Athophysiology of Post Operative Hypovolemia

 Discuss about the Athophysiology of Post Operative Hypovolemia.

1. Pathophysiology of post operative hypovolemia

Hypovolemia is a state that occurs due to blood or fluid loss in which there is a decrease in the circulating blood volume (Waugh, 2015). There are two types of hypovolemia as absolute and relative type. In absolute hypovolemia, either fluid (severe diarrhea, vomiting, diabetes ketoacidosis), blood (severe injury, major surgery), or plasma (burn) is lost (Lewis, 2014, Hinkle, 2014). In relative hypovolemia, fluid moves from the vascular space into extra vascular space as seen in internal bleeding caused by long bone fracture and ascites due to fluid stasis (Waugh, 2015, Lewis, 2014).

When the blood volume decreases below 10-20%, hypovolemic shock develops (Hinkle, 2014). In this, the vascular compartment is unchanged and only the circulating blood/ plasma volume decreases (Lewis, 2014). The physiologic consequences are same for both absolute and relative hypovolemia. Mr. Jensen underwent open reduction and internal fixation and is in post operative period with serous oozes in incision area (right leg) leading to hypovolemic shock.

Due to increased serous loss at the incision site, Mr. Jensen’s intravascular volume is reduced. This causes decreased venous return to the heart and thereby decreasing pre load. This leads to a decrease in stroke volume and also decreasing cardiac output, thus ultimately reducing blood pressure as Mr. Jensen has BP- 104/55 mmHg. This has increased his heart rate to 107 beats /minute, respiratory rate 24 breaths/ minute (Lewis, 2014). This results in decreased perfusion to cells and impairing cellular metabolism which are the hallmark signs of shock as seen in Mr. Jensen that his right leg is cool to touch and pain due to poor perfusion of legs with pain score of 7/10. His oxygen saturation was reduced to SaO2 95% and so 6 liters of oxygen was administered through Hudson mask. Paleness can occur due to poor oxygenation (Hinkle, 2014).

Due to decreased blood flow, rapid, weak and thready pulse can occur with increased pulse rate as the patient presents with heart rate of 107 beats /minute. Due to the stimulation of sympathetic nervous system, rapid and shallow breathing occur as Mr. Jensen’s respiratory rate- 24 breaths/ min. There will be weakness, decreased or absent urine output as Mr. Jensen’s output in foley IDC is >1ml/kg/hr and dilute urine, sweating, anxiety, confusion and unconsciousness (Hinkle, 2014). Decreased tissue perfusion cause hypothermia. Fluid depletion can increase thirst sensation and cause dry mouth especially in older patients as supported by a study conducted by Ahmed in 2014. Therefore for the patient, Hartman’s solution was running at 125mls/ hr through triple lumen central line situated in the right internal jugular vein.

Mr. Jensen has type- 2 diabetes for past 2 years which might also contribute for hypovolemia. His post operative blood glucose level is 17mmols/liter. He has insulin and dextrose infusion running at 2units/hr. In type 2 diabetes, insulin is produced by pancreas but the body cells will show resistance to the action of insulin (Douglas, 2012). Normally from the digested food, glucose enters into circulation. Glucose is also produced by glycogenolysis and gluconeogenesis processes. The glucose will not be metabolized due to the insulin resistance causing hyperglycemia (Ahmed, 2014). This causes glycosuria and polyuria and so the patient lands up in dehydration. The patient has foley IDC >1ml/kg/hr which is dilute. This may lead to decreased cerebral blood flow ending in coma and death (Douglas, 2012).

Due to post operative stress, sympathetic nervous system will be stimulated that leads to release of epinephrine and nor epinephrine. This increases heart rate, blood glucose and oxygen saturation thereby increasing blood pressure as the patient manifest (Douglas, 2012).

Hypovolemic shock develops, if the hypovolemia increases further. This is the most common type of shock (Vincent, 2013). About 1-2% of trauma cases develop hypovolemic shock. Basically, shock is a syndrome that occurs due to decreased tissue perfusion thereby impairing cellular metabolism and has four stages (Gaieski, 2016).

Initial stage– In this, hypoperfusion of tissue causeshypoxia. As the metabolism changes from aerobic to anaerobic, lactic acid accumulates which is harmful to cells causinglactic acidosis (Lewis, 2014).

