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CVS II > Reflexes > Flashcards

Reflexes Flashcards

1
Q

How do excitatory inputs lead to pressor response?

A

arterial chemoreceptors + muscle metaboreceptors (Work) switch on reflexes to increase CO/TPR/BP

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2
Q

How do inhibitory inputs lead to depressor response?

A

arterial baroreceptors switch off reflexes to decrease CO/TPR/BP

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3
Q

How does the body monitor blood flow w/o blood flow sensors?

A 
Monitoring arterial BP shows blood flow
Blood flow (CO)  = BP / TPR  
BP = CO x TPR	
CO = blood flow (both have units of volume/time)
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4
Q

Define baroreceptors?

A

sensors detect arterial wall stretch

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5
Q

Sig of BP sensors?

A

allow specific sensing of blood flow to brain and heart

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6
Q

Location of arterial baroreceptors?

A

Carotid sinus at base of internal carotid

Aorta

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7
Q

Location of arterial chemoreceptors?

A

Carotid body

Aortic bodies

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8
Q

How do baroreceptors respond to changes in pressure?

A

Dynamic (speed of onset)
Sensitivity (relative change to amount of pressure)
Adaptation (change over time)

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9
Q

How do baroreceptors respond to hypertension?

A
  • baroreceptors are less activated
  • threshold becomes greater
  • don’t regulate BP as well
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10
Q

Describe effect of increased BP on baroreflex (loading)?

A
  • baroreceptors activated
  • stimulate carotid sinus nerve
  • BP falls (depressor reflex)
  • bradycardia
  • pulse p falls so lower SV
  • decreased symp + increased para via vagus
  • vasodilation -> decreased TPR -> BP
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11
Q

Describe effect of decreased BP on baroreflex (unloading)?

A
  • increased symp + decreased vagus
  • increased HR + contractility -> increased CO
  • arteriolar constriction
  • increased TPR
  • venous constriction
  • increased CVP -> SV -> CO (Starling’s law)
  • pressor reflex maintains BF + BP to vital organs
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12
Q

Describe effect of severe drop in BP on baroreflex?

A
  • secretion of ADH + A
  • stimulation of RAAS :
  • Ang II production
  • vasoconstriction
  • decreased capillary p
  • absorption of interstitial fluid
  • increased blood volume
  • Ang II production
  • aldosterone secretion
  • Na/H2O reabsorption in kidneys
  • increased blood volume
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13
Q

Diff types of cardiac receptors?

A
  • Nociceptive sympathetic afferents
  • Veno-atrial mechanoreceptors
  • Ventricular mechanoreceptors
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14
Q

What are nociceptive sympathetic afferents?

A
  • chemosensitive ventricular afferent C fibres
  • stimulated by K+, H+ (lactate), bradykinin during ischaemia
  • mediate pain/symptoms of angina + MI
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15
Q

What’s the basis of referred pain?

A

C fibres converge onto same neurones in spinal cord as somatic afferents

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16
Q

Which type of reflex is nociceptive sympathetic afferents?

A

Acute pressor reflex - increases symp: pale, sweaty, tachycardia

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17
Q

What are veno-atrial mechanoreceptors?

A

stimulated by increase in filling/CVP

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18
Q

What’s the Bainbridge effect?

A

reflex tachycardia due to rapid infusion of volume into venous system (veno-atrial mechanoreceptors + pacemaker distension)

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19
Q

Which type of reflex is veno-atrial mechanoreceptors?

A

Initial pressor reflex - increases symp: tachycardia

Longer term depressor reflex - increased diuresis decreases blood volume, feedback loop via changes in ADH, ANP, RAAS

20
Q

What are ventricular mechanoreceptors

A

stimulated by over distension of ventricles

21
Q

Which type of reflex is ventricular mechanoreceptors?

A

Depressor reflex - protective for heart, overrides veno-atrial reflex?

22
Q

What are arterial chemoreceptors stimulated by?

A

low O2 (hypoxia), High CO2 (hypercapnia), H+ , K+

23
Q

Blood flow of arterial chemoreceptors?

A

v high = 20 ml g-1 min-1

24
Q

Role of arterial chemoreceptors?

A

-Regulate ventilation
-Drive cardiac reflexes during:
Asphyxia (low O2/high CO2)
Shock (systemic hypotension)
Haemorrhage (when BP below range of baroreflex)
-Pressor reflex

25
Q

Describe pressor response of arterial chemoreceptors?

