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Causes and Effects of Hypovolemic Shock

Question:

Discuss About The Effects Of The Shock On Different Systems?

Patient Maureen, 77 years old an Australian woman. Presents with what seems to be in the progressive phase of hypovolemic shock. The symptoms she presents are as a result of the effects of the shock on the different systems. The respiratory, nervous, cardiovascular, renal and hepatic systems. The breathing is at 28 breaths per minute. This breath must be shallow as the saturation level of oxygen is undetectable. The heart rate is at 120 beats a minute. Despite this high beats the systolic blood pressure is at 80mmHg. There is evidence of vasoconstriction on the skin as the capillary fill lasts more than 4seconds. This is a classical evidence of shunting as the blood flow is redirected to other vital organs. She presents with hypovolemia. The hemoglobin levels are below average. The blood cells are also below the average. She has signs of ascites and vomits blood which is a huge contributor of fluid volume deficiency. The vomiting is as a result of ulcers on the gastrointestinal as a result of the vasoconstriction. She is also on diclofenac which worsens the ulcers because of its pharmacodynamics. She is pale and unconscious all this points to hypovolemic shock.

Brunner and Saddarth (2013), states that around 60% of an adult’s body weight is composed of fluids, that is, water and electrolytes. This amount is not fixed. It ranges from one person to the other. Gender, age, and body fats are some of the factors that determine the amount of body fluid.  Lewis et al (2014), from the book it has been researched and proven that men have more body fluids that women, Young people has more fluids when compared with old people and the obese people have less water.  (Sloan 2013), According to the book, the body fluids are located in two compartments. The intracellular fluid, that is, the fluid in the cells and the extracellular space. Barret et al (2017), further classifies this compartment. According to them, the intracellular holds two-thirds of the fluids while the extracellular holds the remaining third. They go on explaining that the extracellular fluid is further divided into interstitial, intravascular and trans cellular fluids.

The fluid volume is maintained by the body. The body is equipped with mechanisms to help it balance the fluids. The homeostasis mechanisms. These include the kidney function. The heart and blood vessels function, lung functions, pituitary function, renin angiotensin aldosterone system, parathyroid function, Anti-diuretic hormone and thirst, baroreceptors and the osmoreceptors. These mechanisms ensure that there is a fluid balance because if this balance gets altered it can cause a lot of harm.

Stages of Shock and Manifestations

Brunner and Saddarth (2013), explains that hypovolemia or fluid volume deficit takes place when extracellular fluid volume loss exceeds the volume of the fluid intake. The water and the electrolytes are lost in the same proportion making a deficit in both the extracellular and the intracellular.  Marcin (2016), adds that there is a difference between dehydration and hypovolemia. In dehydration, water is the only thing lost. Fluid volume deficit is accelerated with decreased intake of water. Causes of fluid volume deficit other than inadequate water intake include; vomiting, sweating, diarrhea, gastrointestinal suctioning, Beck, (2015). If the homeostasis mechanisms, for example, the kidney functions are impaired due to a disease, this could cause the fluid volume deficit. A patient with fluid volume deficit has the following presentations: they have an acute weight loss, their skin turgor is decreased, they have oliguria, this small amount of urine is highly concentrated, they present with hypovolemia, their heart rates are fast but weak, the neck veins are flattened, they have increased temperature, their central venous pressure is decreased, they are cool, they have clammy skin due to the vasoconstriction of the vessels peripherally, they are thirsty have muscle cramps and weakness. If this condition is not reversed it can worsen and cause shock which in turn causes death.

Mikhail (2015), Defines shock as a condition that is life threatening. It is usually as a result of inadequate perfusion of tissues. If untreated it causes death. The systemic blood pressure is unable/inadequate in delivering the required amount of oxygen and nutrients to enhance cellular and vital organ function, Balk (2015), Inadequate perfusion ( inadequate oxygen and nutrients), this causes cellular starvation, this progresses to cell death, in turn it causes organ dysfunction which progresses to organ failure and later on death. As mentioned shock is fatal. It progresses rapidly or slowly and it affects all body systems.