Compensatory stage– In this stage, the body attempts to reverse the condition by using physiological mechanisms. As increased carbon dioxide acidifies the blood, the person will try to remove it and improve pH by causing hyperventilation. Hypotension stimulates the baroreceptorsin thearteries and stimulates the release of epinephrine and nor epinephrine (Lewis, 2014, Vincent, 2013). Nor epinephrine causes vasoconstriction with a mild increase in heart rate, whereas epinephrine increases heart rate and blood pressure (Gaieski, 2016).

The fluid is reabsorbed from kidneys by increasing the release of anti-diuretic hormone. The renin–angiotensin mechanism is also activated. Vasoconstriction is caused by these hormones to increase the blood flow to vital organs (Gaieski, 2016, Douglas, 2012). There will be decreased urine output due to decreased blood flow to kidneys. If the hypovolemia is corrected at this time, tissue dysfunction is reversible. Administration of blood is needed, if the loss is greater than 30% (Authority, NB, 2011). There might be a loss of auto regulation in the microcirculation causing irreversible destruction of tissues, if the loss is above 40% (Lewis, 2014, Hinkle, 2014).

3. Progressive stage: In this stage, stimulation of α- adrenergic receptors causes vasoconstriction in capillaries thereby decreasing fluid volume, activates renin-angiotensin mechanism and hypoxemia in lungs causing tissue hypoxia, anaerobic metabolism and metabolic acidosis. β adrenergic receptors are stimulated decreasing cardiac output and landing in hypoxia .

4. Refractory stage: At this stage, the vital organs have failed and the shock can no longer be reversed. Brain damage and cell death are occurring, and death will occur imminently.

2. Mr. Jensen has hypovolemic shock and features are based on that. (Douglas, 2012, Lewis, 2014)

Ineffective tissue perfusion related to decreased oxygen supply to cells and tissues as manifested by presence of severe pain in the right leg with pain score of 7 out of 10, skin of right leg is cool to touch (Walker, ‎2016). Therefore the first priority of care is to improve tissue perfusion which increases blood supply to tissues and organs.

Acute pain (in the incision site) related to poor tissue perfusion secondary to progressing hypovolemic shock as manifested by severe pain in incision site of right leg with pain score of 7 on a scale of 10 (Walker, ‎2016). This is prioritized in second position as the pain is severe and it has to be reduced to prevent shock and gain cooperation from patient for further care.

Decreased cardiac output related to decreased venous return to heart secondary to increased serous loss and reduced the intravascular volume as manifested by decreased systolic pressure- 105mmHg and decreased diastolic pressure- 55 mmHg, tachycardia with heart rate as 107 beats /minute cool, clammy skin in right leg and increased respiratory rate- 24 breaths/ min.

Ineffective breathing pattern related to poor perfusion of lung as manifested by dyspnea, use of accessory muscles. Here the patient has increased respiratory rate- 24 breaths/ minute, SaO2- 95%, oxygen administration of 6 liters through Hudson mask.

Impaired gas exchange related to hypoxemia in lung as manifested by SaO2- 95%, pulse rate- 104 beats/ min and respiratory rate 24 breaths/ min, skin in right leg is cool to touch.

Deficient fluid volume related to post operative blood loss as manifested by poor skin turgor (Walker, ‎2016), patient with Hartman’s solution running at 2ml/hr. The patient has fluid volume deficit as he underwent surgery and is in post operative period. He might have lost more blood and fluid at the time of surgery and also has serous ooze with swelling in the fracture site and pin site of right leg.

Impaired skin integrity related to surgical incision as manifested by presence of incision in right leg with serous ooze.

Anxiety related to severity of condition as manifested by patient verbalization of fear and anxiety, increased respiratory and heart rate.

Risk for infection related to surgical incision.

Potential complication for organ ischemia/ dysfunction related to decreased tissue perfusion. As the patient is hypovolemic shock, the patient may land up in ischemia of vital organs causing multi organ failure.

3. Jensen will maintain adequate tissue perfusion as evidenced by absence of pain in the right leg with pain score of 0 out of 10, normal skin temperature, normal vital signs (Douglas, 2012).

