L04 CVS Physiology Case Introduction Haemorrhage

Overview

This lecture introduces the first CVS physiology case, blood loss and blood pressure regulation, using two contrasting mini-cases: a routine blood donation with no measurable cardiovascular change, and a bleeding gastric ulcer with severe haemodynamic compromise. It then sets out the framework the case is built on: a fall in mean arterial blood pressure after haemorrhage triggers three homeostatic responses on different timescales, immediate (the baroreceptor reflex), intermediate (fluid shift from the tissues into the capillaries, or autotransfusion), and long term (replacement of fluid and red cells). Starling’s equilibrium is used to explain the intermediate response, and the same framework is then applied to two other states that disturb capillary fluid balance, raised venous pressure and low plasma albumin.

Course and case context

CVS physiology comprises:

• 11 lectures
• 3 practicals: cardiac cycle, ECG, blood pressure
• 2 cases: haemorrhage, and heart failure
• Further topics listed: fainting, rhythm, MI, endocarditis

Physiology Case 1 (blood loss and BP regulation) is run as case tutorials in the week of 26 to 30 May, in the Hunter Centre, in the Physiology Module tutorial groups and rooms listed on Moodle (the same as for the Myaesthenia Gravis case). Each stream does an hour of group work followed immediately by the wrap-up in Hunter G30 A&B.

Stream	Date	Group work	Wrap-up
A	Tuesday 27 May	11 to 12	12 to 1, Hunter G30 A&B
B	Thursday 29 May	11 to 12	12 to 1, Hunter G30 A&B
C	Wednesday 28 May	4 to 5	5 to 6, Hunter G30 A&B
D	Monday 26 May	9 to 10	10 to 11, Hunter G30 A&B

Mini-case A: Bill, blood donation

• Bill, 30 years old, height 179 cm, weight 71 kg, giving his twelfth blood donation in Oamaru.
• Immediately before venepuncture, lying arterial blood pressure 125/80 mmHg, pulse 72/minute.
• 440 ml of blood collected over the next twelve minutes from the left antecubital vein.
• Immediately after removal of the needle, lying arterial blood pressure 125/80 mmHg and heart rate 72/minute, that is, unchanged from baseline.

Mini-case B: Ben, bleeding gastric ulcer

• Ben, 42 years old, height 183 cm, weight 81 kg.
• Long history of repeated episodes of intense epigastric pain relieved by antacids; thought to have a gastric ulcer. He had not taken time off his busy life to seek medical care and took no medication for it.
• He had noticed black tarry stools on occasion, and one evening began vomiting small amounts of blood. When this did not stop he went to the Emergency Department.
• On examination: face pale and drawn, sunken eyes, dry shrunken tongue, pulse of poor volume and difficult to feel, heart rate 150 beats per minute, arterial blood pressure 90/75 mmHg.
• Interpretation given: the ulcer has likely eroded into a gastric blood vessel with on-going bleeding into the lumen of the stomach. He will need gastroscopic intervention to stop the bleeding; meanwhile he needs IV fluids to maintain his BP.
• Obtaining intravenous access proved very difficult, but was eventually achieved, and intravenous fluids were infused until cross-matched blood became available.

The two cases bracket the same physiology at different severities: 440 ml lost slowly produces no change in BP or heart rate at all, whereas continuing occult blood loss produces tachycardia (150/min), a narrow low blood pressure (90/75 mmHg), a thready pulse and signs of fluid depletion.

Haemorrhage and hypotension: the three responses

A fall in mean arterial blood pressure (MABP) following haemorrhage elicits homeostatic reflexes to minimise the fall:

1. Immediate: baroreceptor reflex.
2. Intermediate: fluid shift from tissues to capillaries.
3. Long term: replacement of fluid and red cells.

Immediate: the baroreceptor reflex

Sequence as presented: haemorrhage lowers arterial pressure, which reduces firing by the arterial baroreceptors. That reduction in baroreceptor firing produces four efferent limbs:

1. Decreased parasympathetic discharge to the heart acts on the SA node to increase heart rate.
2. Increased sympathetic discharge to the heart also increases SA node heart rate, and acts on cardiac muscle to increase stroke volume (toward normal).
3. Increased sympathetic discharge to the veins increases constriction of the peripheral veins, raising venous pressure (toward normal), which increases venous return (toward normal), which increases end-diastolic volume (toward normal), which increases stroke volume (toward normal) via cardiac muscle.
4. Increased sympathetic discharge to the arterioles increases arteriolar constriction, raising total peripheral resistance.

Converging: increased heart rate and increased stroke volume both raise cardiac output (toward normal); increased cardiac output and increased total peripheral resistance both raise arterial pressure (toward normal).