Jindal et al., (2014), hypovolemic shock is the most common which results in a decrease of 15%-25% of intravascular volume. As mentioned earlier intravascular fluid represents the blood which is an extracellular fluid. The percentage will present a loss of 750 ml to 1300ml of blood given that in a normal physiological man weighing 70kgs has 5lts to 6lt of blood. Hypovolemic shock can be caused by external fluid losses. This could be a traumatic loss of blood (internal bleeding, a wound, GIT bleeding) or internal fluid shift which could be as a result of severe edema, severe dehydration, ascites. Rauen and Munron, (2016), they vividly explain how hypovolemic shock occurs. It starts when there is a deficit in the intravascular fluid. This deficit causes a decrease in the venous return. Due to this reduction, there is a reduced ventricular refilling which in turns causes a reduction in stroke volume and cardiac output. When this happens the blood pressure drops. This compromises the tissue perfusion which progresses to death. The manifestation of the patient depends on which stage they are in.

ISBAR and Interventions

Through the assessment of airway, breathing, circulation, disability and exposure, there are three stages of shock. All systems are assessed. The cardiovascular; that is the systolic blood pressure and the heart rate. The respiratory system checks the breathing rate. The skin for warmth and liver function. The kidney functions. All this are checked up and the findings helps categorize the patient. The first stage is compensatory. The body tries to normalize the fluids. At this phase, the body displays the normal fight or flight response. The heart rate increases, vasoconstriction occurs, the hearts contractility increases, there is a shunt of blood flow to other organs. Blood is redirected to the vital organs, that is, the brain, liver, and kidney. This makes the patients skin feel cold and clammy. The patients’ blood pressure is normal at this stage, heart rate is above 100 beats per minute, the respiratory rates is above 20breaths per minute, there is reduced urinary output, the patient is confused, laboratory findings reveal respiratory alkalosis. At this stage, the body does its best to have a homeostasis. If it is not restored the shock progresses to the next phase which is the progressive stage. Abraham et al., (2015), at this stage the body systems are unable to maintain the blood pressure. The blood pressure falls beyond the average range of the systolic blood pressure. It falls beyond 90 mm Hg. The manifestation of shock at this stage is usually due to two things. One the overworking heart becomes dysfunctional hence poor/ no perfusion to the muscles. This brings about ischemia. Two, the microcirculation auto regulatory function fails because of the biochemical mediators. This makes the venous and arterioles to constrict making the perfusion poorer, Kumar and Haery (2014). The systolic blood pressure is below 80mmHg. The heart rate is above 150beats per minute. The breathing is shallow, rapid and with crackles. The skin has petechial and is mottled. The urinary output is 0.5ml/kg/hr. The patient is lethargic. Lab findings reveal metabolic acidosis. This is the stage where patient Maureen is at. Airway is being compromised by the nervous system as she is semiconscious. Breathing rate is very high although the breaths are shallow. Circulation is not normal as the capillary refill time has lengthen, skin is pale and cold and systolic pressure is at 80mmHg. Disability the patient is at risk of death as circulation and breathing has been compromised. Exposure, her organ are exposed to death if this stage is not reversed. If this stage is not reversed the patient progresses to irreversible phase. At this stage, the cell damage is so severe. The patient is not responsive to any treatment. The patient cannot survive. The patient presents with jaundice due to liver failure. They require mechanical or pharmacological support for the heart function. They require intubation for breathing. They have anuria and requires dialysis. They are unconscious and have a profound acidosis. The heart rate is erratic or asystole.

Conclusion

ISBAR stands for: identification, situation, background, assessment and recommendation. I, Mary, a registered nurse, rotating at the casualty and emergency ward, have assessed patient Maureen. She appears to be in progressive stage of hypovolemic shock. The following are identifies as to why she is in shock. One, her airway/breathing is compromised. She is semiconscious so she requires assistance in breathing. Her breathing rate is so high and her breaths are shallow. Her systolic blood pressure is at 80mmHg. It is hypovolemic shock because she has signs of low hemoglobin count. From the lab investigations her hemoglobin was at 9g/l. She lost blood from vomiting. Has signs of ascites which causes fluid imbalance. The interventions or recommendations that are most appropriate for patient Maureen will be targeting the following. One is to optimize the intravascular volume. The second target is to support the pumping function of the heart. The third thing is to improve the competence and functioning of the vascular system. Fourth is to redistribute the fluid volume and lastly is to find a solution to what is causing the fluid volume deficit. If it is vomiting, anti-emetics will be administered. If it is fluid intake deficiency, fluid replacement therapy is done. Choi et al, (2015), for shock management fluid replacement is necessary so as to restore intravascular volume. This includes fluids like 0.9% sodium chloride and lactated Ringer’s solution. Fein and Calalang (2015), vasoactive medications are important in restoring the vasomotor tone and improving the functioning of the heart. This drug includes, sympathomimetic, vasodilators and vasoconstrictors. Nutritional support is required to take care of metabolic deficiency. During the compensation phase, there was a release of catecholamine's which causes depletion of the stored glycogen. Administration of nutrients is administered as soon as possible. Anti-acids and histamine blockers are administered to help with the stress ulcers.

