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Septic Shock- Causes and Pathophysiology. Julia Moser, Charlotte Farron, and Natalie Ashwood. Definition. Shock:- When the cardiovascular system fails to deliver enough oxygen and nutrients to meet cellular metabolic needs. Sepsis:- Presence of bacteria in the blood stream.
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Septic Shock- Causes and Pathophysiology Julia Moser, Charlotte Farron, and Natalie Ashwood.
Definition • Shock:- When the cardiovascular system fails to deliver enough oxygen and nutrients to meet cellular metabolic needs. • Sepsis:-Presence of bacteria in the blood stream. • Septic Shock:- Begins with the development of septicaemia usually from bacterial infections, but can be viral in origin. This is the most common type of Distributive Shock.
Causes of Septic Shock • As mentioned any type of bacteria in the bloodstream causes septic shock and this can occur from many infections, for example: • The pope died from septic shock caused by a urinary infection • Simon has a chest infection • Other common reasons according to Collins (2000) are, major abdominal surgery and an invasive catheter.
To diagnose septic shock, the following two criteria must be met: Evidence of infection, through a positive blood test. Hypotension, despite adequate fluid replacement. In addition, two out of four of the following must be present also: Heart rate > 90bpm. Body Temp < 36 or > 38˚C. Hyperventilation. White blood cell count < 4000 cells/ mm3 or >12000 cells/mm3. Diagnosis
Physiology • Immune and inflammatory response causes vasodilation, and so reduces venous return and cardiac output. • The immune response is where bacteria invade phagocytes, causing damage or even death to the cell. This leads to the release of histamine and proteolytic enzymes leading to vasodilatation • Also can cause poor tissue perfusion and tissue death (necrosis). When this happens, the body attempts to restore the blood pressure and cardiac output. This is known as the Compensatory Stage.
Decreased blood flow to kidneys ▼ Kidneys then secrete renin ▼ Initiating the renin angiotensen-aldosterone system ▼ Angiotensen stimulates the adrenal cortex secreting aldosterone…hormone that aids the reabsorption of sodium and water. Physiology – Homeostatic responses
Decreased blood pressure ▼ Initiating the pituitary gland to release ADH ▼ Enhancing reabsorption of water by the kidneys ▼ Conserving the remaining blood volume. Physiology – Homeostatic responses
Physiology – Homeostatic responses Sympathetic Nervous System-Hormonal Anterior Pituitary releases adrenocorticoitropic hormone ▼ Stimulates adrenal cortex to release glucorticoids ▼ Blood sugar increases to meet increased metabolic rate.
Physiology This leads on to…. • An increased basal metabolic rate- this is the increased amount of energy used in the functioning of vital organs. When the cardiovascular rate etc increases then more energy is needed and used. Hence causing….. • An anaerobic metabolism- this is where the energy needed is not being supplied by enough oxygen, so it is created through the breaking down of carbohydrates.
If Compensatory Mechanisms Fail…. Progressive Stage of shock. • This is when the heart cannot maintain a satisfactory cardiac output, the blood pressure falls, the patient becomes cold and clammy, urine output is absent, the pulse is fast and thready, respirations begin to fail and the patient loses consciousness.
Physiology Cont… Irreversible Stage of shock. • This is the terminal stage. • The patient demonstrates signs of cardiac, hepatic, renal, respiratory, pancreatic, gastrointestinal, haematological and neurological failure. • Organ damage does not respond to treatment. • Death is imminent. • Mortality rate from septic shock is around 50% (Porth, 1998)
Hmmm……. “NOW I KNOW WHY THEY CALL IT ICU!”
References • Collins, T. (2000) Understanding Shock. Nursing Standard. 14 (49), p.35-39. • Hand, H. (2001) Shock. Nursing Standard. 15 (48), p.45-52. • Hinchliff, S. Montague, S. and Watson, R. (2002) Physiology for Nursing Practice. 2nd ed. Edinburgh: Bailliere Tindall. • Porth, C. (1998) Pathophysiology. Foundations of Disease and Clinical Intervention. Philadelphia: WB Saunders.