Cardiac circulation control Flashcards

1
Q

What is a cardiac reflex

A

◦ “Reflex loops between the heart and central nervous system” which regulate heart rate and peripheral vascular resistance to maintain physiologic homeostasis

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2
Q

List the cardiac reflexes

A

4B’s 2C’s and a ROD

Bainbridge
Baroreceptor
Bezold Jarish
Barcroft Edholm

Chemoreceptor
Cushing

Respiratory sinus arrhythmia
Oculocardiac
Diving

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3
Q

What is the most important cardiac reflex

A

Baroreceptor

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4
Q

What are the 5 domains you need to consider for every reflex and every endocrine system

A

Sensor
Afferent
Processor
Efferent
Effector

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5
Q

Barorecepotr reflex

A

◦ Sensors: mechanoreceptors detect pressure (carotid sinus and aortic arch)
◦ Afferent: vagus and glossopharyngeal nerves
◦ Processor: nucleus of the solitary tract and nucleus ambiguus (vasomotor centre)in medulla oblongata
◦ Efferent: vagus nerve and sympathetic chain
◦ Effect: increased HR and BP (via SVR + increased stroke volume/cardiac output) in response to a fall in BP

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6
Q

Bainbridge reflex

A

◦ Afferent: vagus (atrial stretch) - increase in central venous pressure triggers low pressure mechanoreceptors in great veins and RA
◦ Processor: nucleus of the solitary tract and the caudal ventral medulla
◦ Efferent: vagus nerve and sympathetic chain
◦ Effect: increased RA pressure produces an increased heart rate;

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7
Q

Chemoreceptor reflex

A

◦ Afferent: carotid / aortic chemoreceptors (low PaO2 and/or high PaCO2) - in the context o response to MAP this will only occur under extreme hypotension
◦ Processor: nucleus of the solitary tract and nucleus ambiguus
◦ Efferent: vagus nerve and sympathetic chain
◦ Effect: bradycardia and hypertension in response to hypoxia
‣ (also secondary tachycardia from Bainbridge and Hering-Breuer reflexes)

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8
Q

Cushings reflex

A

◦ Afferent: mechanosensors in the rostral medulla?
◦ Processor: rostral ventrolateral medulla
◦ Efferent: sympathetic fibres to the heart and peripheral smooth muscle
◦ Effect: hypertension and baroreflex-mediated bradycardia

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9
Q

Bezold Jarish reflex

A

◦ Afferent: vagus (mechanical/chemical sttimuli to the cardiac chambers - ventricular) C fibres
◦ Processor: nucleus of the solitary tract
◦ Efferent: vagus nerve and sympathetic chain
◦ Effect: hypotension, coronary artery dilation and bradycardia

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10
Q

Oculocardiac reflex

A

◦ ​​​​​​​Afferent: trigeminal nerve (pressure to the globe of the eye)
◦ Processor: sensory nucleus of CN V; nucleus of the solitary tract
◦ Efferent: vagus nerve and sympathetic chain
◦ Effect: vagal bradycardia, systemic vasoconstriction, cerebral vasodilation

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11
Q

Diving reflex

A

◦ ​​​​​​​Afferent: trigeminal nerve (cold temperature; pressure of immersion)
‣ Processor: sensory nucleus of CN V; nucleus of the solitary tract
◦ Efferent: vagus nerve and sympathetic chain
◦ Effect: vagal bradycardia, systemic vasoconstriction, cerebral vasodilation

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12
Q

Barcroft Edholm reflex

A

◦ ​​​​​​​Afferent: emotional distress, hypovolaemia
◦ Processor: unknown
◦ Efferent: vagus nerve and sympathetic chain
◦ Effect: bradycardia, systemic vasodilation, hypotension

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13
Q

Respiratory sinus arrhtyhmia

A

◦ Afferent: central respiratory pacemaker
◦ Processor: nucleus ambiguus
◦ Efferent: vagus nerve, via the cardiac ganglion
◦ Effect: cyclical increase of heart rate during inspiration

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14
Q

What type of receptor is a baroreceptor? How are they activated?

