Week 10

Question 1

Characteristics of response to emotional stress

Answer 1

Evoked by emotion, mental stress, visual, sound, pain, novel environmental stimuli
Magnitude of response is graded with stimulus strength, but includes:
-increased respiration
-decreased parasympathetic/increased sympathetic activity to heart-> increase cardiac output
-increase symp activity vasoconstriction in kidney, gastrointestinal tract, skin
-vasodilation in skeletal muscle due to:
— decrease symp noradrenergic activity to muscle
—increase circulating adrenaline- B-adrenoceptors
Results in: increase ABP with increase in blood flow to skeletal muscle and pupillary dilation, sweating, piloerection, urination, defaecation
Common to all mammalian species
Appropriate stimulus varies between individuals
Response can show habituation or sensitisation
Response can be conditioned
During strong alerting/defence response, baroreceptor reflex is suppressed.
Therefore ABP can reach very high values

Question 2

Amygdala and brain stem defence areas

Answer 2

By electrical stimulation
Areas from which whole pattern of A/DR can be evoked: periaquaductal grey matter, dorsal PAG, dorsal medulla, ventral hypothalamus, ventral medulla
Areas that can modulate pattern A/DR: prefrontal cortex, orbits frontal cortex
Amygdala defence area -> ventral hypothalamic defences area-> stria terminalis
Remain aroused for a longer time, cardiovascular symptoms

Question 3

Integrating areas for alerting/defence response

Answer 3

Specific cortical regions
— modulation +/-
Afferents:
- amygdala
-ventral hypothalamus
-midbrain preaqueductal grey ———— inhibition of baroreflex at NTS
-dorsal medulla

Ventral medulla
(RVLM, respiratory neurones, N.ambiguus)
Efferent outflow:
-sympathetic, respiration, parasympathetic vagal to heart

Question 4

Clinical significance of alerting/defence response

Answer 4

Increase state of arousal or apprehension
Increase cardiac output redistribution to muscle
-split second advantage if fight/defend/run away or competitive exercise
No obvious values in everyday life
Increase ABP- acute risk for those with:
-coronary artery disease- myocardial infarction
-aneurism, fragile cerebral blood vessels
Chonrically- repeated stress in individuals who do not habituate leads to essential hypertension
Large population studies: those who show largest pressor responses to environmental/mental stressors have 3-4 fold greater risk of hypertension over 10 year period
Parental hypertension also increases risk of hypertension by 3-4 fold

Question 5

A mechanism for essential hypertension

Answer 5

Environmental stressors via defence areas
Genetic and environmental influences modulate
- increase ABP
— hypertrophy of vascular smooth muscle in arterioles
—muscle grows inwards reducing internal lumen
-increases TPR
— increase ABP

Exercise, relaxation therapy, music, yoga etc may break the loop

Question 6

Vasovagal syncope emotional fainting

Answer 6

Profound bradycardia and vasodilation
Profound fall in ABP and faint
Due to:
-sudden increase in vagal activity to heart
-decrease in sympathetic activity to blood vessels
May be preceded by strong tachycardia and increased contractility (baroreflex, exercise induced)
Typically preceded by alerting/defence response
-reflex response and cortical influences (may exaggerate reflex response)
—increased HR and contractility by increased sympathetic activity

Question 7

Vasovagal syncope induced by head-up tilt and lower body negative pressure (LBNP)

Answer 7

LBNP= vacuum chamber, more venous pooling
Baroreceptors reflex
Vasoconstriction in peripheral circulation
Deepen negative pressure:
-Vasovagal syncope: bradycardia and vasodilation pulling BP down and patient faints

Question 8

Vasovagal reflex response

Answer 8

Strong defence response leads to increase HR and contractility
Leads to ventricles contracting fast and very strongly with reduced filling (decrease EDV)- particularly if standing upright (venous pooling)
Torsion of ventricle stimulates high threshold mechanoreceptors in wall in ventricle
Contractility is high volume is low
Afferent activity via vagus to medulla NTS then to lateral hypothalamus (stimulation in area lateral to defence areas evokes Vasovagal syncope)
Reflex increase vagal activity to heart decreasing HR
-decrease sympathetic activity to all blood vessels-> vasodilation
-decrease ABP- patient faints when brain blood flow falls
Cortical influences (modulating lateral thalamic area):
-strong emotion: fear, loss- facilitates ventricular reflex response. Generated by torsion of ventricles

Question 9

Physiological and clinical significance of Vasovagal syncope

Answer 9

Occurs in extreme emotional stress
-may even cause cardiac arrest and death in profound fear and shock. Kidnap, hostage victims
However:
-torsion of ventricle, stimulation of ventricular mechanoreceptors and therefore Vasovagal syncope may also occur:
-following head up tilt with LBNP, sudden large haemorrhage
—increase sympathetic activity to ventricles (baroreflex), but low EDV (low blood volume)
-following strenuous exercise if remain standing upright
—increase sympathetic activity to ventricles (exercise reflex) but low EDV (muscle vasodilation and venous pooling)

Question 10

Treatment

Answer 10

Avoid fainting triggers
Avoid hot crowded places/alcohol
Foot exercise, compression stockings, tensing leg muscles
Adequate salt in diet
Fludrocortisone acetate- expand blood volume
Pacemaker- triggers when HR falls below pre determined level