Regulation of cardiac function - Smaill

Question 1

Water movement between cells and interstitium?

Answer 1

driven by osmotic gradients across the cell membrane, thus water will be distributed so that osmolality in intracellular and interstitial fluids is equalised

Question 2

Water movement between interstitial and vascular compartments is determined by?

Answer 2

nett gradient of hydrostatic na osmotic gradients at the level of capillaries.
Starling equaiton: k[(Pc-Pt) - (Ppl-Pif)]

Question 3

What will happen when you add hypotonic saline to the ECF

Answer 3

this will reduce the osmolality of that compartment causing water to move into the ICF. At equilibrium the osmolality of both compartments will be reduced and the volume of both will be increased.

Question 4

cell volume is determined by?

Answer 4

sodium homeostasis and water balance in the ECF compartment

Question 5

How do osmoreceptors and ADH work?

Answer 5

osmoreceptor cells in supraoptic and paraventricular nuclei of the hypothalamus, sense changes in effective plasma osmolality by altering their volume. This modulates their sensory output to the cells of the posterior pituitary that produce and secrete ADH
Linear relationship between plasma osmolality and ADH over 280-295mOsm/L. When ADH concentration reduced, there is reduced water reabsorption from the CD tubules.
Activation of osmoreceptors by increase plasma osmolality also stimulates thirst centres in the hypothalamus.

Question 6

Reduced cardiac filling leads to

Answer 6

increased sympathetic outflow to the heart and vessels, reduced cardiac vagal activity and increased catecholamine secretion by the adrenal medulla, also elicits humeral responses that affect extracellular fluid volume

Question 7

compare the tie course of effector mechanisms

Answer 7

plasma ADH is elevated minuets after a change in ECF osmolality or volume, aldosterone begins to rise about 1 hours after a fall in plasma volume stimulus.

Question 8

examples of ways tissue fluids and electrolytes can be lost and gained

Answer 8

Blood loss, diarrhoea, vomiting, sweating, diuresis, and change in fluid intake or diet.

Question 9

What happens when blood volume is reduced?

Answer 9

Decrease in peripheral venous pressure, and therefore dec in venous return to heart, dec in cardiac filling and therefore dec in stroke volume.
Dec cardiac filling triggers autonomic responses, increased sympathetic outflow to heart and vessels, dec vagal activity, inc catecholamine secretion by adrenal medulla. Renal sympathetic stimulation is inc therefore inc in ADH and angiotensin II.
CO preserved by inc HR and inotropy
Blood flow diverted from non-essential circulations to maintain coronary and cerebral oxygen supply
Venoconstriction preserves venous return
ADH and RAAs acts to restore volume of blood lost.

Question 10

Fluid shift form interstitial space to plasma?

Answer 10

Reflex constriction of pre capillary vessels reduces capillary hydrostatic pressure, shifts balance between capillary hydrostatic and oncotic pressures in favour of fluid absorption.
So get translocation of fluid into the vascular compartment
Important reservoir = skeletal muscle
Process rapid but limited by dilution of plasma proteins
Upton 800ml of fluid may be mobilised

Question 11

Restoration of ECF volume

Answer 11

Increasing circulating levels of ADH, angiotensin II, aldosterone, favours water and sodium retention by kidney and arguments thirst drive. Alters balance between fluid intake and fluid output so that ECF volume restored.
Serum ADH inc minuets after moderate loss BV, aldosterone begins to rise only an hour after that.
ECFV restored over 12-72 hours.

Question 12

Restoration of red cells and other blood constituents

Answer 12

days to weeks.
Immediately after acute blood loss small amounts of preformed albumin transferred into the circulation, but the bulk of the plasma protein defecit, is restored by hepatic over 3-4 days.
Red cell synthesis stimulated by EPO from the kidneys in response to low oxygen tension takes 4-8 weeks for red cell levels to return to normal after blood loss.

Question 13

what is normotensive haemorrhage

Answer 13

acute loss of BV of 10% or less
MAP unchanged, pulse pressure declines
Neurally mediated reflex mechanisms are sufficient to maintain cardiovascular haemostatsis
Significant dec in firing of cardiac receptors but no change in firing of arterial baroreceptors.
Circulating levels of ADH and aldosterone both increase
Inc in HR and inotropy

Question 14

hYpotensive haemorrhage

Answer 14

blood loss > 10% graded fall in systemic arterial pressures, reflects the extent of blood volume deficit.
Arterial baroreceptor firing is progressively reduced
Further increases in ADH and aldosterone.
Increasing intensity of inc HR and inotropy, and constriction of resistance and capacitance vessels.

