Hypovolaemic Shock: Term Definition - Special Academic Support

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The four features

Reduction in intravascular volume is classified as a hypovolaemic shock (Urden et al, 2006). Low blood pressure, hypoxemia, reduced urine output, and raised pulse rate are features of hypovolaemic shock. Hypovolemic shock is an emergency condition in which severe blood and fluid loss makes the heart unable to pump enough blood to the body (Hypovolaemic shock, NIMH).

Feature 1 Decreased blood pressure 90/60 mm Hg. (Normal 120/80mm Hg.)

Decreased BP is due to the loss of intravascular volume. The blood loss in this study is 600 ml. which comes to about 40% of circulating blood (Newberry and Criddle, 2005). By Newberry and Criddles classification, the blood volume lost, the decreased BP, the urine output, and the cold clammy skin of John are features of Class III while the heart rate and respiratory rate belong to Class II. John could have a Class II hypovolaemic shock progressing to Class III.

Feature 2 Hypoxaemia SpO2 is 92% on room air (Normal 95%-100%).

Hypoxaemia is evident from the data. The loss of intravascular volume reduces the saturation of oxygen in the blood. To facilitate adequate perfusion and thereby increase the oxygen saturation, the body systems that participate to compensate for the loss of intravascular volume are the sympathetic nervous system, renal system, and endocrine mechanisms. John appears to be in the compensatory phase. This phase has origins at the cellular level. With the lesser intravascular volume and oxygen transported, the tissues involved become impaired. The anaerobic glycolytic metabolism is reduced in impact, resulting in excess lactic acid production causing metabolic acidosis. Oxygen supplementation helps in reversing the process.

Feature 3 Decreased urine output 15ml. in last hour (Normal is 1500-2000ml/day.)

A urine output of less than 30 ml. per hour is considered abnormal and requires interventions. The compensatory endocrine response is to stimulate the posterior pituitary so that ADH is released to conserve the intravascular volume. The renin-angiotensin is activated when the renal perfusion is reduced and the sympathetic nervous system is stimulated. Angiotensin I will be stimulated when renin is released. The angiotensin I will then get converted to angiotensin II by the action of the ACE within the lungs. Vasoconstriction of the arteries occurs; simultaneously the adrenal cortex releases aldosterone by preventing the release of sodium and water. Urine output is thus reduced. Both procedures raise the blood pressure towards the end of the development of shock. The increased pulse rate increased respiratory rate and restlessness, and blood pressure changes are features of the compensatory stage of hypovolaemic shock.

Feature 4 Increased heart rate 120/mt. (Normal 72-80/mt).

The sympathetic nervous stimulation causes the adrenal medulla to be stimulated to release adrenalin and noradrenalin. Thereby alpha, beta one, and beta two receptors are activated. The alpha receptors found in abundance in the coronary muscle, skeletal muscle, pulmonary arterioles, abdominal viscera, and renal arterioles produce vasoconstriction. The beta two receptors in the same regions when activated produce vasodilatation. The myocardial contractility produces an increased heart rate. The action produced in the lungs causes a higher respiratory rate. Cardiac output and BP are simultaneously raised. Cardiac output is decreased when there is a lesser pre-load or lesser oxygen-carrying capacity.

The respiratory alkalosis and the hypoxemia further confirm the compensatory phase.

Three interventions before the next surgery

The interventions before the second operation concern the reversal of the shock and preventing the progression, ensuring cardiovascular stability, and maintaining the optimal tissue perfusion. Here the cause is the drainage of 600 MLS. of bright red haemoserous fluid through the UWSD and thereby the loss of intravascular volume. Stopping the bleeding from the site of surgery is of utmost necessity. Subjecting the patient to another surgery is the only positive move to remove the causative problem. The patients condition has to be stabilized before the primary aim of correcting any leakages at the surgery site. Reversing the shock is essential as multiple organ failure is a possible outcome for hypovolaemic shock (Kolecki, 2009).

Knowing more about the physiology and the pathology of bleeding helps one to understand the reasons for the interventions for hypovolaemic shock (Kolecki, 2009). The coagulation mechanism in the haematologic system is triggered by severe blood loss. Meanwhile, the vessels which are bleeding save blood loss by vasoconstriction and activation of thromboxane A2 release. Platelets are activated to form an immature clot. Collagen will be extruded from the damaged vessel and go onto the fibrin deposition. The clot matures within 24 hours (Kolecki, 2009).

