Canonical Question
CVS – Responses
Master answer
Normal circulating Volume ~ 5L
2L Haemorrhage ~ 40% loss without resuscitation – Major Haemorrhage
Immediate:
Baroreceptor Response
- HP BR
- Stretch receptor: ↑ distension of vessel → ↑ discharge rate
- Threshold > 60mmHg → normally has baseline tone.
- Located at Carotid Sinus and Aortic Arch
- Carotid sinus and aortic arch receptors
- Detects > 5-10 % change in plasma volume
- ↓ Plasma volume → Increased central SNS tone and decreased PSNS tone
- ↑’d distension → ↓’d HR/Contractility/SVR
- Provides strict negative feedback to Δ’s in CO
- LP BR
- Located at junction of return vessels and atria, vetricular walls, pulmonary vessles
- Throughout the peripheral vasculature (esp kidney)
- Detect > 10% decrease in plasma volume as decreased atrial stretch
- Reduced ANP release
- Increase SNS output
- 2 types
- A receptors → fire at atrial contraction (a wave)
- B type → fire at atrial filling (v wave)
- 1. Medulla afferents cause
- ↓ SNS (NA) and ↑PSNS (RVLM) outflow → peripheral vascular vaso and venodilation
- ↓ SNS activity to kidney → ↓ Na/H2O conservation
- ↑ SNS activity to sinus node
- 2. Hypothalamic afferents cause
- → ↓ ADH release and ↓ Thirst
- Outcome
- ↓ PL → ↓ CO → ↓BR discharge rate
- → ↓ PSNS medullary outflow
- → ↑ RVLM outflow
- ↑ contractility/HR
- ↑ SVR → autotransfusion and ↑ perfusing pressure (but ↑AL)
- ↓ PL → ↓ CO → ↓BR discharge rate
Chemoreceptor response
- Peripheral CR
- “Carotid bodies” (more important)
- at bifurcation point of common carotid arteries
- supplied by CN IX
- “Aortic bodies” (less important)
- above and below the aortic arch
- supplied by CN X
- PCRs found in “Glomus cells”
- ↓ PaO2 – via inhibition of O2 sensitive K-channels
- ↑ PaCO2 and/or ↓pH – via effect on pH sensitive K-channels
- Type I cells (rich in NAd, DA, ACh)
- Hypoxia causes release of NTs
- NAd/ACh – ↑ AP firing rate of AB or CB afferent fibres
- DA – Damping of type 2 cell responses
- Type II cells (rich in capillary supply)
- ↓ PaO2, ↑ PaCO2 and/or ↓pH
- ↓ IC [ATP] which leads to ↑ NT production and release
- ↑ AP firing rate of AB or CB afferent fibres
- CCRs located Below the ventral surface of the medulla
- ↑ ECF [H+] stimulates ↑ ventilation
- CO2 rapidly diffuses into CSF
- Low CSF protein and HCO3 (c.f. plasma)
- Poor buffering capacity
- ΔCSF pH per ΔPaCO2 is GREATER than that of blood
- Cause
- ↑’s SVR due to
- ↓ hypothalamic perfusion pressure
- ↓ Hct
- ↑’d RR → ↑ venous return
- ↑ ADH secretion (intermediate term response)
- ↑’s SVR due to
Intermediate term response
- Chemoreceptor stimulation (↓’d perfusion → ↑pCO₂:pO₂)
- ↑ ADH secretion
- ↑’d RAAS activation
- ↓ renal perfusion → ↑ renin → ↑AT2 and Aldosterone
- ↑ADH → ↑Na/H2O retention and vasoconstriction
- ↓Hydrostatic pressure
- altered starlings forces
- autotransfusion of 0.25mL/kg/min ~ 1L/hr
Long Term Response
- ↑ RAAS → ↑ Na/H2O retention
- Osmoreceptor response
- Anterior hypothalamic receptors
- Detect 1% decrease from normal (280-300mOsm/kg)
- Threshold 280mOsm/kg
- Promotes release of ADH from posterior pituitary
- ↑thirst
- EPO release
- From adrenal medulla → ↑ RBC mass
- ↑ hepatic plasma protein synthesis
Gladwin 2016
Exam appearances
| Exam | Exact wording | Relationship | Success |
|---|---|---|---|
| 2009B Q02 | Describe the physiological consequences and responses after an acute haemorrhage of 2.0 litres in a healthy 70kg adult if there is no immediate fluid resuscitation. | historical_member | — |