Syncope Flashcards
Syncope
Transient loss of consciousness and postural tone due to temporary reduction in cerebral perfusion
Abrupt and transient
Accounts for 1% to 1.5% of emergency department visits, resulting in high hospital admission rates and significant medical costs.
Common in all age groups
Higher incidence in elderly
Important to distinguish between benign and serious causes
Cardiac syncope is associated with increased morbidity and mortality.
Runser et al, Am Fam Physician 2017 Mar 1;95(5):303-312
ESC definition of syncope
European Society of Cardiology(ESC) definition states that syncope is characterised by:
Rapid onset
Short duration (typically no longer than 20 seconds, but can be several minutes)
Spontaneous and complete recovery (although some disorientation is common with increasing age)
The presence of these three characteristics isstrongly suggestiveof a syncopal episode (i.e. a transient loss of consciousness caused by transient global cerebral hypoperfusion).
Types of syncope
Reflex syncope
vasovagal, situational, and carotid sinus syndrome
Orthostatic syncope
Due to postural changes leading to hypotension.
Cardiac syncope
Arrhythmias, structural heart disease, or ischemic events
Neurological syncope
Seizures, transient ischemic attacks (TIAs).
Reflex syncope
VVS most common form of reflex syncope
Failure in autoregulation of blood pressure, and ultimately, in cerebral perfusion pressure resulting in transient loss of consciousness.
Mechanisms responsible for this are complex and involve both depression of cardiac output as well as a decrease in vascular tone.
Other typesof reflex syncope include carotid sinus syncope and situational syncope, for instance, cough or micturition syncope.
Vasovagal syncope may be triggered by pain or emotional upset, although frequently a specific trigger cannot be identified
Orthostatic syncope
Syncope resulting from a postural decrease in blood pressure.
Reduction in BP of at least 20mmHg systolic or 10mmHg diastolic within 3 minutes of standing or being upright to 60 degrees on the head-up tilt table.
In patients with initial orthostatic hypotension, the decrease in blood pressure occurs within 15 seconds, while in those with delayed orthostatic hypotension it occurs after over 3 minutes of assuming an upright position.
High rate of morbidity and mortality related to this disease process due to frequent falls, leading to multiple hospital admissions.
Caused by both neurogenic and non-neurogenic aetiologies and can also be related to medications.
Most prevalent in patients aged >65years (partly due to impaired baroreceptor sensitivity). Prevalence can be as high as 18.2% > 65 yrs old
Cardiac Syncope
While most syncopal events are innocuous, cardiac syncope is often indicative of a potentially fatal, underlying disease process, carrying a one-year mortality rate of 30%.
Cardiac syncope occurs when the source of one’s loss of consciousness stems from a problem in the heart that prevents it from supplying enough nutrients and oxygen to the brain.
Rhythm disturbance,
Structural problem,
Or structural problem that predisposes a patient to a rhythm disturbance.
Cardiac syncope is estimated to be the cause of syncope in 15% of syncopal events. Distinguishing cardiac syncope from the myriad of other syncopal etiologies can be challenging
Ischemic cardiomyopathy (most common structural cardiac etiology of syncope)
Valvular abnormalities (second most common structural etiology, most commonly aortic stenosis)
Nonischemic/Dilated cardiomyopathy (third most common structural etiology)
Hypertrophic obstructive cardiomyopathy
Aortic dissection
Cardiac tamponade
Obstructive cardiac tumors
Pericardial disease
Pulmonary hypertension
Pulmonary emboli
Arrhythmogenic right ventricular cardiomyopathy
Electrical
TachyarrhythmiaSupraventricular (examples: atrial fibrillation, atrial flutter, paroxysmal supraventricular tachycardia (PSVT), PSVT in the setting of pre-existing accessory conduction pathways)
Ventricular (often secondary to mechanical/structural heart disease or channelopathies, such as Brugada)
PR interval disorders/accessory conduction pathways (WPW, LGL, Mahaim syndrome, Breijo syndrome)
BradyarrhythmiaSinus node dysfunction
Atrioventricular conduction block (typically second or third degree)
Pacemaker malfunction
Inherited channelopathiesQT interval disorders (Long or short QT)Romano-Ward syndrome: Autosomal dominant congenital long QT syndrome
Jervell and Lange-Nielsen syndrome: autosomal recessive long QT syndrome associated with deafness
Brugada syndromeAn autosomal dominant mutation in the SCN5A gene, which encodes for voltage-gated sodium channels found in the heart
Catecholaminergic polymorphic ventricular tachycardiaAutosomal dominant mutation of hRyR2 gene, which encodes for ryanodine receptors
Autosomal recessive mutation of CASQ2 gene, which encodes for calsequestrin-2
Neurological syncope
Seizure-induced arrhythmogenic syncope results from heart rate and rhythm changes during seizures.