Jensen will remain free from pain as evidenced by absence of pain and pain score of 0 out of 10, stable vital signs, increases activity gradually, relaxed facial expression, restlessness decreased (Lewis, 2014).

Jensen will maintain sufficient cardiac output as evidenced by strong pulse, stable vital sign, absence of dyspnea, warm and dry skin sufficient oxygen saturation (Douglas, 2012).

Jensen will maintain effective breathing pattern as evidenced by normal respiratory rate and rhythm, proper oxygen saturation of tissues, synchronous thoraco abdominal movement (Hinkle, 2014).

Jensen will have optimal gas exchange as evidenced by clear lung sounds, patent airway, good oxygen saturation level, nail beds and membranes pink, capillary refilling within 2 seconds, oriented to person (Douglas, 2012).

Jensen will be able to maintain adequate circulating blood volume and fluid volume as evidenced by good skin turgor, normal blood pressure, stable weight, balanced intake and output chart (Lewis, 2014).

Jensen will have improved skin integrity as evidenced by good healing of the incision site, absence of ooze from the site (Hinkle, 2014).

Jensen’s anxiety will be relieved as evidenced by relaxed facial expressions, calm and confident, verbalization of positive attitude (Lewis, 2014).

Jensen remains free from infection as evidenced by absence of ooze from surgical site (Douglas, 2012, Hinkle, 2014).

Jensen will not develop organ ischemia/ dysfunction as evidenced by lack of deviations from acceptable parameters (Lewis, 2014).

4. Jensen will be able to maintain adequate circulating blood volume and fluid volume as evidenced by good skin turgor, normal blood pressure, stable weight, balanced intake and output chart. (Lewis, 2014, Davis, 2014).

A nurse should assess for skin turgor, sunken eyes, dry lips, increased pulse and respiration as these are indicators of fluid volume deficit. Assess for dry mucous membrane and thirst to understand dehydration. Increase oral fluids to restore fluid loss.  Maintain intake and output chart daily to monitor the fluid status (Davis, 2014). Monitor serum electrolyte levels to note for abnormalities and to be reported to the physician.

As the patient is in progressive stage of hypovolemic shock with altered vital signs as heart rate of 107 beats/ minute, respiratory rate 24 breaths/ minute, blood pressure- 104/55 mm Hg, monitor vital signs every 4th hourly. Check weight of the patient daily as decrease in weight indicates fluid loss and to monitor fluid status. A nurse should administer fluid and electrolytes through intra venous catheters to maintain the fluid status. 

In hypovolemic shock, the first main intervention is to restore fluid volume so as to increase blood pressure (Bougle, 2013).  Administer intravenous fluids as ordered to compensate the fluid loss (Naren, 2011). Administration of colloids causes rapid plasma expansion due to increase in oncotic pressure and quickly maintains circulation (Bougle, 2013).  But few studies suggest that even though crystalloids are cheaper, they are more effective than colloids. A study reported that patients with trauma or in post operative period, there is no evidence that colloids are more effective than crystalloids (Bougle, 2013). 

A study suggests that administration of albumin was safe for fluid resuscitation for post operative patients (Perel, 2011). James in 2011 has compared 0.9% saline with hydroxyethyl starch in patients with penetrating injury and surgeries and suggest that these patients require >3 liters of fluid resuscitation. Hypertonic saline infusion is very important in case of hypovolemic shock (Burgler, 2011). Administer 0.9% normal saline and Ringer lactate. This fluid remains in intra vascular space and increases intravascular volume (Kayilioglu, ‎2015). In 2011, Haut suggests that intravenous fluid administration during pre hospital time increasing mortality in trauma patients.

Ringer lactate solution should be administered cautiously in all shock patients as in case of progressive shock, liver cannot convert lactate to bicarbonate. Blood should be administered, if the patient doesn’t respond to IV fluids cautiously (Authority, NB, 2011, Duan, 2015). An indwelling bladder catheter should also be inserted to monitor fluid status.  Instruct the patient take 3L of fluid/ day to replace the lost the fluids and electrolytes in the serum (Duan, 2015).

Mr. Jensen will not develop organ ischemia/ dysfunction as evidenced by absence of parameter deviations (Lewis, 2014, Hinkle, 2014).

