CVS Reflexes Flashcards
What is the pressor response? What receptors are involved?
What is the depressor response? What receptors are involved?
- When excitatory inputs are stimulated, the reflexes are SWITCHED ON to ↑CO/TPR/BP - arterial chemoreceptors, muscle metaboreceptors
- When inhiBitory inputs are stimulated, the reflexes are SWITCHED OFF to ↓CO/TPR/BP - arterial Baroreceptors
What are the roles of the arterial baroreceptors?
Where are they found?
What occurs when there’s an increase in BP?
What’s the effect of Chronic HT on the baroreceptors?
- Maintain blood flow to the brain and heart
- Carotid and aortic bodies
- Baroreceptors are stimulated to send AP’s to the brain - impulse frequency starts off high and then slows down
- They adapt to the change - become used to the high BP
What is Loading of the Baroreceptors?
What is the response of loading?
How does it carry out this response?
- The effect an increased BP has on the Baroreflex e.g. stress
- Responses work to ↓HR, BP, and TPR - DEPRESSOR reflex
- ↓Sympathetic activity and ↑Parasympathetic activity
What is UNloading of the Baroreceptors?
What is the response of Unloading?
How does it carry out this response?
- The effect a decrease BP has on the Baroreflex e.g. haemorrhage
- Responses work to ↑Sympathetic and ↓Parasympathetic activity - ↑HR and contractive force = ↑CO. Vasoconstriction = ↑TPR. Venoconstriction = ↑CVP, SV, and CO - PRESSOR reflex.
- A large drop in BP causes:
• Adrenaline secretion
• ADH secretion
• ↑RAAS = ↑Renin = ↑Ang II
Ang II = Vasoconstriction = ↓Capillary pressure = ↑Reabsorption = ↑Blood volume
Ang II = ↑Aldosterone = ↑Na reabsorption = ↑Blood volume
What is the OVERALL effect of the Cardiac receptors?
What are the 3 types of Cardiac receptors? What stimulates them? What is their effect?
- Depressor Effect
- Nociceptive sympathetic afferents:
• Chemo-sensitive fibres in ventricle
• Stimulated by K+, H+, Bradykinin (released during ischaemia)
• Nerve fibres converge into same neurons in spinal cord as somatic afferents - basis for referred pain
• Cause an ACUTE PRESSOR reflex = ↑Sympathetic activity
- Nociceptive sympathetic afferents:
- Veno-atrial mechanoreceptors:
• Go to NTS
• Stimulated by ↑Cardiac filling/CVP.
• Have an INITIAL PRESSOR REFLEX = ↑Sympathetic activity
• Have a LONGER DEPRESSOR REFLEX = changes in ADH, ANP, RAAS to ↑Diuresis = ↓Blood volume - Ventricular mechanoreceptors:
• Go to NTS
• Stimulated by over-distension of ventricles
• Cause the DEPRESSOR REFLEX = Bradycardia, Vasodilation, ↓BP
Where are the Arterial Chemoreceptors found?
What are they stimulated by?
What is their role?
What is their effect?
- Carotid and Aortic bodies
- Stimulated by low O2, High CO2, H+, K+.
- Regulate ventilation and drives the cardiac reflexes during Asphyxia/Shock/Haemorrhage
- Cause a PRESSOR REFLEX = ↑Sympathetic activity, Tachycardia, Selective vaso/venoconstriction = ↑CO and BP.
They preserve cerebral blood flow during low O2.
Where are the Muscle Metaboreceptors found?
What are they stimulated by?
What is their effect?
- Skeletal muscle
- Metabolites e.g. ATP, K+, lactic acid, Adenosine
- Cause a PRESSOR REFLEX = ↑Sympathetic activity, Tachycardia, ↑Vaso/venoconstriction = ↑CO and BP.
They preserve blood flow to muscles during isometric exercise.
What’s the effect of an increase in signalling from the baroreceptors, arterial chemoreceptors and muscle mechanoreceptors?
LOOK AT DIAGRAM!
↑Baroreceptors:
Excitatory NTS = ↑CVLM = Inhibition of RVLM = SWITCH OFF sympathetic nerves - DEPRESSOR RESPONSE.
↑Arterial chemoreceptors, Muscle mechanoreceptors:
Inhibitory NTS = ↓CVLM = Less inhibition of RVLM = SWITCH ON sympathetic nerves - PRESSOR RESPONSE.
What’s the affect of a drop in BP in the signalling pathways?
LOOK AT DIAGRAM!
↓BP will stimulate baroreceptor excitatory pathway to NTS = Activation of Nucleus Ambiguus (NA). This will make Parasympathetic > Sympathetic activity = Vagal Bradycardia to ↓HR and TPR.
Inspiratory centre is in the medulla. Inspiration will ↓NA to temporarily switch off vagal nerves = Sympathetics dominate = ↑HR during inspiration, called Sinus Tachycardia.
HR then drops back down during expiration, called Respiratory Sinus Arrhythmia.