Cardiovascular regulation Flashcards
Ways we can lose fluid and electrolytes
How does osmolality, volumes and electrolyte concs vary in body fluid compartments
- sweating, diuresis, changes in fluid intake/diet, blood loss, diarrhoea and vomiting
- Vary little despite fluid intake and diet variation
Intracellular fluids and extracellular fluids
Intracellular: 2/3 of TBW. Low in sodium, chloride. High in K+
Extracellular: 1/3 of TBW, consists of interstitial fluid and plasma. No negative proteins in IF. Both high in sodium, bicarbonate, chloride. low in potassium
Water movement recap
Net=k(Pc-Pt)-(Cp-Ct)
Altered by precapillary resistance, if increased, lowers hydrostatic pressure, if decreased increases
Water and ion movement between ECF and cells
isotonic and hypotonic infusion
Driven entirely by osmotic gradients
Cell volume is determined by sodium and water balance in the extracellular compartment\
Between ECF and ICF controlled by pumps.
Isotonic: No ICF change, as osmotic pressure does not change, but increase in ECF increases CO
Hypotonic: reduces ECF osmolality, driving water into ECF
How is ADH secreted, and what does it do.
What is the range of ADH action on renal tubules
supraoptic and paraventricular nuclei in the hypothalamus sense effective plasma osmolality changes. If it increases, ADH secretion will increase thirst and retain water.
threshold, at 280 mOsmol/L ( at this osmolality starts secreting). Will increase ADH secretion as osmolality increases, but max effective conc. is at 295mOsmol/L
ECF volume and its link to arterial pressure
ECF consists of IF and plasma
Plasma and red cell volume makes up blood volume, which in turn effects the hearts filling pressure, which influences CO. Along with TPR, this alters arterial pressure
Thus changes in ECF alter cardiovascular performance
Cardiac receptors role in volume sensing
what percent f BV loss will alter BP
Afferents from the heart sense changes in blood volume, if high, will slightly reduce sympathetic nerve activity. Note small changes, then baroreceptors
If BV is lowered by 10% or more, arterial pressure falls and baroreceptor firing decreases
(BIG)
Neuro-humoral response to a reduction in ECF volume
Cardiovascular receptors decrease firing rate
Increase ADH secretion, increase sympathetic tone
ADH will retain water, and activate thirst
Sympathetic tone increases renin, A2 (activates thirst), aldosterone reducing water and salt excretion
Capillary filtration decreases due to VC
Increase in precapillary resistance due to VC (due to blood loss increasing sympathetic tone) does what
- Reduction in capillary hydrostatic pressure
- shifts to fluid absorption, movement of IF to plasma
Skeletal muscle provides role as big reservoir for internal transfusion, can mobilize about 800mls of fluid, however is limited by dilution of plasma proteins.
Occurs quickly
Time courses of ADH, sympathetic drive, renin
ADH: minutes after loss
Aldosterone: hour
ECF volume can be restored in 12-72 hours
IF transfusion, almost instantaneously
Time course of red cells and plasma proteins following acute blood loss
Days to weeks
Immediately after acute blood loss, preformed albumin put into circulation, however most plasma proteins restored over 3-4 daysby liver. 4-8 weeks for red cells to return
Result of blood volume losses of different amounts
- <10%: mean arterial pressure maintained, pulse pressure reduced. Non-hypotensive haemorrhage
- > 10%: MABP graded fall, hypotensive haemorrhage
- Uncompensated extreme loss of blood: volume deficit replacement may not restore cardiovascular homeostasis, hemorrhagic shock (due to loss of capillary integrity, proteins leak and water follows, DIC)
Time period with progressive blood loss with neuro-humoral effects
(graph Smail pg5)
Less than 10%, little change in baroreceptor firing, however cardiac receptor firing does decrease, increasing levels of ADH, HR (to maintain CO, indicative of sympatheitc drive)
Small VC of precapillary vessles
With a loss of more than 10%, increased baroreceptor, increase ADH, aldosterone, more intense VC, increase HR and inotropic state
Response to altere posture
Upon standing up, blood pools in lower limbs, causing a volume shift from intrathoracically to lower limbs, an internal haemorrhage.
Increases hydrostatic pressure, leads to sequestration of blood in superficial veins, reduced VR
Cardiac receptors start firing, so despite a lowered stroke volume and slight BP lowering, HR increases to try maintain CO, resistance vessel constrict (TPR goes up a bit, keeping BP similar)
Similar to non-hypotensive haemorrhage
Baroreceptor adaptiblity
Sustained high pressures will reset the firing rate of baroreceptors (right shift). Are not set.
Argue that provide info on beat to beat changes in arterial pressure, but does not set mean pressure
