Untitled Flashcards Set

NA Sodium

Arthur’s sodium is increased to high part of normal. I am concerned about this because Arturs sepsis is causing systemic vasodilation, and the body is releasing vasoconstriction such as angiotensin 2 which stimulates aldosterone. This increases sodium and water reabsorption in the nephron. To increase circulatory volume to compensate for the leakage of the fluid into interstitial space. I am concerned by this increased sodium indicates the severity of compensation Arthur is undergoing.

K Potassium

High potassium

Potassium is high intracellular

Arthur’s hypoxia caused by the reduced cardiac output from his sepsis, causing hypoxemia from the infected exacerbated copd. Cells switch to anaerobic respiration to preserve them, as hypoxia continues it can cause ischemia to cells. This leads to cells releasing the high intracellular potassium into the circulatory volume. This causes the increased potassium. I am concerned about this high potassium because it can cause ventricular arrhythmias, which are life threating.

Low potassium

Salbutamol, a β2-adrenergic agonist, primarily relaxes bronchial smooth muscles, leading to bronchodilation. However, it also has some β1 activity in the heart, which can cause tachycardia. Its stimulation of cellular activity increases ATP production, enhancing ion exchange and triggering electrical discharges. This drives potassium into cells, leading to hypokalaemia, which in turn increases the risk of cardiac arrhythmias.

Urea – excretion through the kidney &Creatinine increases

Arthur’s sepsis is causing reduced cardiac output which reduces oxygen perfusion to the glomerulus filtration membrane which filters blood into urine. This causes ischemic death to the glomerular filtration membrane causing acute kidney injury. This reduces the filtration of waste products, increasing creatine and urea. I am concerned of this because there is a greater loss of more than 50% of kidney function and indicates the severity of Arthurs AKI.

Heamoglobin low

In COPD, chronic inflammation increases inflammatory mediators in circulation, affecting the kidneys and altering erythropoiesis, leading to reduced haemoglobin levels. This decreases the oxygen-carrying capacity of the blood, contributing to hypoxemia. In cases of sepsis, cardiac output is further compromised, reducing oxygen delivery and worsening hypoxia. These combined factors—low haemoglobin, reduced oxygen transport, and impaired circulation—can lead to cell death and organ dysfunction, posing a serious risk to the patient

White blood cell and leucocytes

Arthur’s sepsis and infected exacerbated COPD will trigger an immune response to fight the infection leading to an increase in neutrophils which are the first defence, rapidly increase in response to infection. Monocytes also rise to help with pathogen clearance. I am concerned about this because it indicates intense inflammatory response which shows the severity of the sepsis and infected exacerbation COPD within Arthur.

Platelet lower part and PT ratio higher part

The prothrombin and APPT these enzymes create fibrin and mesh attach to platelet to stabilize and form the thrombus/ clot.

In sepsis, the body releases cytokines to fight infection, causing vasodilation and capillary damage. Bacterial endotoxins worsen this, leading to bleeding from the damaged endothelium. To stop the bleeding, platelets activate, forming clots with fibrin mesh. However, because this happens systemically, platelets are used up, causing their levels to drop. As sepsis progresses, prolonged clotting time and the formation of microthrombi can lead to ischemia and cell death. Eventually, clotting factors become depleted, increasing prothrombin time (PT) and raising the risk of Disseminated Intravascular Coagulation (DIC)—a severe condition where the body both over clots and bleeds, potentially leading to multi-organ failure.