Vasopressin Case Study

Hypovolemic shock is an urgent condition of rapid reduction of circulatory volume in the body, which can be created due to blood or plasma or body fluids loss (Kettley & Marsh, 2016, p. 31; Perner & Backer, 2014, p. 613). Blood loss can be induced by internal or external injuries, excessive perspiration or diuretics (Craft & et al, 2015, p. 852). Maureen Hardy’s hypovolemia has been precipitated by hematemesis.

As sepsis progresses, tissues become less perfused and acidotic, compensation begins to fail, and the patient begins to show organ dysfunction. The cardiovascular system also begins to fail, the blood pressure does not respond to fluid resuscitation and vasoactive agents, and signs of end-organ damage are evident (e.g., renal failure, pulmonary failure, hepatic failure). As sepsis progresses to septic shock, the blood pressure drops, and the skin becomes cool, pale, and mottled. Temperature may be normal or below normal. Heart and respiratory rates remain rapid. Urine production ceases, and multiple organ dysfunction progressing to death occurs. Adventitious lung sounds occur throughout the lung fields, not just in the upper fields of the lungs.

As previously mentioned, the left ventricle is no longer as compliant and therefore cannot fill with blood without encountering resistance. The use of diuretics decreases overall volume, which as a result decreases overall pressure. This lost pressure may be needed in order for blood to pump with added pressure against the resistance into the ventricle. Once pressure is lost the patient is said to have hypotension and is at risk for blood not being able to perfuse to vital tissues (Burchum et al., 2016, pg.

The unresolved infection has landed the patient on septic shock. Sepsis is the body’s response to inflammation of a particular or unknown infection. The presence of hypotension despite adequate fluid infusion and inadequate tissue perfusion is the result of septic shock. The treatment of shock is centered on the restoration of blood pressure to normal, the presence of adequate tissue perfusion, making sure organs return to functioning well, and avoiding further complications (Lewis, Dirksen, Heitkemper, Bucher, & Harding,

Septic shock is a subset of severe sepsis and was defined as “sepsis-induced hypotension persisting despite adequate fluid resusci- tation” (see Fig. 12.1). While the quantity of fluid that qualifies as “adequate fluid resuscitation” is controversial, we believe septic shock is best defined as a “mean arterial pressure (MAP) less than 65 mmHg after a fluid challenge of 20 mL/Kg body weight (given 30–60 minutes) in patients with sepsis and in the absence of other causes for hypotension” (also see Chap. 14). According to the ACCP/SCCM defini- tions, three stages in the hierarchy of the host’s response to infection were recognized, namely, sepsis, severe sepsis and septic shock, with sepsis having the best prognosis and septic shock the worst. While the use of the SIRS criteria to define sepsis is some- what controversial [3–6], many consider sepsis to be best defined as the “systemic response to infection with the presence of some degree of organ dysfunction”

The fundamental principle of the phenomenon known as sepsis is an amplified immune response to a pathogen. It is important to note that the insult originates from the excessive host response to, rather than the pathogenicity of, the infective agent1. The upregulation of pro-inflammatory (TNF-α, IL-1α/β, IL-6, IL-12, IFN-γ, and MIF) and anti-inflammatory (IL-10, TGF-β, and IL-4) mediators have been found in various sepsis states2. The exact function, value, and limits of this peculiar, and extravagant, immune response is not fully understood3. Historically, sepsis and processes within the sepsis spectrum have been difficult to truly identify and diagnose1. In 2012, the Surviving Sepsis Campaign identified three major categories of the phenomenon: sepsis, severe sepsis, and septic

Septic shock is the stage of sepsis when multiple organ failure is evident and uncontrolled bleeding of the body occurs. Septic shock results from the complication of an infection where toxins initiate a full body inflammatory response. Viral, fungal, and bacterial infections can all lead to septic shock, but the most common causes of sepsis are gram- negative bacteria and gram-positive bacteria. Sepsis causes severe hypovolemic shock and hypodynamic cardiac function to affect the body, platelets and clotting factors are consumed and thus the body cannot clot blood. Capillary leak occurs and cardiac contractility is poor from cellular ischemia (Ignatavicius & Workman, 2011). For a person to be diagnosed with septic shock, they must have symptoms

Since the arterial vasodilatation seems to be a key mechanism in the pathogenesis of HRS, vasoconstrictors have been used as a bridging therapy to definitive therapy; liver transplantation. The vasopressin analog terlipressin is the most widely studied drug, especially in type 1 HRS

