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Shock - a decrease in tissue perfusion and impaired cellular metabolism.…
Shock - a decrease in tissue perfusion and impaired cellular metabolism.
4 main categories of shock
Cardiogenic shock - reduced cardiac output resulting dysfunction of the heart pumping action (either systolic or diastolic). A decrease in the fiilling of the heart reduces stroke volume.
common causes include: acute MI, arrhythmia, and cardiomyopathy.
Signs and symptoms include: tachycardia, hypotension, poor pulse pressures, tachypnoea, crackles on auscultation, cyanosis, sweating, cool and clammy, poor capillary refill, confusion, decreased bowels sounds, nausea, and vomitting.
~60% mortality rate.
Hypovolaemic shock - occurs when there is a loss in intracellular fluid volume. This causes a decrease in preload, stroke volume, and capillary refill.
Immediate hypovolaemia - fluid lost through haemorrhage ie. vomitting, diarrhoea, diuresis.
Relative hypovolaemia - third spacing: this is caused by the shift in the extracellular space from the vascular space. May be observed in burns patients.
Signs and symptoms include: tacchycardia, tachypnoea, decreased urine output, cool and clammy, confusion, and absence of bowel sounds.
Distributive shock - maldistribution of circulatory flow and volume.
Neurogenic shock - pooling of blood in the blood vessels caused by vasodilation without compensation. Caused by injury to the T5 of above. Signs and symptoms- bradycardia, hypotension, and low body temperature.
Anaphylactic shock - Hypersensitivity reaction to an allergen, causes increased capillary permeability, causing fluid to leak into interstitial space. Signs and symptoms - bronchospasm, dizziness, chest pain, swelling, incontinence, and rash; onset of symptoms is usually sudden
Septic shock - systemic response to an infection. Signs and symptoms - hypotension even with fluid resuscitation, high and low temperatures, crackles, respiratory failure, decreased urine output, changes to mental status, paralytic ileus, and GI bleeding.
Obstructive shock - Blood flow is physically obstructed along with a decreased cardiac output. This leads to a decrease in preload.
Caused by: tension pneumothorax, abdominal compartment syndrome, and pulmonary embolism.
Signs and symptoms include: hypotension, tachypnoea, decreased urine output, cool and clammy, confusion, and decrease in bowel sounds.
Stages of shock
Compensatory - The body attempts to maintain homeostasis, the clinical signs and symptoms are beginning to reflect what is happening the body's oxygen supply and demand.
Signs and symptoms: confusion, hypotension, narrowed pulse pressures, tachypnoea, decreased bowel sounds,.
Progressive - Begins when the compensatory stage fails. Signs and symptoms: Delirium, hypotension, tachycardia, arrhythmia, decreased capillary refill, ARDS, GI bleeding, decreased urine output, hypo or hyperthermia, jaundice, and cool and clammy.
Irreversible - the body's compensatory mechanisms have failed, sending the organs into failure.
Signs and symptoms: Unresponsive, hypotension, bradycardia and irregular, hyperaemia, respiratory failure, ischaemic gut, no urine output, changes to metabolic function from the wastes accumulating, hypothermia, and skin looks mottled and blue.
Treatment options
oxygen and ventilation: this is directed at increasing the body's oxygen supply as well as decreasing the demand.
Fluid resuscitation: fluid used depends on the fluid that has been lost. The main goal is to restore tissue perfusion.
Drug therapy - directed at correcting decreased tissue perfusion.
Sympathomimetic drugs are used to mimic the action of the SNS to cause vasoconstriction.
Vasodilators drugs are used to decrease contractility, useful for maintaining blood pressure.
Nutritional therapy - To maintain protein/calorie balance in the body.
Reference: Seckel, M. (2015). Shock, systemic inflammatory response syndrome and multiple organ dysfunction syndrome. In D. Brown., H. Edwards., L. Seaton & T. Buckley. (Eds.). Lewis’ medical – surgical nursing. Assessment and management of clinical problems (4th ed., pp.1706-1725). Sydney, Australia: Elsevier