Intermediate: autotransfusion

The intermediate response is a shift of fluid from the interstitium into the capillaries, described as autotransfusion:

1. Arterial pressure falls.
2. The fall in arterial pressure also acts through the baroreceptor reflexes to increase arteriolar constriction.
3. Both the fall in arterial pressure and the arteriolar constriction reduce capillary hydrostatic pressure.
4. Reduced capillary hydrostatic pressure increases fluid absorption from the interstitial compartment.
5. Increased absorption raises plasma volume, restoring arterial pressure toward normal.

Starling’s equilibrium at the capillary

Fluid movement across the capillary wall is set by the balance between hydrostatic pressure (HP), which drives fluid out, and colloid osmotic pressure (COP), which draws fluid in. Fluid left in the interstitium drains via the lymphatics. Four states were presented (pressures in mmHg as labelled on the slides).

Normal

• Arterial end: HP 35 against COP 25, so net filtration out of the capillary.
• Venous end: HP 15 against COP 25, so net reabsorption into the capillary.
• Fluid leaves the capillary at the arterial end, returns at the venous end, and the residual interstitial fluid drains as lymph.

Blood loss

• Arterial end HP falls from 35 to 28; COP unchanged at 25 at both ends; venous HP unchanged at 15.
• Outward flow at the arterial end is reduced and return at the venous end is increased, so the balance shifts toward reabsorption of interstitial fluid into the capillary. This is the autotransfusion described above.

Increased venous pressure (for example heart failure)

• Arterial HP unchanged at 35; venous HP raised from 15 to 30; COP 25 at both ends.
• Outward movement now occurs at the venous end as well as the arterial end, and there is no reabsorption.
• Result: excess interstitial fluid, that is, oedema.

Reduced COP, low albumin (for example malnutrition)

• HP unchanged (35 arterial, 15 venous); COP reduced from 25 to 15 at both ends.
• Arterial end: increased filtration out of the capillary.
• Venous end: HP 15 and COP 15 are roughly balanced, and the slide marks the direction of net movement at the venous end with a ”?” [slide does not elaborate].
• Result: excess interstitial fluid, that is, oedema.

Long term: volume replacement

• Reduced renal perfusion leads to RAA activation, which retains Na and H2O.
• ADH release, retaining water.
• Thirst.
• Erythropoiesis, to replace the cells.

Coverage note

Slides 13 and 14 of the PDF are handout thumbnail pages (6-up grids duplicating slides 1 to 6 and 7 to 12) and contain no additional content.

Self-test

1. List the three homeostatic responses to a fall in MABP after haemorrhage, with the timescale of each.
2. Describe the afferent limb of the baroreceptor reflex following haemorrhage.
3. List the four efferent limbs that follow reduced baroreceptor firing, and the immediate effector target of each.
4. Explain how increased sympathetic discharge to the veins ends up increasing stroke volume.
5. Explain why both cardiac output and total peripheral resistance need to change for arterial pressure to be restored.
6. Describe the steps of the intermediate autotransfusion response, from fall in arterial pressure to restoration of pressure.
7. Explain why arteriolar constriction lowers capillary hydrostatic pressure rather than raising it.
8. State the normal hydrostatic and colloid osmotic pressures at the arterial and venous ends of a capillary, and the direction of net fluid movement at each end.
9. Explain why colloid osmotic pressure is the same at both ends of the capillary in the normal state while hydrostatic pressure is not.
10. After blood loss, which Starling pressure changes and by how much, and what is the consequence for net capillary fluid movement?
11. Distinguish the capillary pressure changes in raised venous pressure from those in low plasma albumin, and explain why both produce oedema.
12. Predict what happens to net fluid movement at the venous end of the capillary when COP falls to 15 and venous HP is 15, according to the slides.
13. List the four long-term mechanisms of volume replacement after haemorrhage, and state what each one restores.
14. Explain why reduced renal perfusion is the trigger for the long-term response.
15. Bill gives 440 ml of blood over twelve minutes and his lying BP and heart rate are identical before and immediately after donation. Explain how blood pressure can be unchanged despite the loss.
16. Ben presents with a heart rate of 150/min, BP 90/75 mmHg, a thready pulse, pale drawn face, sunken eyes and a dry shrunken tongue. Explain which of the three homeostatic responses his findings reflect, and why his blood pressure has fallen despite them.
17. Explain why Ben’s presentation includes black tarry stools and haematemesis, given the stated site of bleeding.
18. Ben’s management is IV fluids until cross-matched blood is available, then gastroscopic intervention. Explain what each of these achieves in terms of the three-tier framework.
19. Integrative: trace the fate of a haemorrhaged patient’s plasma volume across all three timescales, naming the mechanism that acts on it at each stage.