Reversing the shock

John may be positioned well by allowing him to lie flat on his back but with the head and legs slightly elevated. The Trendelenberg is not opted for as more blood loss is possible from the wound site. Intracardiac catheterization, fluid resuscitation, and oxygen supplementation constitute the main interventions in John prior to the surgery for correction of the bleeding from the surgical site.

Intervention One

An intracardiac catheter may be inserted and connected to the USWD to recirculate the lost fluid so that the volume being lost is minimal. The catheter also allows the measurement of the blood pressure within the heart chambers and the rate of blood flow in the heart. The significant reason for its use is that it can detect abnormalities of the heart too.

Medication can also be administered through the ICC into the coronary vessels with the assistance of tomography (Mosbys Medical Dictionary, Elsevier). The intervention is performed by the cardiologist. This move would reduce the loss of blood volume. Drainage of the haemoserous fluid would decrease and be observed by the nurse. The decrease in the drained fluid would suggest an improvement in the situation to the nurse. An increase would suggest a worsening of the situation. Similarly, the blood pressure rise would suggest an improvement and a falling pressure would mean that the situation is worse.

The patient may be having hypothermia. He must be kept warm so that his temperature is 360C. The hypothermia at mild status may be corrected by removing wet blankets and using a warm one instead. Wet materials may be removed. The hypothermia is moderate when the temperature is between 32- 340C and severe when it drops below 320C.

Active external methods may be used here: a space blanket, warm fluids, a bear hugger, and a headcover. The nurse would be able to detect the temperature by clinically measuring it with a thermometer. A temperature below 340C is suggestive of hypothermia.

Pain in the post-operative period can be managed by administration of opioids, NSAIDs(nonsteroidal anti-inflammatory drugs), local anesthetic agents, or inhalation agents. Morphine, an opioid, is the best and first line of treatment for pain (Pillai and Neal, 2004). It is carefully titrated to the response and as necessary by the patient. Johns pain is a perioperative breakthrough pain that is caused by movement treated by drugs with rapid onset and short duration of action. The intravenous person-controlled analgesia is effective for John. Postoperative complications and morbidity are reduced by the effective management of acute perioperative pain (Pillai and Neal, 2004). Pain causes the release of stress hormones and catecholamines which in turn causes stress on the heart functions.

Intervention two: Supplemental oxygen

Maintaining optimal tissue perfusion of vital organs is essential (Nolan, 2001). A patent airway is maintained. Oxygen supplementation must be actively done with observation. The oximeter would be observed to monitor the oxygen saturation of the supplemental oxygen given. The arterial oxygen (PaO2) should be maintained at 85mm Hg. The cardiac output and the content of oxygen in the arterial blood and the saturation of hemoglobin with oxygen determine the oxygen delivery (Parillo and Dellinger, 2001). During hypovolaemia, the saturation of hemoglobin for a given partial pressure can be observed from the oxyhemoglobin dissociation curve as the hypovolaemia gets corrected. A decrease in cardiac output reduces oxygen delivery to the tissues producing focal ischemia. The critical oxygen delivery is 8ml/kg./min. in humans. When this is reduced in hypovolaemia, anaerobic metabolism takes over and leads to lactic acidosis in the blood (Parrillo and Dellinger, 2001). The body needs critical oxygen delivery. This is raised in hypovolaemic shock because of increased respiratory muscle activity and increased catecholamines. The nurse is the person who is responsible for the oxygen delivery.

Taking care to alleviate fear and emotional anxiety helps in improving the situation of tissue perfusion by reducing the stress hormones circulating. Showing concern and respecting the patient would provide confidence in meeting the crisis and allay the impending doom. The soothing effect of calm and pleasant facies is undeniably reassuring to the patient. Any new equipment or procedure must be explained in due detail so that he knows what is happening. His family members must be informed about the procedures being adopted. The nurse observes the oximeter and notes the oxygen saturation level improving as the shock is reversed. The systolic blood pressure rises and the pulse becomes normal in rate and volume. These are indications that the nurse observes to understand that the shock has been reversed and the patient would become more stable with the halt of the progression in the compensatory phase of shock.

