Joys blood pressure is low, especially for a patient who is normally hypertensive. Patient is on Carvedilol 50mg BD, which is a beta-adrenergic-blocking agent; antihypertensive. (MIMS Online, 2019). The patients blood pressure must normally be very hypertensive as the patient is on the maximum dose. (MIMS Online, 2019). Blood pressure has dropped by from 95 to 90 systolic over the past 30/60.
Her temp is high, especially for a patient who is on TDS Panadol Osteo which is a pyrogenic. (MIMS Online, 2019).
Joys blood glucose level is elevated, especially for a non-diabetic patient who has lost her appetite over the past 3 days as stated by her husband.
SP02 has dropped from 94% to 93%, the patients work of breathing is increasing as well as the respiration rate over the past 30/60.
The patients venous gas was results were stable and within normal limits. Except for the blood glucose and haemoglobin. Which means that the metabolic and respiratory systems are working efficiently at the moment. The water and acid base in balanced also. Oxygen and carbon dioxide levels are within limits.
Heart rate has increased the past 30/60 from 105 to 116 and is now weak. The patient is tachycardic. Considering the patient is taking Carvedilol; a betablocker, the medication suppresses the heart rate and could be masking the severity of the patients tachycardia (MIMS Online, 2019).
When following the adult sepsis pathway, (NSW Government Health Clinical Excellence Commission 2016) the patient is treated with having sepsis. As the patient has 5 observations in the yellow zone. The patients blood pressure is just on 90 systolic, anything below this is a red zone observation which is escalated to severe sepsis/septic shock. Pathophysiology below is written accordingly.
Sepsis is a host response to infection that is dysregulated that has the potential to cause organ dysfunction that is life threatening. (Singer et al., 2016).
Sepsis can be caused by any microbe that is pathogenic. Sepsis may arise from the lungs, abdomen, kidney, urinary tract, skin or other parts of the body. Bacteria is the most common causative organism of sepsis. Sepsis can affect anyone; however, some individuals may be at a higher risk. Including elderly, newborns, those who are immunosuppressed; suffer chronic illnesses, invasive medical procedures and those who have recently undergone surgery (Nagalingam, 2018). Women have a high rate of UTI throughout their lives because the openings to the urethra and rectum in women are near one another (Carson-DeWitt, 2018). My patient is an elderly woman therefore she is at a higher risk of developing sepsis. Her 3/10 pain and stinging upon urination coupled with fever is indicative of a potential urinary tract infection. (Berria, 2017) (Carson-DeWitt, 2018).
Pattern recognition receptors initiate the innate response when pathogen associated molecular patterns are discovered which could be bacteria, viruses of fungi. This triggers the inflammatory cascade. Cytokines, complement, immune cells, the endothelium and coagulation proteins are the effectors of the innate/ non-specific immune response. When the innate immune response becomes dysfunctional and amplified it leads to an imbalance between anti-inflammatory and pro-inflammatory responses which causes systemic inflammatory responses (SIRS); a prolonged immune and inflammatory response. (Censoplano, Epting and Coates, 2014). Otherwise known as distributive shock.
In SIRS uncontrolled cytokine release may lead to vasodilation and increased capillary permeability, and breakdown of normal epithelial cell walls that ideally serve as protective barriers, due to the release of pro-inflammatory mediators. Cytokines include interleukins, interferons, tumour necrosis factor, transforming growth factor, and other lymphokines, chemokines, and growth factors. The resulting leakage syndrome can cause hypotension in septic patients.
The complement system is a cascade of protein activations that help to break down pathogens and identify as well as label foreign molecules. The complement proteins when activated multiply the effects of the local immune reactions by putting more cytokines into play. (Neviere, 2013).
In sepsis, inflammation is accompanied by coagulation activation, thrombin generation, and disseminated intravascular coagulation (DIC). The primary coagulation pathway activated in sepsis is the tissue factor pathway which results in upregulation of monocyte/macrophage membranes and damage to the endothelium. The intrinsic or contact factor pathway amplifies clotting in an autoactivation manner leading to widespread vasodilation and generation of bradykinin, causing further vasodilation. (Boomer, Green and Hotchkiss, 2013).
The bodys compensatory mechanism due to the low blood pressure is to be increasing the work of the heart, which is why an individual may become tachycardic. (Nagalingham, 2018).
Tachypnoea is related to the patients hypoxia and increased levels of carbon dioxide. The aetiology of tachypnoea and hypoxia in sepsis is secondary to the decreased gas exchange within the alveoli due to proteins and fluids leaking into the tissues of the lungs. (Nagalingham, 2018). Caused by the increased permeability of pulmonary and alveolar capillary endothelial cells, due to inflammatory mediators. This leads to an increased respiratory rate to compensate for the reduced surface area for oxygenation; hypoxia. (Kim and Hong, 2016).
Raising the bodys temperature is intended to impair pathogen replication and survival. This is achieved in the hypothalamus, where an altered inflammatory milieu increases the internal thermostat set point. Heat must be generated as a by-product of metabolism, thus the rate of energy expenditure by the cells increases dramatically. To meet the demand for oxygen, the cardiac output must increase, explaining why tachycardia is an almost universal sign of fever generation. With increased oxygen consumption, the production of carbon dioxide increases, resulting in compensatory tachypnoea. (Censoplano, Epting & Coates, 2014).
When oxygen delivery is insufficient to meet metabolic demand; tissue hypoxia, the body gives rise to lactate production as a by-product of anaerobic cellular glycolysis. (Ebrahim, 2011). Lactate levels help indicate how poor perfusion and oxygenation are within the body during sepsis. The mortality rate of a patient with lactate levels greater than two are significantly higher.
When the body enters a state of shock, the patients fight or flight response is triggered. Cortisol activates enzymes which are involved in hepatic and also inhibit the ability of the peripheral tissues to uptake glucose. Adrenaline and noradrenaline activate hepatic gluconeogenesis and glycogenolysis, consequently increasing blood sugar levels. As the body is fighting infection, an inflammatory substance called C-reactive protein is released in order to combat the infection. C-reactive protein induces insulin resistance, meaning that the body cannot effectively use its own insulin. The result of this will be a raised blood sugar.
As blood flow to the brain reduces, so conscious levels can be affected. This can present as confusion, drowsiness, slurred speech, agitation, anxiety, or a decreased level of consciousness. A further consideration is that when the body enters a state of shock, in order to preserve the internal organs, the body pulls its circulating volume into its core. The brain is the only internal organ not to sit in the core of the body. So, when the body pulls its circulating volume into its core, the brain does not receive adequate oxygen to function.
Early in the progression of sepsis, the patient may look remarkably well, despite a low blood pressure. Patients may present with warm peripheries and often capillary refill times that are normal. Later, as the circulating volume becomes depleted and the compensatory mechanisms become exhausted, the circulation begins to fail and the patient will look much worse; with cool peripheries, often a prolonged capillary refill time and signs of organ dysfunction.