Assessment Although a patient in severe sepsis may be transferred to the intensive care unit (ICU), medical-surgical nurses must be able to recognize early signs and symptoms of sepsis to ensure prompt treatment before the patient requires ICU admission. Severe sepsis Severe sepsis occurs when a patient with documented sepsis goes on to develop acute organ dysfunction with hypoperfusion and tissue hypoxemia. Simple prevention strategies Without proper assessment and early identification, patients with sepsis can deteriorate quickly, suffering compromised tissue oxygenation and organ dysfunction for many hours. Be aware that although blood pressure readings are crucial in assessing and planning care for the septic patient, mean arterial pressure

Sepsis is a systemic response to infection that leads to severe sepsis and septic shock (Dellinger et al., 2013). Severe sepsis and septic shock are major health concerns, affecting millions of people, and killing one in four (Dellinger et al., 2013). Multisystem organ failure (MOF) is one of the leading causes of death of hospitalized patients with the underlying condition of sepsis (Rittirsch, Redl, & Huber-Lang, 2012).

According to the National Trauma Institute, hypovolemic shock is the second leading cause of death in people with traumatic injuries. [1] This makes the initial identification and management of Hypovolemia detrimental to the outcome and survival of many patients involved in traumatic events. Hypovolemia refers to a medical condition in which rapid fluid loss results in multiple organ failure due to inadequate circulating volume and consecutive inadequate perfusion. [1,2,3]

The author Julianna Kettlewell, a BBC News Online science staff member, uploaded an article on Wednesday June 16, 2004 which gives us information on how a new gene can alter the Don Juan of voles to go from not caring for their wives or children to an excellent home-loving husband. She describes how a new gene called vasopressin boosts pair-bonding in voles. Before this experiment, the prairie voles would not have sentimental relationships with their partners and have multiple partners at once, likely due to the fact that scientists found that the voles had little vasopressin (V1a) receptors in their forebrain, known as the ventral pallidum region. Scientists hypothesized that if they would inject these vasopressin hormones into the forebrain section they would get a “taming” effect and make a loving husband.

This clinical report will be discussing the potential life threatening effects “from cellulitis to septic shock”. Cellulitis is the starting cause of an infection that will lead through the sepsis cycle, finishing with the severe part septic shock (Swartz, 2004). Analysation of the interrelationships between localised infection, systemic inflammation response syndrome (SIRS), and the sepsis course will be discussed throughout this report. Additionally, this report will incorporate comprehensive detail of the physiological systemic weakening that can prompt septic shock. Finally, in-depth details about the investigation towards the red flags of disintegration, for example, intense respiratory trouble disorder will be analysed.

Pathophysiology when it comes to Sepsis which is a “clinical syndrome of life-threatening organ dysfunction caused by a dysfunction response to infection, there is critical reduction in tissue perfusion; acute failure of multiple organs, including the lungs, kidneys, and liver. The pathogenesis of septic shock is not completely understood. An inflammatory stimulus (eg, a bacterial toxin) triggers production of pro inflammatory mediators, including TNF and IL-1” (Maggio,2016, ).“These cytokines cause neutrophil–endothelial cell adhesion, activate the clotting mechanism, and generate micro thrombi. They also release numerous other mediators, including leukotrienes, lipoxygenase, histamine, bradykinin, serotonin, and IL-2. They are opposed by anti-inflammatory mediators, such as IL-4 and IL-10, resulting in a negative feedback mechanism. Initially, arteries and arterioles dilate, decreasing peripheral arterial resistance; cardiac output typically increases” (Maggio, 2016). “Shock occur cardiac output may decrease, BP falls (with or without an increase in peripheral resistance), signs include fever, hypotension, oliguria, and confusion. Diagnosis is primarily clinical combined with culture results showing infection; early recognition and treatment is critical” (Maggio,2016

Sepsis is defined as the invasion of infection into the bloodstream (septicaemia) and start to affect other organs in the body (Foster, Whetsone, Prevost, & S, 2012). Septic shock can cause multiple organ failure and also can cause blood clots to form thus compromising the vital organs with enough oxygen and nutrients .Sepsis can cause a decrease in tissue perfusion which results in systemic vascular dilation .In this essay progression of infection will be explained, stages of septic shock, major causes of septic shock and the effects on perfusion and microcirculation on major vital organs (Foster, Whetsone, Prevost, & S, 2012).