WEEK SEVEN Flashcards
Shock occurs when?
Inability to meet metabolic demands of the tissues
Hypoperfusion results in cellular dysfunction
There is homeostatic imbalance between nutrient supply and demand
Adaptive responses can no longer accommodate circulatory changes
Types of shock?
-Hypovolaemic
-Cardiogenic
Obstructive (blockage of circulation by impedance of outflow)
-Distributive Shock
Sepsis
Anaphylaxis
Neurogenic
Clinical markers of shock
Markers of global Hypoperfusion indicate severity of shock
Lactate and acid base disturbances
Early marker of mitochondrial dysfunction
Cellular Hypoperfusion
Assess acidaemia
Ph
Serum Lactate
BE
Increased lactate – warning sign of organ failure
Early indication of shock
Early detection and management Improves patient outcome Tachycardia Altered consciousness Cold diaphoretic skin Tachypnoea Shallow resps Decreased urine output (<30 mls/hr) Hypotension (SBP <90) – Late/misleading - emergency
Hypovalemic shock
Low Volume of Blood’ Can be any fluid. Caused by : Bleeding – internal/external Diarrhoea / vomiting Dehydration
Hypovalemic shock management
Fluid resuscitation Increases preload – cardiac output Fluid infused reflect fluid lost Burns – Plasma Massive haemorrhage – Blood Colloid or crystalloid??!!! Caution Fluid replacement can result in overload Fluid shift Inflammatory response Bolus dose – Volume/Kg – haemodynamic response Local policy must be followed
Cardiogenic shock
Inability to maintain adequate perfusion despite adequate circulatory volume
Circulatory failure from cardiac dysfunction
Usually occurs within 48hours of MI
40% or more left ventricle ischemic
Mortality rate of 50-80%
Main cause from LVF
Clinical manifestations of cardiogenic shock
Low Cardiac output Hypotension (<90SBP) Sever pulmonary congestion High CVP Oliguria < Peripheral perfusion Anxiety Dyspnoea/tachypnoea Resp alkalosis/acidosis Distended neck veins Cause of cardiogenic shock ie CP, Cardiac arrhythmias etc
Disruptive shock
Impaired oxygen and nutrient delivery to the tissues Failure of the vascular system Widespread vasodilation Septic shock Anaphylaxis neurogenic
Septic shock
Now incorporated into: Systemic Inflammatory Response Syndrome (SIRS) Systemic Inflammation caused by Sepsis Burns Pancreatitis Trauma Septic Shock Severe Sepsis
Clinical manifestations of septic shock
Infectious agents in blood cause haemodynamic compromise Ineffective tissue oxygen delivery Inappropriate vasodilation Normal or increased CO Hypovolaemic due to >vasodilation Pt presentation Warm, pink well perfused Cell death Caused by decompensation leads to multiple organ failure
Anaphylaxis
Sever allergic reaction
Normally immunoglobulin E (IgE), an antibody, links to an antige destruction of the antigen.
Abnormal response in an allergic individual excess of IgE, which binds to tissue mast cells
Following a subsequent exposure to the antigen (allergen) the complex which is formed between the antigen and the IgE attached to the cells wall
damage to the cell wall
release of histamine
Vasodilation
Neurogenic shock
Know as Spinal Shock Loss of Vasomotor tone (sympathetic) Disruption/inhibition neural output Spinal cord injury above T6 Decreased vascular resistance Vascular dilation Commonly cased by Trauma Can be as result of anaesthesia (spinal)
Signs and symptoms of neurogenic shock
Hypotension <90 – 100 SBP Bradycardia <80bpm Skin warm and dry No Obvious cause HR does not occur Parasympathetic nervous system Blockage of sympathetic compensatory response
Nursing care of a shocked patient
Rapid assessment of patient (A – E) Support of patient Physical Emotional Psychological Holistic care Family Maintain Communication Patient Staff Family Interventions Fluids Observations Scribe Medications transfer