A
  • Baroreceptors are mechanoreceptors which respond to stretch stimuli.
  • This strecth deforms mechanically sensitive sodium channels (DEG/ENaC, degenerin/epithelial sodium channels)
  • With sufficient stimulus, sodium current increases to the point where the membrane potential reaches the threshold of local voltage-gated sodium channels, and generates a propagating action potential
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15
Q

Where are baroreceptors located

A
  • Arterial baroreceptors (“high pressure baroreceptors”) are located at the junction of the intima and media of the aortic arch and carotid sinuses
    ◦ stretch sensitive mechanoreceptors
    ◦ Carotid sinus - small neurovascular structure in the adventitia in the dilated portion of the common carotid artery (carotid bulb) at its bifurcation. Not to be confused with the carotid body which is a PaO2/PaCO2 sesning chemoreceptor at the same location at the bifurcation of the vessels
    ◦ sinus senses stretch, and body senses breathing
    ◦ Aortic arch - medio-adventitial junction mainly confined to a saddle shaped area between the brchiocephalic trunk and the origin of the left subclavian
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16
Q

What layer of the vessel are baroreceptors in

A
  • Arterial baroreceptors (“high pressure baroreceptors”) are located at the junction of the intima and media of the aortic arch and carotid sinuses
    ◦ stretch sensitive mechanoreceptors
    ◦ Carotid sinus - small neurovascular structure in the adventitia in the dilated portion of the common carotid artery (carotid bulb) at its bifurcation. Not to be confused with the carotid body which is a PaO2/PaCO2 sesning chemoreceptor at the same location at the bifurcation of the vessels
    ◦ sinus senses stretch, and body senses breathing
    ◦ Aortic arch - medio-adventitial junction mainly confined to a saddle shaped area between the brchiocephalic trunk and the origin of the left subclavian
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17
Q

Where is the carotid baroreceptor

A
  • Arterial baroreceptors (“high pressure baroreceptors”) are located at the junction of the intima and media of the aortic arch and carotid sinuses
    ◦ stretch sensitive mechanoreceptors
    ◦ Carotid sinus - small neurovascular structure in the adventitia in the dilated portion of the common carotid artery (carotid bulb) at its bifurcation. Not to be confused with the carotid body which is a PaO2/PaCO2 sesning chemoreceptor at the same location at the bifurcation of the vessels
    ◦ sinus senses stretch, and body senses breathing
    ◦ Aortic arch - medio-adventitial junction mainly confined to a saddle shaped area between the brchiocephalic trunk and the origin of the left subclavian
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18
Q

Where is aortic baroreceptor

A
  • Arterial baroreceptors (“high pressure baroreceptors”) are located at the junction of the intima and media of the aortic arch and carotid sinuses
    ◦ stretch sensitive mechanoreceptors
    ◦ Carotid sinus - small neurovascular structure in the adventitia in the dilated portion of the common carotid artery (carotid bulb) at its bifurcation. Not to be confused with the carotid body which is a PaO2/PaCO2 sesning chemoreceptor at the same location at the bifurcation of the vessels
    ◦ sinus senses stretch, and body senses breathing
    ◦ Aortic arch - medio-adventitial junction mainly confined to a saddle shaped area between the brchiocephalic trunk and the origin of the left subclavian
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19
Q

How does the baroreceptor receptor respond to changes in BP –> how does it convey the change to the controller

A
  • Increased blood pressure (increased stretch, increased receptor firing rate)
  • Decreased blood pressure (decreased receptor firing rate)
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20
Q

How does the carotid baroreceptor get to the central controller

A
  • From the carotid sinus: carotid sinus nerve, a branch of the glossopharyngeal nerve - courses anteromedially to the internal carotid artery and joins the body of the glosspharngeal nerve at the base of the skull where its cell bodies lie in the petrosal ganglion
    ◦ Carotid sinus receptors are innervated by the sinus nerve of Hering, which is a branch of the glossopharyngeal nerve
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21
Q

How does the aortic baroreceptor get back to the central controller

A
  • From the aortic arch: aortic nerve, a branch of the vagus nerve - cell bodies also in the petrosal ganglion which is in the jugular foramen where the nerves then synapse with NTS
  • Both of these nerves travel through the jugular foramen to enter the medulla
    ◦ Both myelinated (A) and unmyelinated (C) fibres - fast response and baseline slower regulation
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22
Q

What is the processor of the baroreflex?

A

Nucleus of the solitary tract
* Sensory interneurons in the posteiror medulla (caudal ventrolateral medulla)
* Roles
◦ ANS
◦ Taste information - mediating cough and gag
◦ Middle ear - tympanic branch of CN9

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23
Q

What does the NTS do?

A

Nucleus of the solitary tract
* Sensory interneurons in the posteiror medulla (caudal ventrolateral medulla)
* Roles
◦ ANS
◦ Taste information - mediating cough and gag
◦ Middle ear - tympanic branch of CN9

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24
Q

What connections does the NTS have?

A

◦ Excitatory glutamate-mediated neurotransmission to the nucleus ambiguus translates the afferent signal into increased vagal activity
◦ GABA-ergic inhibitory neurons of the caudal ventral medulla translate the afferent signal into the inhibition of the rostral ventrolateral medulla (vasomotor centre - constant tonic output), which coordinates sympathetic tone
◦ Effrent fibres to the hypothalamus help coordinate the humoural response to changes in blood pressure.

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25
Q

Where is the PSNS 1st order neurons coming from?

