The Cardiovascular System

at a Glance

Fourth EditionPhilip I. Aaronson, Jeremy P.T. Ward & Michelle J. Connelly

Case Studies

Case 6 – Haemorrhage and shock

You are a casualty officer in a busy department in the late evening. A young man comes in supporting his friend; he gives his name as John, and that of his friend as Bill. He is very worried about Bill, who he says was hurt when they were involved in a traffic accident. Bill’s legs are covered in blood from a wound in his thigh, which has been inexpertly bandaged. He also has a livid bruise on his forehead. John appears very pale, nervous and uncomfortable, and is evasive about the accident; it is not clear how long ago this occurred, although he implies that it was within the last half hour. Both John and Bill smell of alcohol, and although John says they are 18 years old, they both look a couple of years younger. You suspect they may have been joy-riding. While you are uncovering Bill’s wound, John says he feels dizzy and nauseous; you suggest he goes out and sits in the waiting room.

Bill is conscious, but unable to stand unsupported and is only partly coherent. When you get him lying on the trolley you find his skin is pale and clammy, his pulse rate 110 beats/min, and his blood pressure 110/70 mmHg. He has a raised respiratory rate. On investigation, you find that the wound is not as serious as it appeared, although there has clearly been significant blood loss. You decide that blood transfusion is required, and take a blood sample for cross-matching and measurement of haematocrit. The blood tests reveals a haematocrit of 0.43, which does not reassure you, and an AB blood group. Within an hour of transfusion Bill becomes coherent, his pulse falls to 95 beats/min, and his blood pressure is 115/80 mmHg.

  • (a) In Bill’s case, what symptoms and signs should alert you to hypovolaemic shock? (b) What are they caused by?

    Note: Refer to Chapter 29 for all answers. (a) and (b) The loss of blood is obvious, but the cold clammy skin, high heart rate and confusion are strongly suggestive of cardiovascular shock. Reduced blood volume will lead to activation of the baroreceptor reflex which may allow blood pressure to be maintained by vasoconstriction and diversion of blood from the periphery and splanchnic circulations. Sympathetic activation of the skin also causes sweating, and thus the clamminess. If the fall in blood pressure is sufficient, reduced blood flow through the carotid bodies would cause chemoreceptor activation and an increase in rate of breathing, although in this case it may be just anxiety. Reduced blood flow also causes acidosis which will similarly activate the chemoreceptors. The disorientation, especially initially when standing, could be due to reduced cerebral perfusion and consequent hypoxia, but the bruising to the forehead might indicate some concussion.

  • (c) Why are you not reassured by Bill’s haematocrit? Why might you suspect that the accident happened rather longer ago than John said?

    Bill’s haematocrit is towards the bottom of the normal range for males (0.43 compared to the normal value of 0.47). He could be normally slightly anaemic, but this might reflect haemodilution due to movement of fluid from the tissues into the blood (internal transfusion). As the latter takes place over a few hours, this would suggest that the accident occurred at least a couple of hours ago. He may also have drunk a lot of fluids. It is likely that Bill and John delayed coming to the hospital because they were afraid of being caught for joy-riding and drunk-driving.

  • (d) What blood group could be used for Bill’s transfusion, and why?

    Bill’s blood group is AB, and as his red blood cells therefore have both A and B antigens (agglutinogens), he has no antibodies (agglutinins) to either. He can therefore receive blood of any group. People of group AB are often called universal recipients, and those of group O universal donors. However, in massive transfusions agglutinins in the donor blood could reach a level to cause problems, and close matching is required unless these have been previously removed.

  • (e) What did you omit to do concerning John?

    John was also involved in the accident. You initially noted he was pale and obviously uncomfortable, and soon after he said he felt dizzy and nauseous. As a minimum, you should have asked whether he had suffered any injury himself. It later transpires that he has also lost a significant amount of blood to internal bleeding; early correction might well have prevented the later complications.

  • Bill asks for John so he can call his family. However, when the nurse goes to the waiting room she finds that John had kept asking for water and then became abusive; security, believing him to be drunk, had escorted him outside and told him to go home. An hour later a young man is brought in having been found looking very ill on a bench by the bus stop. It is John. He is very disorientated, his skin is cold and clammy, and he has abdominal discomfort. His heart rate on the trolley is 115 beats/min, and his blood pressure 100/70 mmHg. When helped to stand his blood pressure falls to 85/40 mmHg and he faints. His haematocrit is 0.44. You are unsure of the diagnosis, so he is admitted overnight for observation.
  • (f) Why was John so thirsty? Why might security have thought he was drunk?