Neurologic ischemia– perform neurological assessment and monitor the level of consciousness, orientation to time, place and person, memory and intellectual capacity once in every hour to understand the cerebral blood flow status (Louis, 2015). Note for any changes in patient’s behavior. Provide safe environment to protect confused patients from injury. Provide a noise free environment and allow taking rest (Hinkle, 2014).

Renal ischemia– monitor for signs of renal ischemia as this most often occurs in case of hypovolemic shock and multiple organ failure (Joseph, 2011). Monitor intake output daily to note for decrease urine output which indicates progressive renal ischemia. Send samples for examination of specific gravity, blood, sodium and albumin in urine. Monitor serum BUN, creatinine levels, and electrolytes level to assess renal function (Davis, 2014). To accurately measure urinary output, insert bladder catheter. Check weight daily to monitor fluid status and evaluate renal function (Lewis, 2014). Administer fluids as ordered to maintain adequate renal perfusion. Monitor for fluid overload to identify for over treatment. Note for renal parameter deviations.

Gastro intestinal ischemia: monitor for presence of gastro intestinal ischemia. Monitor for presence of abdominal pain, distention, nausea, vomiting, anorexia, diarrhea, thirst to know the gastro intestinal status (Daniel, 2016). Auscultate bowel sounds every 4th hourly to note for changes. Monitor weight daily to know the fluid balance. Start enteral nutrition to meet the nutritional needs. If ordered administer parenteral nutrition quickly to meet the metabolic demands.

Peripheral Vascular ischemia– Monitor for presence of cool, clammy skin. Assess for cyanosis especially in extremities to rule out ischemia. The peripheral pulse should be checked. Assess for tingling and numbness necrosis and gangrene in extremities. Note for deviations in peripheral perfusion to plan treatment modalities. Check the capillary refill once in every 15 minutes. Assess the intensity, severity of pain which indicates progressive vascular ischemia (Lewis, 2014). Maintain the properly by following all the skin measures to prevent pressure ulcers and maintain skin integrity (Hinkle, 2014). Keep patient warm and dry to prevent vasoconstriction.

Respiratory ischemia– Monitor for the use of accessory and abdominal muscles for respiration to know the respiratory status. It is a major type of ischemia (Louis, 2015). Monitor for rate, rhythm and depth of respiration. Note for dyspnea and cyanosis to assess for respiratory distress (Lewis, 2014). Auscultate the breath sounds for crackles, wheezes and unequal breath sounds to note for fluid accumulation. Take ABG samples to monitor gas exchange and acid base balance (Davis, 2014). Instruct the patient to practice deep breathing exercise to improve gas exchange. Bougle in 2013 suggested that oxygen should be administered until the bleeding stops (Bougle, 2013). Suction if needed to remove secretions.


Ahmed, (2014). The pathophysiology of fluid and electrolyte balance in the older adults- surgical patient. vol:33(1). 6-13 doi: 10.1016/j.clnu.2014.Authority, NB Australia. (2011). NBA – patient blood management guidelines:

module 1 – critical bleeding massive transfusion. Retrieved from, A. (2013). Resuscitative strategies in traumatic hemorrhage shock. Retrieved from www.>PMC3626904.Bulger, E. (2011).

Out-of-hospital hypertonic resuscitation after traumatic hypovolemic shock: a randomized, placebo controlled trial: Ann Surg. 3:431–441. doi: 10.1097/SLA.0b013e3181fcdb22.Daniel, G. (2016). Mesenteric Ischemia: The New England Journal of medicine.

Medical Surgical Nursing: Assessment and Management of Clinical Problems. (9th ed.). Missouri: Mosby. Louis, R. (2015). Vertebrobasilar Ischemia and Hemorrhage. Retrieved from jOAhULgI8KHS5 ABIIQ6AEIUzAI#v=onepage&q=respiratory%20ischemia&f=falseNaren, C.T.


Review of fluid resuscitation and massive transfusion protocols. Retrieved from www. defence.>health>adfh_2011.Perel, P. (2011). Colloids versus crystalloids for fluid resuscitation in critically ill patients: Cochrane Database Systemic Review. 3. › PubMed 21412866Vincent, J.L. (2013). Circulatory shock: National England Journal med. oct: 369 (18): 1726- 34 PMID 24171518.Walker, J.A. (‎2016). 

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