Intervention Three: Fluid Resuscitation

Fluid resuscitation also helps the tissue perfusion and reverses the shock. The type of fluid selected will depend on the situation. Some prefer Hartmans solution while others prefer colloids (Shafi and Kauder, 2004). The studies of Pryke (2004) and Moore et al (2204) have shown that there are no real reasons to select either. Crystalloid solutions are the choice volume expanders: blood and blood products are used in people who have hemodynamic instability especially when bleeding is proceeding or ongoing. Sisson (ITIM) has also said the same thing. Stammers et al advise the use of rapid infusion devices and autologous transfusions if the loss is speedy and enormous (2005). Their study used two systems for performing the rapid infusion and found that the Myocardial Protection System was better with more safety features. The complications of hypothermia, coagulopathy and abdominal compartment syndrome are associated with massive infusions (Shafi and Kauder, 2004). It is essential to detect loss of circulating volume before it turns the condition of the patient into a critical one but it is a difficult proposition (Diprose and Sleet, 1993). If 0.9% Normal saline is used it has to be given carefully infused to avoid metabolic acidosis. Fluid resuscitation must be done to revive the vital signs and normal ABG results. If ABG results are not available, the normal mental status, the normal heart rate, skin perfusion, normal urine output, and systolic blood pressure at 80-90 mm. Hg. are the indicators (Sisson, ITIM). Human albumin solution is known to be used as a volume expander in critically ill patients but Alderson and his team found that this idea may not be right after all as concrete evidence has not been obtained: moreover, albumin is costlier than other crystalloids and colloids (2002). The nurse can identify whether fluid resuscitation has been achieved by observing the urine output and blood pressure.

Drug therapy to increase tissue perfusion is done after the fluid resuscitation is started. The decreased tissue perfusion should be instituted to increase the perfusion to show a MAP of more than 60mm Hg. Positive inotropes adrenaline, dopamine, or dobutamine may be administered. The vasopressor action of adrenalin and noradrenaline also may be resorted to but they are believed to cause tissue ischemia. They may be used if fluid resuscitation is not successful (Mullner et al, 2004). Mullner and his team conducted randomized trials of eight studies to determine the role of vasopressors in the treatment of shock. They could not however gain conclusive evidence to support their idea.

References

Alderson et al, (2002). Human albumin solution for resuscitation and volume expansion in critically ill patients Cochrane Database Systematic Review, (1), CD001028 Pubmed.

Cardiac catheter.

Diprose, P. and Sleet, R.A. (1993). How well do doctors resuscitate patients with haemorrhagic shock. Arch. Emergency Medicine, Vol. 10 (3), p. 135-137.

Hypovolaemic shock.

Kolecki, P. and Menckhoff, C.R. (2009). Hypovolaemic shock.

Moore, F.A., McKinley, B.A., Moore,E.E. (2004). The next generation in shock resuscitation. Lancet, Vol.363 (9425), p. 1988-1996.

Mullner, M. et al, (2004). Vasopressors for shock. Cochrane Database Systematic Review, (3), CD003709 Pubmed.

Newberry, L, Criddle, L.M. (2005). Sheehys Manual of Emergency Care 6th ed. Elsevier, Philadelphia. pp.362.

Nolan, J. (2001). Fluid resuscitation for the trauma patient. Resuscitaion, Vol. 48(1), p. 57-49.

Parillo, J.E. and Dellinger, R.P. (2001). Critical care medicine: principles of diagnosis and management in the adult Gulf Professional Publishing, 2001.

Pillai, P. and Neal, R. (2004). The management of perioperative pain in (Eds. ) Core topics in perioperative medicine by Jonathan Hudsmith, Dan Wheeler, Arun Gupta, Cambridge University Press.

Pryke, S. (2004). Advantages and disadvantages of colloid and crystalloid fluids. Nursing Times, Vol. 100 (10), p. 32-33.

Shafi, S. and Kauder, D.R. (2004). Fluid resuscitation and blood replacement in patients with polytrauma. Clinical Orthopaedic Related Research, Vol. 422, p. 37-42.

Sisson, G., Hypovolaemic shock: Adult trauma clinical practice guidelines. Institute of Trauma and Injury Management.

Stammers, A.H., Murdock, J.D. and Klayman, M.H. et al, (2005). Utilisation of rapid infuser devices for massive blood loss. Perfusion, Vol. 20, No.2, p. 65-69, Pubmed.

Urden, L., Stacy, M. & Lough, M. (2006). Thelans Critical Care Nursing 5th edition. Mosby. St.Louis.

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