A
  • increased symp
  • tachycardia
  • increased selective arterial/venous constriction
  • increased BP/CO
  • preservation of cerebral blood flow during low O2 (asphyxia/haemorrhage)
26
Q

What are muscle metaboreceptors?

A

work receptors

27
Q

Where are muscle metaboreceptors?

A

sensory fibres in Group IV motor fibres in skeletal muscle

28
Q

How are muscle metaboreceptors activated?

A

via metabolites; ATP, K+, lactate, adenosine

29
Q

Role of muscle metaboreceptors?

A
  • Pressor response

- During isometric exercise

30
Q

Describe pressor response of muscle metaboreceptors?

A
  • increased symp
  • tachycardia
  • increased arterial/venous constriction
  • increased BP/CO
31
Q

Why are muscle metaboreceptors important in isometric exercise?

A
  • joint angle and muscle length don’t change when weight lifting / handgrip
  • maintains blood perfusion to contracted muscle
  • muscle undergoes metabolic hyperaemia
  • blood flow to contracted tissue
32
Q

Effect of local anaesthetic (LA) in muscle?

A
  • metaboreceptor afferent fibres blocked

- prevent pressor response

33
Q

Role of cerebral cortex?

A

-Controls hypothalamus, limbic system etc
-Tells body we’re about to do exercise to increase
HR + CO

34
Q

Role of hypothalamus?

A

Trigger areas in medulla:
Rostral Ventral Lateral Medulla (RVLM)
Caudal Ventero Lateral Medulla (CVLM)
Nucleus Tractus Solitarius (NTS).

35
Q

Describe effect of increase baroreceptors

A
  • baroreceptors detect increase in BP
  • afferents to excitatory NTS
  • increase CVLM
  • inhibition of RVLM
  • inhibitory pathway acts as ‘thermostat’
  • switch off sympathetic nerves - DEPRESSOR
  • decrease BP
36
Q

Describe effect of increase arterial chemoreceptor/muscle work receptors

A
  • inhibitory NTS
  • inhibit CVLM
  • switch on RVLM and sympathetic nerves - PRESSOR
37
Q

Effect of destroying spine (spinal transection)?

A
  • sympathetic fibres in spinal cord to CVS destroyed/lost
  • so only vagal system remains of baroreflex
  • acute hypotension
38
Q

What do vagal parasympathetic fibres innervate?

A

SAN + AVN (vagal outflow to pacemaker),

39
Q

Describe the baroreflex

A

-aortic baroreceptors stimulated by increase in BP
-afferents to nucleus tractus solitarius
-nucleus tractus solitarius stimulates nucleus ambiguus
-vagal parasympathetics from nucleus ambiguus to SAN
-decrease HR (bradycardia) + CO
-decrease BP
The is
also under

40
Q

What controls nucleus ambiguus?

A
  • Controlled directly from higher centres : limbic system (one of the reasons someone can experience a vaso-vagal reflex)
  • Receives communication from inspiratory centre (what is controlling breathing is also linked to the vagal control of heart)
41
Q

Describe effect of inspiration on inhibitory control

A

-nucleus ambiguus receives communication from inspiratory centre
-every inspiration inhibits nucleus
ambiguus
-switch off vagal activity to SAN
-sinus arrhythmia (normal)
-sinus tachycardia when you breathe in.
-seen in the ECG

42
Q

Describe effect of expiration of inhibitory control

A
  • expiration
  • inhibitory pathway is turned
  • allows vagal activity on heart
  • HR slows
  • HR changes due to breathing
  • sinus arrhythmia (normal rhythm change in course of breathing)
43
Q

What’s limbic system?

A

emotional centre

44
Q

Describe how fainting/syncope/vaso-vagal attack occurs?

A

-sudden drop in arterial BP via:
Vagal bradycardia
Sympathetic activity – further decrease in HR due to vasodilation
Peripheral vasodilatation (decerased TPR)
-decreased cerebral BF
-(reduced oxygen delivery)

45
Q

What happens if you denervate baroreceptors?

A

spread around mean BP

46
Q

What happens if you denervate baroreceptors + cardiac receptors?

A

mean BP rises, less variation stable BP

47
Q

What happens if you remove CVS reflexes?

A

less controlled + higher BP because reflexes stabilise BP

CVS II (19 decks)

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