syncope Flashcards
what is syncope
cerebral hypoperfusion–> loss of consciousness and postural tone, fainting
Abrupt, complete, transient
what to ask with syncope
first time, past med hx
Vitals- bp, hr, temp, RR, puls ox
HEENT- trauma, contusions
Neck- bruits jugular v distension, thyromegaly
Lungs- clear to auscultation and percussion
CV- murmurs, arrythmias, orthostatic
Abdomen-
Neuro- CN2-12 strength, sensationand coordination
Skin- warm, thyroid
Post ictal- after seizure- youre confused
Transient loss of consciousness - should look into history and blood glucose levels what else can cause syncope
Prolonged recovery (post ictal)- consider seizure (check neuroimaging, EEG)
Trauma–> head injury
Hypoglycemia
Intoxication
Neurologic symptoms/signs–> cerebrovascular disease (posterior circulation)
Syncope–> cardiac syncope, orthostatic hypotension, reflex syncope
EKG
Rate- find a qrs and count the big boxes (300/#)
rhythm- is there a QRS every beat
Sinus- A p wave before every QRS and a QRS after every P wave
Axis- if lead 1 is up and AVF then youre good, if avf is down, lead 2 is up
Intervals- between P and QRS should be under 1 big box (3-5 little boxes), short= wpw syndrome
QT intervals- T wave should end 1/2 between 2 QRS
Vasovagal syncope
when the heart randomly stops and then starts up again tachycardic
Neurocardiogenic dysfunction
inappropriate neurogenic slowing of the heart- blood vessels vasodilate, decreased perfusion
autonomic regulation of the CV system
moment to moment pressure
Senosory receptors in periphery
Baroreceptors
Mechanoreceptors- in heart
Chemoreceptors- pH and O2 changes
Heart is innervated by vagus (parasympathetic)- and it innervates the SA and AV node, SLOW the HR and deccrease contraction
Sympathetic- constriction, inntervates the SA and AV and increases contractility and HR
Medullary control of the Autonomic outflow
Baroreceptors in the carotid sinus, aoritc arch, heart ventriclessench pressure changes–> medullary (via 9 and 10)
increase in stretch–> increase in firing rate of inhibitory medullary control, decreases tone in CV system
Central control
Inputs through central pathways can either excite or inhibit medullary CV centers
Emotion, pain, motor activity, can influence CV status
Pathophysiology of vasovagal syncope
Prolonged standing, venous pooling–> decreased venous return
Pain or anxiety–> sympathetic surge–> vigorous cardiac contraction
–> markedly reduced end systolic volume–> Vagal reflex–> Bradycardia and vasodilation–> hypotension and syncope
Bezold jarisch reflex
venous pooling–> sympathetic activation–> vigorous contraction of a poorly filled ventricle–> brain–> hypotension
–> brainstem–> increased vagal efferents–> bradycardia
Vaasavagal syncope diagnosis
ECG, echo, tilt table test, holter monitor, implantable loop recorder
vasovagal syncope treatment
Non pharm- patient education (avoid triggers, recognize symptoms, lie down), Hydration, salt
Pharmacological- a1 agonists- midodrine, Not as effective (B blockers, fludrocortisone)
Pacemaker- if severe, recurrent and refractory to other treatments >490 with asystole on implantable loop recorder
20 yr old male with syncope at exersice
HCM- hypertrohoic cardiomyopathy
Most common cause of CV death in young athletes, syncope develops in 15-25% of pt
Outflow tract obstruction due to Left ventricular Hypertrophy wihtout loading conditions (HTN AS)
Complications: heart failure, angina, sudden cardiac death, atrial fibrillation
DIAGNOSIS OF HOCM
hypertrophic obstructive cardiomyopathy
outflo tract obstruction
Classic murmur- Harsh systolic murmur at apex and lower LSB, increases from squating to stanging, decreases with passive leg elevation
EKG- LV wall thick, septal hypertrophy
Pt has syncope with a family hisoty of SCD
burgada syndrome,
Intermittent ventricular tachycarddia, mutation in Na cnhannel gene, structurally normal heart
ST Elevation, with down slope in v1-v3
Treatment- AICD