A

◦ Excitatory glutamate-mediated neurotransmission to the nucleus ambiguus translates the afferent signal into increased vagal activity
◦ GABA-ergic inhibitory neurons of the caudal ventral medulla translate the afferent signal into the inhibition of the rostral ventrolateral medulla (vasomotor centre - constant tonic output), which coordinates sympathetic tone
◦ Effrent fibres to the hypothalamus help coordinate the humoural response to changes in blood pressure.

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26
Q

Where is the SNS first order neurons coming from?

A

◦ Excitatory glutamate-mediated neurotransmission to the nucleus ambiguus translates the afferent signal into increased vagal activity
◦ GABA-ergic inhibitory neurons of the caudal ventral medulla translate the afferent signal into the inhibition of the rostral ventrolateral medulla (vasomotor centre - constant tonic output), which coordinates sympathetic tone
◦ Effrent fibres to the hypothalamus help coordinate the humoural response to changes in blood pressure.

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27
Q

What are the efferent nerves to the heart? What supplies the SA node? What supplies the AV node

A
  • Sympathetic fibres to the heart and peripheral resistance vessels
  • Vagal efferents to the cardiac ganglion (heart rate)
    Effector: Myocardium, SA and AV nodes, vascular smooth muscle
  • The right vagus does the SA node and the left vagus does the AV node, with enough overlap that the loss of a vagus does not produce total parasympathetic denervation. PSNS more important in HR control
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28
Q

Describe how circulating volume changes SV, CO and HR using a graph

A

In response to arterial hypotension:
◦ Decreased receptor discharge rate
◦ Thus, decreased vagal and disinhibited sympathetic efferents
◦ Thus, systemic vasoconstriction and tachycardia
* In response to arterial hypertension:
◦ Increased receptor discharge rate
◦ Thus, increased vagal and inhibited sympathetic efferents
◦ Thus, systemic vasodilation and bradycardia

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29
Q

How long does a baroreceptor response take?

A

0.5 - 1 seconds

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30
Q

What is the first and fastest response of the baroreceptor reflex

A

Increased or decreased HR due to PSNS or vagal supply - rapid effect of vagal on HR is through inward rectifying potassium channels

cAMP system is slower

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31
Q

When is the baroreceptor response active?

A

Constantly, constant tonic activty

Immediate and proportionate response to changes

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32
Q

What is the minimum value for change for baroreceptor firing change

A

Depends on the baseline state - more sensitive at the higher and lower range of pressures and depends on abruptness of change

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33
Q

Which baroreceptor is more sensitive to hypotension?

A

Carotid

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34
Q

Which baroreceptor is more sensitive to hypertension

A

Aortic

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35
Q

How is firing of baroreceptors related to change in pressure?

A

Generally proportional within the normal ranges however has hysteresis

  • Assymmetry: the firing rate has a hysteresis, i.e. it increases exponentially with increasing carotid sinus pressure, but also plateaus at very high pressures. the steepest part of the response seems to be around the normal systolic pressure range, i.e. 100-140 mmHg.
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36
Q

Describe how mechanosensors sense stretch

A
  • Stretch activates sodium current which then reaches membrane potential threshold for voltage gated channels –> action potential
    ◦ The more stretch the more frequently the receptors fire
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37
Q

What is a stronger stimulus - Bainbridge or baroreflex

A

Baroreflex

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38
Q

Bainbridge reflex

A
  • Stimulus - pressure/stretch (increased CVP) - sensitive to a volume change of 5-10% in either direction
  • Sensors - stretch sensitive low pressure mechanoreceptors in atria, great veins and pulmonary arteries (type B receptors)
    ◦ Type A receptors - activated by changes in atrial wall tension during systole
    ◦ Type B - diastolic low pressure receptors
  • Afferent: vagus triggers low pressure mechanoreceptors in great veins and RA
  • Processor: nucleus of the solitary tract and the caudal ventral medulla
  • Efferent: vagus nerve (cardiac ganglion) and sympathetic chain
  • Effect: increased RA pressure produces an increased heart rate;
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39
Q

What happens with increased RA pressure as an isolated phenomena

A

INcreased Bainbridge reflex firing –> tachycardia

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40
Q

What are the two mechanoreceptor subtypes in the Bainbridge reflex

A
  • Stimulus - pressure/stretch (increased CVP) - sensitive to a volume change of 5-10% in either direction
  • Sensors - stretch sensitive low pressure mechanoreceptors in atria, great veins and pulmonary arteries (type B receptors)
    ◦ Type A receptors - activated by changes in atrial wall tension during systole
    ◦ Type B - diastolic low pressure receptors
  • Afferent: vagus triggers low pressure mechanoreceptors in great veins and RA
  • Processor: nucleus of the solitary tract and the caudal ventral medulla
  • Efferent: vagus nerve (cardiac ganglion) and sympathetic chain
  • Effect: increased RA pressure produces an increased heart rate;
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41
Q

How is the chemoreceptor involved in BP control?