Conclusion

From the above, it is clear how hypovolemia develops. How it progresses to hypovolemic shock. The stages of the hypovolemic shock and the manifestations at each stage clarifying why they occur. The organ systems effects during shock. The role of a nurse during shock. With all that knowledge it was easy to relate it to the case study that was presented. Maureen is at progressive shock stage. She has all the signs and symptoms. The shock could have resulted from the effects of the medications she is on. They could have caused stomach ulcers which caused blood loss. The other possible cause is the ascites. The interventions were mentioned and if followed to the later the patient might be able to recover.

References

Abraham, E., Matthay, M. A., Dinarello, C. A., et al. (2014). Consensus conference definitions for hypovolemia, hypovolemic shock, acute lung injury, and acute respiratory distress syndrome: Time for a reevaluation. Critical Care Medicine, 28 (1), 232–235

Balk, R. A. (2015). Pathogenesis and management of multiple organ dysfunctions or failure in severe hypovolemia and hypovolemic shock. Critical Care Clinics, 16(2), 337–351.

Barrett, E., Barman, M., Boitano, S., (2017) Ganong’s review of medical physiology. Lange basic science. 24th edition.

Beck, L. H. (2015). The aging kidney. Defending a delicate balance of fluid and electrolytes. Geriatrics, 55(4), 26–28, 31–32.

Brunner and Suddarth, (2013). Textbook of medical and surgical nursing, 13th edition

Choi, P. T., Yip, G., Quinonez, L. G., & Cook, D. J. (2014). Crystalloids vs. colloids in fluid resuscitation: A systematic review. Critical Care Medicine, 27(1), 200–209.

Fein, A. M., & Calalang-Colucci, M. G. (2014). Acute lung injury and acute respiratory distress syndrome in sepsis and septic shock. Critical Care Clinics, 16(2), 289–313.

Guyton, A. C. (2015). Textbook of medical physiology (13th ed.). Philadelphia: W. B. Saunders

Jindal, N., Hollenberg, S. M., & Dellinger, R. P. (2015). Pharmacologic issues in the management of hypovolemic shock. Critical Care Clinics, 16(2), 233–248.

Kreimeier, U. (2016). Pathophysiology of fluid imbalance. Critical Care (London), 8, Suppl 2:S3–S7.

Kumar, A., Haery, C., & Parrillo, J. E. (2015). Myocardial dysfunction in hypovolemic shock. Critical Care Clinics, 16(2), 251–281

Lewis, l., Dirksen, R., McLean, M., (2013) medical-surgical nursing: assessment and management of clinical problems, 8th edition.

Marcin, J., (2016). Hypovolemic shock. Medical review journal. 21st edition.

McKinley, M. G. (2014). Shock, Introduction to critical care nursing (10th ed.). Philadelphia: W. B. Saunders.

Mikhail, J. (2015). Resuscitation endpoints in trauma. AACN Clinical Issues, 32(1), 10–21.

Rauen, C. A., & Munro, N. (2015). Shock. In M. R. Kinney, S. B. Dunbar, J. A. Brooks-Brunn, N. Moleter, & J. M. Vitello-Cicciu (Eds.), (2013). AACN’s clinical reference for critical care nursing (12th ed.). St. Louis: Mosby

Vincent, J. L., & Ferreira, F. L. (2016). Evaluation of organ failure: We are making progress. Intensive Care Medicine, 26(6), 1023– 1024

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