Question 15

Cardiac receptors play a central role in maintaining cardiovascular homeostasis for blood volume fluctuations of?

Answer 15

10% or less

Question 16

Hemorrhagic shock

Answer 16

In situations where substantial blood loss remains uncompensated for long periods, hemorrhagic shock may occur, under these circumstances, replacing the blood volume originally lost may not restore cardiovascular haemostatsis.

Question 17

Cardiovascular adjustments which company alterations in posture are identical to those which are seen in? explain…

Answer 17

non-hypotensive haemorrhage.
Gravitational effects increase the hydrostatic pressures acting on blood vessels in lower extremities.
Superficial veins in the legs and ankles defer and 400-500mlof blood volume shifts from central thoracic reservoir to lower limbs.
“internal haemorrhage” dec cardiac filling and therefore SV. Neurally mediated reflex mechanisms inc HR and inotropy to minimise fall in CO.
Overall MAP remains relatively unchanged.

Question 18

Arterial pressure during exercise

Answer 18

the fast neurally mediated responses that drive short term regulation of arterial pressure are substantially altered by descending inputs from higher centres the the CNS and by afferent traffic from exercising muscle not present at rest.
Central command from cerebral cortex activates curcits that inc motor activity and arterial pressure, HR and ventilation.
Exercise pressor reflex comes from Thin fiber muscle afferents are also activated by contraction. Triggered by mechanical and metabolic stimuli.
Both contribute to different cariovasular responses associated with static and dynamic exercise.

Question 19

Dynamic exercise

Answer 19

Rhythmic exercise involving a large proportion of the bodys muscle groups (running, cycling…)
substantial fall in peripheral resistance and closely matched increase in CO, inotropic state and HR increase
Pulse and MA (slight) pressure increase

Question 20

Static exercise

Answer 20

Isometric contraction the involves a more restricted set of muscle groups.
No fall in peripheral resistance but CO does increase
susbtaninal increase in MAP, HR and inotropic state both inc
Normal reflex control of arterial pressure is being overridden,
increases HR and CO graded to the intensity of the isometric exercise effort, despite substantial increase in systemic arterial pressure

Question 21

What happens with systemic arterial baroreceptors in long term regulation of systemic arterial pressure

Answer 21

The entire baroreceptor function curve is shifted to the right in hypertension so normal levels of firing occur at higher arterial pressures. “resetting”
Baroreceptor afferents provide information on beat to beat changes in arterial pressure, but cannot be a reliable source of information on systemic arterial pressure because studies suggest baroreceptor function is modified via efferent nerves from the CNS
Animal studies: much wider variation of arterial pressure when arterial baroreceptors are eliminated, average arterial pressure increases for a short period only in enervated animals then returns to control levels, so arterial baroreceptors buffer short term changes in arterial pressure (e.g. postural hypotension) around a set point.

Question 22

cardiac receptors

Answer 22

powerful aggregate activity
Majority of vagal afferents are unmylinated and conduct slowly.
groups of receptors in the atria and ventricles contribute a tonic inhibitory influence over cardiovascular function.
Cardiac receptors cannot sense rapid fluctuations inCV function and they monitor the extent of cardiac filling, which is closely associated with BV.
They are also slowly adapting like arterial baroreceptors, they contribute to setting steady levels of arterial pressure around which the arterial baroreceptors operate
Denervation of these receptors produce wide fluctuations in pressure

Question 23

renal sympathetic innervation causes?

Answer 23

Increases in renal sympathetic nerve activity, cause construction of renal arterioles with a resultant decrease in glomerular filtration rate and increased tubular reabsorption of salt and water. Also stimulates renin release and activates the RAA cascade

Question 24

Juxta glomerular cells?

Answer 24

at the terminal end of the afferent arteriole are directly influenced by altered pressures, when arterial pressure falls renin production is increased, activating the RAAs cascade.

Question 25

Structural remodelling and arterial pressure

Answer 25

in pre-capillary resistance vessels smooth muscle proliferation causes wall thickening and reduces blood vessel lumen. This increases peripheral resistance and reduces vascular distensibility. Similarly in hypertension the wall thickness of cardiac chambers increased and their distensibility is reduced.
The reduction in arterial and cardiac distensibility decreases the firing rate of both arterial baroreceptors and cardiac receptors, likewise remodelling of the renal circulation may influence the responsiveness of the JG cells to pressure change. Finally structural changes scubas renal artery stenosis and fibrosis may themselves be a primary cause of hypertension.