Answers

Reveal answers

1. Immediate, the baroreceptor reflex; intermediate, fluid shift from tissues to capillaries; long term, replacement of fluid and red cells.
2. Haemorrhage lowers arterial pressure, which decreases firing by the arterial baroreceptors.
3. Decreased parasympathetic discharge to the heart (SA node); increased sympathetic discharge to the heart (SA node and cardiac muscle); increased sympathetic discharge to the veins (peripheral veins); increased sympathetic discharge to the arterioles (arterioles).
4. Venoconstriction raises venous pressure toward normal, which increases venous return, which increases end-diastolic volume, which increases stroke volume via cardiac muscle.
5. Increased heart rate and increased stroke volume raise cardiac output toward normal, and arteriolar constriction raises total peripheral resistance; both cardiac output and total peripheral resistance feed into arterial pressure, so both limbs contribute to returning it toward normal.
6. Arterial pressure falls; the fall also acts via the baroreceptor reflexes to constrict arterioles; the fall in pressure and the arteriolar constriction together reduce capillary hydrostatic pressure; fluid absorption from the interstitial compartment increases; plasma volume rises; arterial pressure is restored toward normal.
7. The arterioles are upstream of the capillaries, so constricting them reduces the pressure transmitted downstream into the capillary bed, lowering capillary hydrostatic pressure.
8. Arterial end HP 35 and COP 25, giving net filtration out; venous end HP 15 and COP 25, giving net reabsorption in. Residual interstitial fluid drains as lymph.
9. COP is shown as 25 at both ends, unchanged along the capillary, whereas HP falls from 35 to 15 along its length, so the balance reverses from filtration to reabsorption.
10. Arterial end hydrostatic pressure falls from 35 to 28 (COP 25 at both ends and venous HP 15 are unchanged). Outward flow at the arterial end is reduced and venous return of fluid is increased, so the net balance shifts toward reabsorption of interstitial fluid into the capillary.
11. Raised venous pressure: venous HP rises from 15 to 30 with COP unchanged at 25, so fluid leaves the capillary at both ends and there is no reabsorption. Low albumin: HP is unchanged (35 and 15) but COP falls to 15 at both ends, so filtration at the arterial end increases. Both leave excess fluid in the interstitium, which is oedema.
12. HP 15 and COP 15 are roughly balanced, and the slide marks the net direction with a ”?”, so it does not state the answer.
13. Reduced renal perfusion causing RAA activation, retaining Na and water; ADH release, retaining water; thirst; and erythropoiesis, which replaces the red cells. The first three restore fluid volume, the last restores cells.
14. Haemorrhage lowers arterial pressure and hence renal perfusion, and it is that fall in renal perfusion that activates the RAA system to retain sodium and water.
15. The homeostatic reflexes minimise the fall in MABP; the immediate baroreceptor reflex raises heart rate, stroke volume, venous return and total peripheral resistance to hold arterial pressure at normal, and the loss is small and slow enough that no change in measured BP or heart rate results.
16. He shows a maximal immediate baroreceptor response, with marked tachycardia and a thready low-volume pulse from vasoconstriction and a low stroke volume, plus signs of fluid depletion (dry shrunken tongue, sunken eyes) reflecting the fluid shift out of the tissues. Blood pressure has still fallen to 90/75 mmHg because the bleeding is on-going, so the volume lost exceeds what the reflexes can compensate for.
17. The ulcer has eroded into a gastric blood vessel, so blood is bleeding into the lumen of the stomach; some is vomited as haematemesis and the rest passes through the gut and appears as black tarry stools.
18. IV fluids replace plasma volume immediately when the intermediate autotransfusion response is exhausted and the long-term mechanisms are too slow, holding up BP; cross-matched blood also replaces the red cells that would otherwise take erythropoiesis weeks to restore; gastroscopic intervention stops the on-going loss, without which no homeostatic response can restore pressure.
19. Immediately, plasma volume is not restored at all, and the baroreceptor reflex compensates by raising heart rate, stroke volume, venous return and total peripheral resistance. In the intermediate phase, the fall in arterial pressure plus reflex arteriolar constriction lowers capillary hydrostatic pressure, so interstitial fluid is absorbed into the capillaries and plasma volume rises (autotransfusion), diluting the remaining red cells. In the long term, reduced renal perfusion activates the RAA system and ADH is released to retain sodium and water, thirst drives intake, and erythropoiesis replaces the red cells.