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Year 3 Academic Weeks > A7- Syncope > Flashcards

A7- Syncope Flashcards

1
Q

WHat is syncope?

A

the suddent transient loss of consciousness and postural tone with spontaneous recovery.

Loss of consciousness occurs within 10 secinfd of hypoperfusion of the reticular activating system in the mid brain.

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2
Q

What is presyncope? Symptoms?

What is another name for presyncope?

A

Pre-syncope is the feeling that you are about to faint. Someone with pre-syncope may be lightheaded (dizzy) or nauseated, have a visual “gray out” or trouble hearing, have palpitations, or feel weak or suddenly sweaty. When discussing syncope with your doctor, you should note episodes of pre-syncope as well.

Symptoms include: dizziness, lightheadedness or faintness, weakness, fatigue, and visual and auditory disturbances

Syncopal prodrome

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3
Q

______ causes of syncope have the highest mortality rates

A

Cardiac causes of syncope have the highest mortality rates

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4
Q

How can syncope impact someones life

A

Cause anxiety/Depression

Alter Faily Activities

Restricted Driving

Change Employment

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5
Q

Explain the maintenance postural Normal tension

A

When standing there is a pooling of 500-1000mL of blood in the lower extremities and slanchi circulation.

There is a decrease in venous return to the heart and reduced ventricular filling that result in diminished cardiac output and blood

These haemodynamic changes provoke a compensatory reflex response, initiated by the baroreceptors in the carotid sinus and aortic arch, resulting in increased sympathetic outflow and decreased vagal nerve activity

The reflex increases peripheral resistance, venous return to the heart, and cardiac output and thus limits the fall in blood pressure

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6
Q

Syncope causes can be split into 5 groups.

What are they?

A

Neurally-Mediated

Orthostatic

Cardiac Arrhythmia

Structural Cardio-Pulmonary

Non Cardio-Vascular

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7
Q

Example of Neurally mediated syncope causes?

A

Vasovaal

Carotid Sinus

Situational

  • Cough
  • Post-Micturition
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8
Q

Example of Orthostatic syncope causes?

A

Drug induced

ANS Failure: Primary or Secondary

Brady: Sick Sinus, AV Block

Tachy: VT, SVT

Long QT Syndrome

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9
Q

Example of Structural Cardio-Pulmonary syncope causes?

A

Aortic Stenosis

HOCM

Pulmonary Hypertension

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10
Q

Example of Non-Cardio Vascular syncope causes?

A

Psychogrnic

Metabolic eg hyper-ventilation

Neurological

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11
Q

What are some causes of syncope in a younger patients?

A

Vasovagal

Situational

Psychiatric

Long OQ

Brugada Syndrome

WPW syndrom

RV

Dysplasia

Hypertophic Cardiomyopathy

Catecholamnergic VT

Other genetic syndromes

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12
Q

What are some causes of syncope in a older patients?

A

Cardiac: Mechanical, Arrhythmic

Orthostatic hypotension

Drug induced

Neurally mediated

Mutifactorial

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13
Q

What is Cardiac Syncope?

A

Severe obstruction to cardiac output or rhythmn disturbace can lead to syncope

a) due to strucural abnormalites leading to flow: exertional syncope is a common mindeststion of all types of heart diseae in which cardiac output is fixed an ddoes not rise or may fall with exercise
b) LVOTO: common conditiona AS,HCM

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14
Q

Syncope occurs in what percentage of people with aortic stenosis?

A

<42%

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15
Q

What is the mechanism of syncope for people with aortic stenosis?

A

Due to fixed CO, CO Decreases on exertion due to reflex fall in perioheral vascular resistance

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16
Q

30 % Hypertophic cardiomyopathy patients have syncope

Explain its mechanism

A

Dynamic LVOTO is worsened by an increase in LV contractility (stinulatin the LV mechanoreceptors), decrease in chamber size, or decrease in after-load.. (Hence, a Valsalva maneuver, severe cough or drugs precipitates hypotension and syncope.

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17
Q

How does RVOTO cause syncope?

A

inability to incrase CO in association with a reflec fall of peripheral resistance results in hypotension and syncope

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18
Q

How does CAD cause syncope?

A

sudden pump failure producing hypotension and decreased perfusion of the brain

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19
Q

What is the common arrhythmia that causes syncope?

A

Ventricular tachycardia?

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20
Q

What is the normal response to upright position (standing):

A

The decrease in venous return, stroke volume and arterial pressure lead to increase sympathetic and decrease parasympathetic activity, thereby maintain BP and heart rate

21
Q

Patho of vasovagal syncope

A

In vasovagal syncope: facilitating factors teigger baroreceptors and medullary centes through afferent fibres, activating the parasympathetic tone but inhibiting the sympathetic tone through vagal efferent fibres resulting in hypotesion and bradycardia and there by syncopy.

22
Q

Neurally mediated syncope can be caused following a _______ ___________

what does this mean

A

Cardiac catheterisation

Pain associated with femoral puncture and groin compression after sheath removal may produced vasivagal episode and result in syncope.

23
Q

What is micturational syncope?

What sub category does it fit in?

A

Often seen in younger men after rising from the bed in early morning and men who with sudden LOC during or immediately following voiding .

Situational Syncope

24
Q

Mechanism of situation syncope?