A
  • Regional hypoxia is one of the metabolic stimuli for local vasodilation - systemic hypoxia causes systemic peripheral vasoconstriction
  • Afferent: carotid body glomus (Glossopharyngeal) / aortic body glomus (aortic tract of vagus) chemoreceptors (low PaO2 and/or high PaCO2) - in the context o response to MAP this will only occur under extreme hypotension
  • Processor: nucleus of the solitary tract and nucleus ambiguus
  • Efferent: vagus nerve and sympathetic chain
    ◦ To the SA node, AV node and vascular smooth muscle
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42
Q

What is the effector response to chemoreceptor triggering cardiovascularly

A
  • Effect:
    ◦ Primary effects
    ‣ Vagal - bradycardia
    ‣ Symapthetic effects - hypertension (tachycardia often absent)
    ◦ Secondary effects
    ‣ Increased preload due to increased ventilation –> Bainbridge reflex increasing HR
    ‣ Activation of pulmonary stretch receptors and thus activation of the Hering Breuer reflex increasing HR
    ‣ Due to significant hypertension tachycardia is often not marked due Baroreceptors
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43
Q

Where is the receptor for the cushings reflex

A

mechanosensors in the rostral medulla?/cerebral meduallary vasomotor centre ischameia

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44
Q

Cushings relfex

A
  • Stimulus - ICP or cerebral ischaemia
  • Sensors - mechanosensors in the rostral medulla?/cerebral meduallary vasomotor centre ischameia
  • Afferent nerves - fibres from the medullary mechanosensitive areas to sympathetic ganglia, descending inhibitory control from cerebral hemispheres to medullary vasomotor centre
  • Processor: rostral ventrolateral medulla
  • Efferent: sympathetic fibres to the heart and peripheral smooth muscle
  • Effect: hypertension and tachycardia –> baroreflex-mediated bradycardia
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45
Q

Where is the vasomotor centre

A

Rostral ventrolateral medulla

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46
Q

Bezold Jarish reflex is triggered by

A

vagus (mechanical/chemical sttimuli to the cardiac chambers - ventricular) C fibres
◦ Responds to ventricular or atrial stretch; as well as chemical ATP/capsacin/snake venoms
◦ Loss of stretch decreases firing rat eof C fibre mediated vagal afferent limb, and increased stretch stimulates the reflex

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47
Q

What processes the Bezold Jarish reflex? What does it result in?

A
  • Processor: nucleus of the solitary tract
  • Efferent: vagus nerve and sympathetic chain
  • Effect: hypotension, coronary artery dilation and bradycardia
  • Its physiological role is implicated in haemorrhage or profound hypovolaemia where the vasoconstriction is greater than would purely be seen from barorecepetors and is thought to be due to decreased reflex
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48
Q

Oculocardiac reflex triggered by?

A
  • Stimulus - pressure to the globe of the eye or traction on eye muscles
  • Sensor - mechanosensitive stretch receptors in the facial muscles, especially periorbital muscles, and in the globe of the eye
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49
Q

What does oculocardiac reflex result in?

A
  • ​​​​​​​Afferent: trigeminal nerve - long and short ciliary nerves
  • Processor: sensory nucleus of CN V; nucleus of the solitary tract
  • Efferent: vagus nerve and sympathetic chain
  • Effect: vagal bradycardia, systemic vasoconstriction, cerebral vasodilation
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50
Q

Diving reflex triggered by?

A
  • Stimulus: trigeminal nerve sensory distribution
    ◦ Pressure to the globe of the eye, or traction on the eye muscles
    ◦ Pain in the trigeminal nerve distribution
    ◦ Temperature (cold)
    ◦ Chemical stimulus of the anterior ethmoidal nerve (noxious)
  • Sensors: Pain, temperature, chemical and mechanosensitive stretch receptors in the trigeminal nerve distribution
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51
Q

What is the processor fo the diving reflex?

A
  • Processor:
    ◦ Nucleus of the solitary tract: vagal response
    ◦ Rostral medulla: sympathetic response
    ◦ Ventral medulla: apnoea
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52
Q

What is the effect of the diving reflex

A
  • Effects:
    ◦ Vagal: bradycardia
    ◦ Sympathetic: cerebral vasodilation, systemic vasoconstriction
    ◦ Respiratory: apnoea
    ◦ The net effect is to prevent aspiration and to maximise the blood flow to the central nervous system at the expense of the skin, muscle and splanchnic organs.
53
Q

What is the vasovagal reflex called

A

Barcroft Edholm

54
Q

Why is the Barcroft Edholm reflex thought to exist?

