Syncope Flashcards
DEFINING SYNCOPE
i) what is it? name three things it is characterised by?
ii) name the four main things that can lead to transient loss of conciousness
iii) what is reflex syncope aka? name four potential triggers? which syndrome falls into this group?
iv) name two other groups of syncope
i) transient loss of conciousness due to cerebral hypoperfusion
- charac by rapid onset, short duration, spontaneous complete recovery
ii) TLOC > syncope (reflex, orthostatic, cardiac), epileptic seizure, psychogenic (dx of exclusion after organic causes have been ruled out), rare causes (subclav steal synd, sub arach haemm)
iii) reflex syncope = neurocardiogenic syncope = simple faint
- vasovagal > triggered by standing/emotional
- situational > cough, micrutition
- carotid sinus syndrome
iv) orthostatic hypotension and cardiac syncope
MECHANISMS OF SYNCOPE
i) what underlies syncope? name the two main things that influence this?
ii) name three things that can happen in orthostatic HTN
iii) name two things that can ppt cardiac syncope?
i) low BP/cerebral hypoperfusion
ii) volume depletion, venous pooling > inadequate venous return
iii) arrhythmia, struc cardiac abnorms
RED FLAGS
i) name three symptoms related to a syncopal event that are a red flag syncope during which two times is a red flag?
ii) name four red flags on ECG
iii) what length of prodrome is more concerning?
iv) name three things in the PHM that raise a red flag
v) name three exam findings that are a red flag
i) new onset chest pain, breathlessness, abdo pain, headache
- syncope when supine or during exercise
ii) mobitz type II/ 3rd degree heart block, ischaemic change, VT, channelopathies eg long QT, type 1/2/3brugada
iii) very short prodrome (<10s)
iv) FH of sudden cardiac deatg, structural heart disease, coronary artery disease, low EF (heart failure) > more at risk of malignant arrhythmias
v) SBP <90mmHg, suggestion of a GI bleed (haematuria, melanea) and new systolic murmur
INVESTIGATIONS
i) which imaging should be done?
ii) what is a holter monitor?
iii) what is an implantable loop recorder? when may this be useful in syncope?
iv) whic test can identify the cause of syncopal events?
i) echo
ii) portable ECG (ambulatory monitoring) - records continuously over a 24/48/1wk period
iii) ILR - implanted device under the skin that can constantly monitor for 3/4 years (useful for infrequent episodes of syncope)
iv) tilt table test
TILT TABLE TEST
i) how does it work? why is it done?
ii) which two parameters are measured?
iii) what may be seen on the trace in reflex syncope?
iv) what may be seen in orthostatic HTN?
i) done to work out the cause of unexplained syncope
- strap patient to the board and move from supine to standing to mimic standing whilst recording HR and BP
ii) measure HR and BP on moving position
iii) reflex syncope > increased HR and BP at the start (inc symp tone) and low HR and BP at the end (tilt down)
iv) OH - drop in BP on standing and a slight increased HR to compensate
REFLEX SYNCOPE
i) what is it? name three things it can be due to?
ii) what normally happens on standing? (ANS response)
iii) what happens differently in reflex syncope?
iv) what happens when there is an emotional trigger?
v) which region of the brain is triggered? name four things that can precipitate this? how does it affect vagal tone? what then happens to cause syncope
i) abnormal reflex mechanisms > reduced sympathetic tone and increased psym tone
- can be due to orthostatic/emotional vaso vagal syncope, situational syncope (cough, defecation), carotid sinus syncope
iii) on standing 300-800mls blood thorax > lower limbs where it pools
- venous pooling leads to reduced venous return
- normally sympathetic tone increases leading to maint of BP
iii) in reflex syncope > there is vigourous contraction of an underfilled LV > stimulates mechanoreceptor C fibres
- this overrides the baroreceptor responses > withdraw of symp tone and increased psym tone > dramatic drop in HR and BP
iv) emotional trigger eg pain/sight of blood > higher cortical centres increase psym activity and reduce sym activity
v) stim of medullary vasopressor region
- stim by cardiac C fibres (hypovol, dehy, valsalva), cardiopulm receptors (head turn, carotid massage), cerebral cortex (fright), cranial nerves (GP nerve neuralgia), GI/GU symptoms (defacation)
- leads to increased vagal tone (bradycardia) and decreased symp tone (vdil)
- reduced venous return and decreased CO > cerebral hypoperfusion > syncope
REFLEX SYNCOPE - INC PARASYMP TONE
i) give four symptoms of increase psym tone?