- Tachycardias commonly accompany seizures, though rarely lead to symptoms.
- Bradyarrhythmias are rarer, usually associated with left sided partial seizure onset, and lead to loss of consciousness which is syncopal rather than primarily due to the seizure.
Intermittent obstructive hydrocephalus, present as occipital “pressure” headaches building over seconds before loss of consciousness.
Transient ischaemic attacks rarely lead to loss of consciousness, and then only with involvement of the posterior circulation; there are usually associated brainstem symptoms including vertigo, ataxia, diplopia, and parasthesiae.
Migraine syncope usually manifests as a gradual onset loss of consciousness in the context of other migraine symptoms and is typically associated with familial hemiplegic migraine.
Clinical evaluation steps
History Taking:
Circumstances of the event, associated symptoms, and medical history.
Physical Examination:
Vital signs, neurological assessment, and cardiac examination.
Risk Stratification:
Use of validated scoring systems (e.g., San Francisco Syncope Rule).
History taking
Presenting complaint
“What’s brought you here”.
“can you tell me more about this”
History of presenting complaint
-Triggers
-During the period of syncope
-Duration
-Other clinical features
-After syncope (time to recover, relieving factors)
ICE (ideas, concerns, expectations)
Summarising
Signposting
Physical examination
Brief screen for symptoms in other body systems
Systemic: fevers (e.g. cerebral abscess, meningitis), weight change (e.g. malignancy)
Cardiovascular: palpitations (e.g. arrhythmia), chest pain (acute coronary syndrome), shortness of breath (e.g. heart failure)
Respiratory: dyspnoea, cough (e.g. pneumonia), pleuritic chest pain (e.g. pulmonary embolism)
Gastrointestinal: diarrhoea, vomiting (e.g. dehydration/hypotension)
Genitourinary: oliguria (e.g. dehydration/hypotension)
Neurological: visual symptoms (e.g. pre-syncope), headache (e.g. brain tumour), motor or sensory disturbances (e.g. stroke)
Musculoskeletal: trauma (e.g. secondary to syncope)
Dermatological: rashes (e.g. meningococcal sepsis)
Personal history
Drug history
-Prescribed medications
-Over the counter remedies
Family history
-Hx CVD or seizures
-Age the disease developed
-Relatives deceased
Social history
-General context
-Smoking
-Alcohol
-Recreational drug use
-Fluid intake
-Occupation
-Driving
Risk stratification
Syncope is a diagnostic challenge.
Initial risk stratification aims to identify high-risk patients that require hospitalization,
Intermediate-risk patients that should be further investigated and treated to prevent syncope recurrences,
Low-risk patients that needreassurance, education on avoidance of triggers and employment of physical counter-measures, improved hydration and salt supplementation.