A

◦ Clotting hypothesis - protective reflex for slowing of circulation in response to haemorrhage allowing permissive hypotension ti minimise blood loss and maximise clot formation

55
Q

Neurocardiogenic syncope triggers

A

◦ For “true” vasovagal syncope:
‣ Emotional distress
‣ Orthostatic changes (decreased preload with changes in posture)
◦ For “situational” neurocardigenic syncope:
‣ Micturition
‣ Increased intrathoracic pressure:
‣ Defaecation
‣ Cough, sneeze, laughter, playing a brass instrument
‣ Following exercise
‣ “Carotid sinus syndrome”

56
Q

What is the afferent, sensor and processor of the vasovagal response?

A

ensors: Central (descending) as well as peripheral
◦ Mechanoreceptors located in the wall of the left ventricle, the aorta, atria and the pulmonary trunk
◦ Numerous other strecth receptors, eg. splanchnic, bowel,
* Afferent nerves: Unknown! Presumably, both central nervous system and peripheral sensory nerves are involved
* Processor: Unknown! Presumably at some stage the nucleus of the solitary tract and the nucleus ambiguus are involved.

57
Q

What is the efferent response to vasovagal (4)

A
  • Efferent nerves:
    ◦ Vagus nerve, via the cardiac ganglion
    ◦ Sympathetic nervous system
  • Effector: SA node, AV node, peripheral smooth muscle
  • Effects:
    ◦ Vagal: bradycardia
    ◦ Sympathetic: systemic vasodilation (mainly muscles)
    ◦ Vasovagal syncope is thought to have four distint phases:
    ‣ phase 1: early stabilization (by normal baroreceptor reflex)
    ‣ phase 2: circulatory instability (baroreflex vasoconstriction)
    ‣ phase 3: terminal hypotension (bradycardia, cerebral hypoperfusion, systemic vasodilation)
    ‣ phase 4: recovery
58
Q

4 phases of vasovagal syncope

A
  • Efferent nerves:
    ◦ Vagus nerve, via the cardiac ganglion
    ◦ Sympathetic nervous system
  • Effector: SA node, AV node, peripheral smooth muscle
  • Effects:
    ◦ Vagal: bradycardia
    ◦ Sympathetic: systemic vasodilation (mainly muscles)
    ◦ Vasovagal syncope is thought to have four distint phases:
    ‣ phase 1: early stabilization (by normal baroreceptor reflex)
    ‣ phase 2: circulatory instability (baroreflex vasoconstriction)
    ‣ phase 3: terminal hypotension (bradycardia, cerebral hypoperfusion, systemic vasodilation)
    ‣ phase 4: recovery
59
Q

Respiratory sinus arrhythmia is mediated by? Why does it occur?

A

the normal variation in HR which occurs cyclically in response to normal respiration
* It is not mediated by the Bainbridge reflex instead it is through interaction between medullary respiratory and cardiac centres
* Its role is to potentially increase pulmonary circulation efficiency during inspiration by maximising blood flow across the exchange surface

60
Q

Describe the respiratory sinus arrhythmia pathway

A
  • Stimulus: presumably, the Pre-Bötzinger complex (“respiratory pacemaker”)
  • Sensors: none (unless you count respiratory control chemoreceptors)
  • Afferent: central respiratory pacemaker - Pre Botzinger complex - interneurons between it and the nucleus ambiguus
  • Processor: nucleus ambiguus
  • Efferent: vagus nerve, via the cardiac ganglion
  • Effect: cyclical increase of heart rate during inspiration
61
Q

What is the vasomotor centre

A

Medullary centres controling SA node rate and peripehral muscle tone

62
Q

What afferent supply goes to vasomotor centres

A
  • Afferents include:
    ◦ carotid sinus and aortic arch baroreceptors
    ◦ “low pressure” baroreceptors in the atria
    ◦ Cerebral hemispheres, thalami and hypothalamus
63
Q

How are pacemaker cells rapidly slowed by the vagus

A
  • Efferents release acetylcholine at the pacemaker cells, which opens a ligand-gated potassium channel and hyperpolarises the pacemaker cells
  • These effects are more rapid than those of sympathetic regulation
64
Q

What is the main parasympathetic structure in the medulla?

A

◦ Nucleus ambiguues contains preganglionic vagal neurons (PSNS) –> Sends efferent fibres to the cardiac ganglia via the vagus nerve –> Cardiac ganglia are near the SA node, AV node, and in the atria
‣ Release of acetylcholine activates Ik ACh channels (ligand gated pottasium channel - hyperpolarises the membrane through K out of the cell and delays the rate of depolarisation)
◦ Involved in the Baroreflex, Bainbridge reflex, Barccroft-Edholm reflex and vasovagal syncope mechanisms

65
Q

What is the regulator of the nucleus ambiguues and the rostral ventrolateral medullary SNS group?

