4 1D Cvs Syncope Em

Front 1

Causes of syncope can be divided into three large groups. Focal hypoperfusion of the brain, systemic hypoperfusion (causing CNS dysfunction) and 'non-perfusion related' CNS dysfunction. Give some examples of each

Back 1

1. Focal hypoperfusion - cerebrovascular disease (e.g. posterior circulation TIA affecting RAS - rare), subclavian steal, SAH, basilar arterty migraine

2. Systemic hypoperfusion
a) outflow obstruction - PE, tamponade, AS, HOCM
b) reduced cardiac output - tachy and brady arrythmias, long QT, pacemaker/ICD malfunction, aortic dissection, MI, cardiomyopathy
c) Vasomotor/neurally mediated - vasovagal (neurocardiogenic), carotid sinus sensitivity, miscellaneous reflex e.g. cough/sneeze/GI/micturition
d) Other causes hypoperfusion - ORTHOSTATIC HYPOTENSION (including via volume depletion - e.g. ectopic pregnancy), anaemia, drug induced

3. CNS dysfunction 'non perfusion related'
Hypoglycaemia, hypoxaemia, psychogenic, toxic (drugs, CO), seizures (not considered true syncope by many texts) R194

Front 2

What is the commonest cause, and what are the life threatening causes?

Back 2

Commonest - neurocardiogenic/vasovagal

Life threatening
1) Commonest - MI and arrythmia
2) Less common - CVA (SAH, post circ TIA), toxic-metabolic, structural cardiac lesions eg. AS
3) Rare but catastrophic - Aortic dissection, SAH, massive PE, haemorrhage/hypovolaemia e.g. ectopic pregnancy

Front 3

The most important part of the assessment is the history and examination. What features should be sought on hx and what special features should not be forgotten on exam?

Back 3

Hx - setting (e.g. postprandial, exercise - during UL exercise suggests subclavian steal syndrome, exertional suggests AS, HOCM), position (lying/sitting/standing), prodrome, rate of onset, duration, events during (tonic clonic vs myoclonic jerks, tongue biting and incontinence), rate and completeness of recovery, events after e.g. postictal period

Exam - don't forget PR and postural BP (BP after 5minutes supine, then after 1 and 3 minutes standing, decrease of >20mmHg in SBP or SBP <90mmHg is abnormal but nonspecific)

R194

Front 4

Who needs monitoring, IV access etc?
Who needs admission e.g who is at high risk?

Back 4

Monitor those with repeated episodes, abnormal vitals or significant associated Sx

Admit those who have
1) CP with event, significant signs of CCF and valvular disease
2) Abnormal ECG esp vent dysrhythmia, ischaemia, prolonged QT, new BBB
3) Consider admitting >60year, preexisting CVD and congential heart disease, FHx SCD, exertional syncope (risk AS and HOCM)

R196

Front 5

What are the San Francisco syncope rules, what are the designed to predict and what are their limitations?

Back 5

Serious ST and LT outcomes (a pt with any one of the features has a 12% risk of serious outcomes in 7 days)

1. SBP <90 at triage
2. SOB
3. Hx CCF
4. new ECG changes
5. HCt <30%
6. not in SR

Highly sensitive 95% but poorer specificity 60% and applying rigidly increases admissions by 9%

D94

Front 6

Which classes of medications can be responsible for syncope?

Back 6

CVS - anything that can cause hypotension or logn QT, antiarrythmics
Psychoactive - all except SSRI, SNRI, antipsychotics
Other mechanisms - drugs of abuse (ETOH, cannabiscocaine, heroin), insulin/OHG, dig, NSAIDs?!, bromocriptine

R195

Front 7

Which two Ix are 'mandatory'?

Which other Ix could be considered as an IP? As an OP?

Back 7

ECG and BSL

IP - FBE, UEC, bHCG, CTB, Echo, VQ/CTPA, 'carotid sinus massage' (part of examination, in a monitored resus area, +ve if >50mmHg reduction SBP or vent pause >3seconds)

OP - holter, Echo, tilt table, psychiatric evaluation

Front 8

How should these be managed - neurally mediated (vasovagal), orthostatic, suspected cardiac

Back 8

Vasovagal - ensure ECG and BSL NAD, explain, reassure

Orthostatic - give IVF if needed, exclude bleeding, establish oral intake, evaluate medications for cause

Suspected cardiac - MI workup, admit to monitored bed, consider echo

C398