A&E presentation: no consensus for use of algorithms and risk score
Clinical judgement still goldstandard
Outpatient settings, syncope units add refinement of diagnosis and management benefits
Canadian Syncope Risk Score
https://www.mdcalc.com/calc/3951/canadian-syncope-risk-score
EGSYS (Evaluation of Guidelines in SYncope Study) Score for Syncope
https://www.mdcalc.com/calc/3948/egsys-evaluation-guidelines-syncope-study-score-syncope#pearls-pitfalls
San Francisco Syncope Rule
https://www.mdcalc.com/calc/93/san-francisco-syncope-rule
ROSE (Risk Stratification of Syncope in the Emergency Department) Rule
https://www.mdcalc.com/calc/3949/rose-risk-stratification-syncope-emergency-department-rule
CHB pathway -syncope
stabilise patient
identify and treat reversible causes - electrolyte abnormalities
temp pacing - used in emergency settings when patient is haemodynamically compromised: following MI, severely symptomatic bradycardia, following surgery (CABG, valve surgery), during procedure (TAVI, rotablation), Brady-induced tachycardia
- when the underlying cause is reversible and expected to resolve
- when benefits outweigh infection risk
- to provide a normal heart rhythm until a permanent pacemaker can be implanted
- dual chamber pacemaker implantation
Investigation
12-lead ECG.
BP sitting and standing
Bloods
Ambulatory ECG monitoring remarkable? N/A
ILR implant
INDICATIONS FOR ILR implant
- Patients with clinical syndromes or situations who are at increased risk of cardiac arrhythmias.
- Patients who experience transient symptoms such as dizziness, palpitation, syncope or chest pain that may suggest a cardiac arrhythmia.
BHRS indication for ILR
“The ESC guidelines give a class I recommendation for ILR implant where there is recurrent syncope of uncertain origin, absence of high‐risk criteria and a high likelihood of recurrence within the battery life; Also in those with high‐risk criteria in whom a comprehensive evaluation has not demonstrated a cause of syncope and who do not have conventional indications for primary prevention ICD or pacemaker. A IIa recommendation is given for ILR implantation for patients with suspected or certain reflex syncope presenting with frequent or severe syncopal episodes”
ILR benefits
- more diagnostic yield than ECG, holder monitoring and external loop recorder
- patient initiated symptom episode
Wide complex tachycardia - differential diagnosis
VT
Abberency
Pre-excitation
paced-rhythm
Acute VT management
- assess the patient immediately
pulseless - CPR as per ALS
Pulse - Sync DC cardio version, oral BB, if recurrent consider IV amiodarone - treat reversible causes:
check K+, MG++
Look ischaemia
QT prolonging drugs
Bradycardia - CCU
- Interrogate ICD if present
Further investigations:
Echo - EF? DCM? -> ICD
Tilt testing pros/cons
Normally around 25% of circulating blood volume is in the thorax.
On standing, gravity produces a downward displacement of approx 500ml to abdomen and lower extremities.
Quick compensatory increase in heart rate and peripheral vascular resistance
contraindications
Relative
Carotid Bruit
Prior VT/VF
Absolute
MI, Stroke, other embolic event in last 3 months
HOCM, Severe Aortic / Mitral Stenosis
Severe proximal coronary artery disease
Significant symptomatic carotid artery disease
Positive CSM
Tilt Testing - protocol
Rest in supine position for at least 5 minutes (set up)
Tilt at angle between 60 to 70 degrees
Passive phase of minimum 20 mins and maximum 45 mins.
Use of either I.V. isoprenaline / isoproterenol or Sublingual GTN after negative passive phase. Drug challenge phase 15 to 20 min.
GTN – fixed dose of 400mcg sublingually, administered in the upright position
results:
Relationship between the onset of hypotension and bradycardia. BP drop occurs just prior to HR drop.
Afferent signals from the peripheral vagus elicit an efferent, abrupt and rapidly reversible parasympathetic response causing transient relative sinus bradycardia.
There is also a sudden disappearance of muscle sympathetic nerve activity at a time of diminishing cardiac output causing vasodilation and hypotension.
The 2 processes, parasympathetic activation and sympathetic inhibition, are linked but not necessarily concomitant.
cardiology investigations
ECG
Echo
Ambulatory monitoring
ICM
ETT
Tilt