A

NTS

66
Q

Where does vasomotor SNS output come from?

A
  • Rostral ventrolateral medulla (RVLM)
    ◦ Glutamate-secreting presympathetic neurons which act as the tonic “pacemarker” of sympathetic cardiovascular control
    ‣ Tonic activity here dictates baseline vascular smooth muscle tone
    ‣ RVLM sends descending projections to sympathetic preganglionic neurosn in the thoracic intermediolateral spinal cord
67
Q

How does 1000ml loss of blood affect the cardiovascular system?

A

20% circulating volume
Acute –> baroreflex + low pressure volume receptors +/- chemo receptors –> central controller
- Autonomic
1. Decreased vagal
2. Increased sympathetic
Net effect
1. SBP and DBP drop is reduced
2. Tachycardia
3. Reduction in pulse pressure
4. Cardiac output returns to close to normal

  • Neurohormonal
    1. Renin
    2. Vasopressin
    3. Catecholamines
    4. ANP

Net - reduced urine output and increased Na and water retention

Effect of rate of blood loss
Medium to long term response

68
Q

How does blood loss trigger a response

A
  • Arterial hypotension causes baroreflex activation + low pressure volume receptors of the right atrium and great veins + if severe (with reduced cardiac output/fall in pH) may also induce chemoreceptor activation peripherally accentuating the response
69
Q

How does sympathetic system respond to blood loss 6

A
  1. Increased PVR
  2. Redistribution of blood volume away from cutaenous, skin, splanchnic
  3. Preacpillary vasoconstriction –> autotransferusion
  4. Venoconstriction mobilising venous capacitance (including liver and lung capacitance vessels)
  5. Cardiac - tachycardia, increased inotropy and cardiac output
  6. Stimulation of renin and vasopressin release
70
Q

What are the 4 main systems that are part of the neurohormonal response to blood loss?

A
  • Renin secretion causes:
    ◦ Vasoconstriction (by angiotensin)
    ◦ Increased sodium retention (by aldosterone) leading to increased reabsorption of water
    ◦ Increased thirst
  • Vasopressin release causes:
    ◦ Vasoconstriction (by V1 receptors), augments noradrenaline mediated arteriolar vasoconstriction
    ◦ Increased water retention (by V2 receptors)
  • Venous hypotension decreases atrial natriuretic peptide secretion, which causes:
    ◦ Decreased renal blood flow
    ◦ Decreased urinary water and sodium excretion
  • Catecholamines - see above
71
Q

How does rate of blood loss affect response?

A
  • A more rapid rate of blood loss places increased stress on the cardiovascular system to maintain haemodynamic homeostasis
  • Healthy individuals will be better able to compensate for more rapid rates of blood loss by increasing their heart rate and cardiac contractility
  • Patients with compromised cardiac function (eg. ischaemic heart disease or heart failure) will have impaired compensatory mechanisms and will not be able to compensate for even relatively slow blood loss
72
Q

How much does pressure change occur with height in the cardiovascular system

A

1m difference in height corresponds to 73mmHg difference in pressure

73
Q

How does posture influence the arterial and veinous tree

A

Equal pressures exerted, diffferent compliance so has slightly different effects

74
Q

How does posture influence the arterial tree?

A

‣ Arterial effects: protected in part by high pressure and muscualraity of the walls, as well as only 15-20%^ of the blood being within the arterial circulation
* Decreased perfusion pressure in superior regions
* Increased perfusion pressure pressure in dependent regions

75
Q

How much blood is in the arterial circulation at any one time?

A

15-20%

76
Q

What % of blood is in the veinous system at any one time?

A

‣ Venous effects: Thinner more compliant walls, 70% of blood volume

77
Q

How does posture affect the veinous system

A

‣ Venous effects: Thinner more compliant walls, 70% of blood volume

		* Redistribution of venous blood volume (70% of total) into dependent regions due to high venous capacitance - 10% of BV
		* Thus, decreased venous return (MSFP is unchanged so the vascular function curve alteration is not exactly as depitcted below)
78
Q

How is MSFP changed by posture?

A

It is not

79
Q

What is a hydrostatic indifference point?

A

◦ The point inside the static circulatory system where pressure and therefore wall stress remains stable irrespective of the change in position.
‣ Venous
* Potentially a few CM below the diaphragm
* 7+/- 4cm below the 4th intervostal space
‣ Arterial - at the level of the heart

80
Q

What is the name of the point at which static circulatory pressure is unaltered by position

A

Hydrostatic indfference point

81
Q

Where is the venous hydrostatic indifferent point

A

◦ The point inside the static circulatory system where pressure and therefore wall stress remains stable irrespective of the change in position.
‣ Venous
* Potentially a few CM below the diaphragm
* 7+/- 4cm below the 4th intervostal space
‣ Arterial - at the level of the heart

82
Q

Where is the arterial hydrostatic indifference point

A

at the level of the heart

83
Q

Why is the hydrostatic indiffernt point of value?