Name some predisposing factors

A

SImilar ot vasogal, the mechanoreceptors in bladder are triggered in the oresence of predisposing factors causing syncope

Predisposing factorsL fatigue, decreased food intake, alcohol ingestion, recent UTI , bladder pathology.

25
Q

Defecation syncope

Mechanism

Predisposing factors

Facilitating factors

A

Mechanism: Triggering of mechanoreceptors in th egut wall in the presence of predisposing and facilitating factors

Predisposing factors: Fatigue, decreased food intak , alcohol consumption, GIT pathology

Facilitating factors: Change in the sleep, valsalva manuever during defecation, orthostatic hypotension

26
Q

Cough syncope can also be known as

A

tussive/ post tussive laryngeal vertigo

27
Q

Who usually experiences cough syncope

A

middle aged men who drink alcohol, smoke and have a chronic lung disease

28
Q

What receptors are triggered in cough syncope?

A

Pulmonary mechanoreceptors

severe coughing increases intrathoracic pressure which deceases venous return and in turn CO

Transmission of high intrathoracic oressur eto the subarachnoid space during coughin may increase the cerebrovascular resistance and reduce the cerebral blood flow.

29
Q

Mechanism of carotid sinus hypersensitivity

A

Triggering of carotid sinu s(located in the ICA just above the bifurcation of CCA) and medullary centres via afferent fibres (glossopharyngeal and vagus nerves) activates parasympathetic and inhibits sympathetic tone via vagal and sympathetic efferent fibres results in profund bradycardia and hypotension

30
Q

Which type of people have Carotid sinus hypersensitivity?

A

asymptomatic elder males

31
Q

Defecation syncope most occurs in

A

elders, sually arising dro m bed at night or during manual disimpaction of the rectum.

32
Q

What are the 3 types of carotid sinus hypersensitivity and explain them?

A
33
Q

What is orthostatic syncope?

A

A decline of >20mmhg in systilic or >10mmhg in diastolic BP upon assuming upright posture is often defined as orthosatic hypotension

It is a disorder in which assumption of upright oosture results hypotension assocuated with light headness blurring of vision and sense of profound weakness

34
Q

What blood supply is affected in neurological syncope?

A

Vertebrobasilar system

Subclavian artery

35
Q

12-18% of patiets with migraine may have syncope and orthostatic hypotension due to hyperresponsiveness of _______ receptors with the inhibition of _______ centre and _______ reaction secondary to pain

A

12-18% of patiets with migraine may have syncope and orthostatic hypotension due to hyperresponsiveness of dopamine receptors with the inhibition of vasomotor centre and vasovagal reaction secondary to pain

36
Q

Migraine related syncope is usually seen in what type of people

A

young women and has a strong menstrual association

37
Q

What to ask for a history of syncope?

A

Mode of onset

Duration of episode

Precipitating factors (triggers)

Associated factors- before (prodromes, aura), during and after (postictal)

Predisposing factors

Family history

38
Q

What do you specifically ask in family history for syncope

A

fhx of epilepsy may be present in seizures

postive family history in HOCM, long QT syndrome

39
Q

What is the difference between Seizure and Syncope

onset

duration

jerks

headache

confusion after

incontinence

eye deviation

tongue biting

prodrome

EEG

A
40
Q

What blood pressure measurements should be obtained during presentation of syncope

A

BP measurement for detection of orthostatic hypotension: supine BP and heart rate measured after patient has been lying down for at least for 5 mins

Standing measurements should be obtained immediately and for at least 2 min and should be continues for 10 min when there is a high suspicion of orthostatic hypotension

41
Q

What are some heart monitoring options

A

12- lead

holter monitor

Event Recorders

42
Q

What is Carotid sinus massage

A

Method is to massage for 5-10 seconds in a supin and upright posture

43
Q

What is head up tilt test HUTT

A
44
Q

Tx for syncope

A

principal goals of treatnent:

  • prevent recurrences
  • reduce risk of mortality
  • prevent injuries associated with recurrences
  • imprive quality life
45
Q

Tx of cardiac arrhythmias as primary cause

  • prevention of symptom recurrence
  • improvement of quailty of work- reduction of mortality risk
A
46
Q

What is the first line therapy for treament of syncope AV block (1 and B)

A

Cardiac pacing

47
Q

Tx for orthostatic hypoT

A

Class 1 recommendation

Syncope due to orthostatic hypotension should be treated in all patients. In many instances treatment entails only modification of drug treatment for concomitant conditons

48
Q

Management of Neurogenic Orthoststic HypoT

A
49
Q

Management of Neurogenic Orthostatic Hypotension

drugs

A

Midodrine: α‐1‐adrenoceptor agonist that constricts arteriolar and venous vasculature producing an increase in BP. SH is common with midodrine. Dose: start at 2.5mg bd/tds; max: 10mg tds

• Droxidopa: licenced in USA (L‐threo‐3,4‐dihydroxyphenyl‐serine) or L‐DOPS is a synthetic amino acid, which, after oral administration, is converted to the naturally occurring sympathetic neurotransmitter norepinephrine. Patients with NOH retain the ability to convert droxidopa into norepinephrine and thereby increase their BP.

• Fludrocortisone: mimics the action of aldosterone and raises BP

Year 3 Academic Weeks (40 decks)

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