    (See Chapter 27) Activation of the baroreceptor reflex leads to increased activity of renal sympathetic nerves, and therefore release of renin and consequently increased production of angiotensin II. The fall in blood volume and reduction in atrial stretch receptor activation may also have been sufficient to cause increased production of antidiuretic hormone (ADH). Both ADH and angiotensin II are strong stimulators of thirst.

    It is clear that John’s cardiac output and blood pressure must have been low, leading to insufficient cerebral perfusion and consequent hypoxia. This would impair cognitive function, leading to behavioural differences, slurred speech and unsteadiness – not dissimilar to the effects of alcohol. Moreover, it is clear that he had been drinking as he smelt of alcohol.

  • (g) Why might John’s blood pressure fall so much on standing?

    (See Chapter 25) John’s blood pressure and central venous pressure when lying down are being maintained by the baroreceptor reflex, peripheral vasoconstriction and venoconstriction. On standing, blood pools to the legs and because the baroreceptor reflex is now unable to provide any further support for central venous pressure, cardiac output falls due to Starling’s law of the heart, and consequently so does blood pressure. He faints because this is insufficient to maintain adequate cerebral perfusion.

  • The next morning Bill has recovered well. John, on the other hand, still has a raised heart rate, and his haematocrit has fallen to 0.35. He has not passed any urine. A CT scan reveals an accumulation of more than 2 L of blood in the peritoneum, and subsequent surgery a torn peritoneum and renal artery. On the recovery ward John’s blood pressure is shown to be 120/80 mmHg, but you remain concerned, and place him under ongoing observation.
  • (h) Why did John’s haematocrit fall, and why was he not passing any urine?

    (See Chapters 18 and 27) A fall in capillary pressure due to a generalized arterial vasoconstriction will reduce the hydrostatic pressure, so that the plasma oncotic pressure due to proteins now predominates, with the result that fluid moves from the interstitial space into the tissues (internal transfusion). However, this will cause haemodilution, and so reduce the haematocrit. Urine production is severely reduced because vasoconstriction of the renal afferent arterioles, activation of the renin–angiotensin axis and increased production of ADH reduce renal filtration and increase reabsorption of Na+ and water.

  • (i) Why are you concerned about John, considering his blood pressure has recovered and his urine output is improved?

    In view of the volume of blood loss and the delayed treatment, John would need ongoing observation to exclude underlying ischaemia in other organs. Typically, the gut is most affected by this type of ischaemia, which then allows translocation of bacteria from the bowel to the blood, causing sepsis that can then cause multiorgan failure (MOF) and irreversible shock. However, it would be unusual for a young man to go into MOF this quickly (although less so in a 75-year-old man). MOF usually occurs after some time in intensive care.

  • John’s urine output, which partially recovered after the operation, gradually decreases and after 8 hours ceases. He shows some signs of oedema. Acute renal failure is diagnosed, and he is put on a regime of low fluid, salt and protein intake to reduce accumulation of toxins. While Bill is discharged the following day, John’s renal function takes 3 days to recover, and he remains in hospital for more than a week. It is several months before he is well enough to return to work.
  • (j) What might have caused the acute renal failure?

    Prolonged activation of the sympathetic system with vasoconstriction of the renal circulation can lead to renal ischaemia, and ‘acute renal necrosis’. The renal medulla is particularly sensitive to ischaemia and hypoxia, as the counter-current system of the vasa recta means that the PO2 of the deep medulla is relatively hypoxic even under normal conditions. In acute renal necrosis function normally returns in 3–21 days; renal replacement therapy (dialysis or haemofiltration) might be necessary if function was still impaired after 4–5 days.

  • (k) Why might he develop oedema, and why would it take a few days to recover?

    (See Chapter 19) Prolonged vasoconstriction can lead to peripheral ischaemia and raised metabolites, damaging the vascular endothelium and causing it to become leaky to plasma proteins. Movement of these proteins into the interstitium would reduce the net oncotic pressure across the capillary wall, leading to fluid loss to the tissues. If he received saline instead of blood or plasma during the operation, the resulting haemodilution and thus decreased plasma protein concentration would also reduce oncotic pressure and thus lead to fluid loss to the tissues. Plasma proteins are synthesized in the liver, and it takes around a week for normal levels to be restored.

  • (l) How long will it take for John’s haematocrit to return to normal?

    (See Chapter 6) About 3 weeks, due to increased erythropoietin and thus erythropoiesis. Concluding remarks. This case emphasizes the need for suspicion of internal injury and blood loss following trauma. Both the amount and rate of blood loss are important. A very rapid loss of 30% can be fatal, where 50% over 24 h may be survived. The risk of developing irreversible shock is drastically increased if treatment is not initiated within the ‘golden hour’ after major haemorrhage.

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