A

It is a point about whihc the baroreceptor position will regulate what blood pressure they detect - so not only does a change in position affect preload it also directly via gravitational potential energy effects wall stretch

84
Q

Explain the response to standing from a cardiac perspectie

A

Decreased venous return, increased venous pooling –> decreased cardiac output
Raised hydrostatic indifferent point –> supine to standing lowers the cerebral perfusion pressure by 30mmHg at the carotid and 44mmHg at the midbrain

Baroreceptor reflex activated –> increased HR, delayed increase in peripheral vascular resistance and venous return (muscle contraction of standing does aid somewhat)

Net effects
- Increased BP, increased HR
- Reduced cardiac output and SV
- Reduced cerebral perfusion pressure but stable cerebral perfusion (autoregulation)

Both these factors stimulate the carotid baroreceptors

85
Q

What is the effect on BP, CO, HR, SVR and cerebral blood flow of supine to seated transition?

A
  • BP increases 0-40%
  • Cardiac output reduces by 15%
  • HR largely unchanged
  • SVR increases by 50-80%
  • Cerebral blood flow decreases by 15%
86
Q

What is the effect on BP, CO, HR, SVR and cerebral blood flow of supine to Trendelenburg

A
  • BP increases 0-40%
  • Cardiac output reduces by 15%
  • HR largely unchanged
  • SVR increases by 50-80%
  • Cerebral blood flow decreases by 15%

Trendelenburg - 15-20 degrees head down
* BP increases by 5%
* Cardiac output unchanged
* HR unchanged
* SVR decreases by 5%
* Pulmonary artery wedge pressure increases by 3-4mmHg
* Reduced cerebral perfusion due to poor venous drainage

87
Q

Transition from supine to Prone causes what changes in the below measures
- BP
- HR,
- Cardiac output
- Stroke volume
- PAWP

A

Prone positioning - main change comes from compressing abdominal structures because no hydrostatic change but most efforts to prone people try to avoid this
* MAP increased by 3.5%
* Cardiac output decreased by 8.6%
* HR decreased by 10%
* Stroke volume decreased by 8%
* PAWP increased by 3-4mmHg

88
Q

How does ARDS influence impact of prone positioning

A

Prone positioning - main change comes from compressing abdominal structures because no hydrostatic change but most efforts to prone people try to avoid this
* MAP increased by 3.5%
* Cardiac output decreased by 8.6%
* HR decreased by 10%
* Stroke volume decreased by 8%
* PAWP increased by 3-4mmHg

In ARDS however prone positoining
* INcreased RV preload if welll filled - if no resistance to venous return from IVC compression
◦ Decreased RV preload due to abdominal compression
* RV afterload
◦ Increased due to high pressure ventilation
◦ Improved if prone positioning improves pulmonary compliance with better recruitment, decreased pulmonary vascular resistance as well as improving oxygenation and ventilation which improves it further
* Increased SVR over time
* Increased or stable cardiac output if
◦ RV afterload was the rate limiting step and is releived
◦ Abdominal organs are compressed improving venous return without increasing venous resistance
* Decreased total cardiac output if:
◦ The RV ends up having no added afterload reduction (i.e. prone position did not have any of it desired effects on oxygenation and lung recruitment)
◦ The abdominal contents is compressed to the point where there is increased resistance to venous return from the lower body
◦ The RV pressures increase due to increased preload and afterload to the point where interventricular interdependence affects left ventricular diastolic filling

89
Q

Using a cardiac function curve illustrate the impact of exercise

A
90
Q

Exercise cardiovascular response consists of 4 main domains

A
  1. Local muscle tissue vasodilation
  2. Increased cardiac output
  3. Central control
  4. Haemodynamic variables
91
Q

How does exercise impact regional muscle blood flow? How?

A
  • This increased demand is met by increasing blood flow to exercising muscle
    ◦ Increased from 1-4ml/100g/min to 400ml/100g/min
  • The increase in blood flow is mediated mainly by a regional decrease in vascular resistance
    ◦ It is accompanied by increasing coronary blood flow, decreasing visceral blood flow and increasing skin blood flow (temperature control)
  • The mechanisms for this vasodilation are:
    ◦ Vasoactive substrates, hypoxia and products of muscle metabolism,
    ‣ eg. CO2, lactate, hydrogen peroxide and potassium ions
    ‣ Regional decrease in pH produces vasodilation independent of CO2 and lactate
    ◦ Vasoactive mediators released by the endothelium,
    ‣ eg. nitric oxide (NO), ATP, adenosine, prostaglandins and endothelium derived hyperpolarisation factors (EDHPF)
    ◦ β-2 adrenoceptor activation - systemic adrenaline release increases muscle blood flow and increases cardiac output
    ◦ There is also corresponding vasoconstriction of other vascular beds, redirecting blood flow away from viscera and skin
92
Q

Cardiac output in exercise can reach?