ii) what does this cause to happen in the heart?
iii) how does it affect vascular resistance? why?
iv) what does it ultimately lead to? (3)
v) how can a patient terminate the event
i) nausea, diaphoresis (sweating), light headed, warm and clammy, ringing in ears = prodrome
ii) causes cardioinhibitory response > inappropriate bradycardia
iii) withdraw of symp tone = vasodepressor response = reduced SVR
iv) ultimately leads to low BP and reduced ceb perfusion > TLOC
v) can be terminated by lying down with legs up
TREATMENT FOR REFLEX SYNCOPE
i) name three lifestyle measures that can be done?
ii) what counter pressure manouevre can be done? how does this work?
iii) which therapies should be discontinued?
iv) which mineralocorticoid receptor agonist can be given? how does it work to prevent reflex syncope? what did the POST2 trial show?
v) name an alpha agonist that can be given? how does this work? (2) what have trials shown about this drug?
i) increased fluid and salt intake, avoid triggers, early recognition of prodrome
ii) lock fingers and pull hands apart > transiently increases BP
iii) discontinue anti hypertensives
iv) fludrocortisone > increases salt and fluid reabs in the kidneys to inc BP
- POST2 trial had unimpressive results > marginal nonsignfic reduc in syncope in fludro arm
v) midodrine > causes periph vasoconstriction and helps counteract abnormal vasodilation due to psym activation
- effective in small trials but systematic review = moderate results
CAROTID SINUS SYNDROME
i) what is it defined as? ventricular pause/fall in SBP? following what?
ii) in which group of patients is carotid sinus hypersensitivity a common finding?
iii) name three things that may ppt syncope?
iv) what two things is the response usually due to? when may a pacemaker be considered?
i) ventricular pause >3s, fall in SBP >50mmHg
- leading to syncope
- following carotid sinus massage
ii) hypersens is common in men >40yrs old with no hx of syncope
iii) turning head, shaving, tight collar etc > anything that puts pressure on the carotid sinus
iv) combo of cardio inhibitory and vaso depressor response (one mech may predominate)
- if cardio inhib predominates then may require PM (not a strong reccom and needs MDT discussion)
POSTURAL HYPOTENSION
i) what is it? (3)
ii) how much blood usually shifts to lower limbs on standing? what does this lead to stimulation of? how does this lead to BP being maintained?
iii) what happens in PH?
i) fall in BP on standing
- >20mmHg systolic
>10mmHg diastolic
fall is systolic to <90mmHg
ii) usually 300-800mls of blood shifts from thorax to lower limbs on standing > leads to stim of carotid baroreceptors
- increases symp actvitiy leading to inc SVR and maint of BP
iii) in PH there is reduced venous return leading to reduced CO
- also reduced vascular resistance
CAUSES AND TX OF POSTURAL HYPOTENSION
i) name three drugs that can cause it?
ii) name two things that cause primary autonomic failure / two things that cause secondary autonomic failure and therefore PH
iii) name four ways it can be treated
iv) how may yoga help with recurrent vasovasgal syncope?
i) vasodilators, diuretics, tricyclics, DA agonists
ii) primary autonomic fail > PD, MSA, dementia with lewy bodies
secondary > diabetes, amyloid, spinla cord injury
iii) fluid resus, adequate hydration and salt intake, head up tilt sleeping, review medications, give medication eg fludro and midodrine
iv) yoga (breathing and relaxation) > increase vagal tone and curtail sympathetic overdrive phase and interrupt activation of C fibre mechanoreceptors
