) or entirely negative (QS) complexes, with no RS complexes seen
Rhythm:
Axis: LAD
Fusion beat = VT
Where is VT = RBBB = left VT (septum!) [not lateral]
L-axis (through the spetum)
Value of EP Study in Syncope
Treatment of Previous Myocardial Infarction with Ventricular Tachycardia
- Anti-heart failure
- Anti-ischaemic
- Implantable cardioverter defibrillator
(Give anti-arrhythmic drugs or cath ablation of accessory pathway)
- Axis: RAD
- Chamber enlargement: V1 P wave is very small (monophasic) = R atrial enlargement
- RIght ventricular enlargement:
– Big S wave in V5, V6
– Big S wave in lead I
Q wave in lead III (inverted)
Pulmonary embolism
- Sympathetic activation: sinus tachycardia
- Right ventricular dilatation
Rate:
Rhythm
Axis: RAD
QT: 0.6 (one big square in 0.2, small square is 0.04)
R Atrial Enlargement
R Ventricular Enlargement
S1Q3T3
4 common causes of prolonged QT
- drug
- electrolytes
- ischaemia
- idiopathic
Rate: <60
Axis: LAD
Prolonged PR interval
QRS complex is wide
No monophasic P wave (atrium looks normal)
Left ventricular normal
V2 through V3 (Pathological Q wave)
ST changes: ST elevation in leads V1-6, aVL
Anterolateral STEMI
What could cause exercise-induced syncope?
L-sided obstruction
Atrial myxoma (obstruct L ventricle)
Turner syndrome
R-sided obstructoin
Pulmonary hype
Ventricular arrhythmia, SVT
CPVT
Marfan’s syndrome? Aortic dissection (basketball, super tall)