A

30L/min

93
Q

How is cardiac output increased in exercise

A

Increased HR and increased stroke volume

Increased workload

94
Q

When in exercise is the peak response of stroke volume?

A

At 50% maximal workload

After this HR causes too much reduction in diastole and SV declines

95
Q

What happens to CVP and PCWP during exercise

A

Increase

96
Q

How does SBP change in exercise

A

Increased

97
Q

How does MAP change in exercise

A

Increased
◦ Increase in cardiac output greater than the decrease in PVR so MAP rises slightly

98
Q

How does pulse pressure change with exercise?

A
  • Diastolic blood pressure decreases - despite tachyardia due to drop in PVR
  • The pulse pressure widens
99
Q

How is exercise cardiac output requirements fed back to the body?

A

◦ Increased muscle activity is sensed by stretch receptors and chemoreceptors in the muscle tissue
◦ Decreased peripheral vascular resistance, translating into decreased blood pressure, is sensed by the baroreflex
◦ The central nervous system itself can generate the afferent signals for exercise-related cardiovascular responses in anticipation of effort

100
Q

What is a valsalva manouvre?

A

Expiratory effort against an obstructed airway e.g. closed glottis

101
Q

What sort of pressure do you achieve with Valsalva manouvre?

A

+40mmHg

102
Q

How long does a Valsalva manouvre go on for?

A

15-20 seconds

103
Q

How many phases are there to a Valsalva manouvre?

A

4

104
Q

Describe phase 1 of Valsalva manoeuvre

A
  1. Increased intrathoracic pressure due to voluntary breath hold against closed glottis
  2. Reduced venous return
  3. Decreased LV afterload with temporarily increased LV preload leading to increase in cardiac output and BP due to increased SV
  4. Reflexive decrease in HR immediately
105
Q

Describe early phase 2 of the Valsalva manouvre? and late phase2

A
  1. Decreased venous return to the LV due to decreased RV output –> decreased cardiac output and decreased pulse pressure with reduced SV
  2. Increasing HR baroreflex mediated
  3. The baroreflex vasoconstriction to bring BP back up is slightly slower and so there is a little lag and dip in BP

Late phase 2
- Restored cardiac output (increased HR compensating for drop in SV)
- Resotred BP due to sympathetic increase in SVR

106
Q

Phase 3 of the valsalva manouvre

A
  1. Release of breath hold –> drop in intrathoracic pressure and increased venous return to the RH
  2. Increase in LV afterload, interventricular independence, and reduction in venous return further to the LV with reducing intrathoracic pressure –> BP drops, and HR reflex increase, pulse pressure narrowed
107
Q

Phase 4 of the Valsalva manouvre

A
  1. With increase in RV output LV experiences boost in preload –> persistent increase in contractility and elevated SVR –> increased BP and restored cardiac output
  2. Reduction in HR with slower resolution of BP and SVR due to delay in SNS action
108
Q

Draw a line representing MAP and HR during a valsalva manouvre

A
109
Q

Septic shock does what to cardiac index

A

Increeases

110
Q

Septic shock has what effect on PCWP

A

Normal or reduced

111
Q

Septic shock affects CVP how?

A

Normal or reduced

112
Q

Septic shock has what effect on PVR

A

Reduced

113
Q

Septic shokc has what effect on DO2

A

Increased

114
Q

What are the parameters required when dioscussing shock

A

CI
PCWP
CVP
SVR
DO2

115
Q

How does cardiogenic shock influence CI

A

Reduced

116
Q

How does cardiogenic shock influence PCWP

A

Increases

117
Q

How does cardiogenic shock affect CVP

A

Normal or reduced

118
Q

How does cardiogenic shock affect PVR

A

Increases

119
Q

How does cardiogenic shokc influence DO2

A

Reduced

120
Q

How does hypovolaemic shock affect CI

A

Reduced

121
Q

How does hypovolaemic shock affect PCWP

A

Decreases

122
Q

How does hypovolaemic shock affect CVP

A

Reduced

123
Q

How does hyopovolaemic shock affect SVR

A

Increases

124
Q

How does hypovolaemic shokc affect DO2

A

Decreased

125
Q

How does obstructive shock affect CI

A

Decreased

126
Q

How does obstructive shock affect PCWP

A

Normal or increased

127
Q

How does obstructive shokc affect CVP

A

Increases

128
Q

How does obstructive shock affect SVR

A

Increases

129
Q

How does obstructive shock influence DO2

A

decreases