Distributive shock
What bodily responses are expected in neurogenic shock?
Massive vasodilation leading to decreased SVR and thus decreased CO
What is the best management of septic shock? What treatment is provided to patient in septic shock?
PREVENTION! 1) Finding and eliminating the source of infection 2) Fluid resuscitation 3) Vasoconstrictors 4) Inotropic drugs 5) Maximize O2 delivery
When can sepsis syndrome be diagnosed?
SIRS with confirmed infectious process associated with organ failure or hypotension.
Define "septic shock".
Sepsis with hypotension (despite fluid resuscitation) and evidence of inadequate tissue perfusion.
What is the most common etiology of neurogenic shock?
Spinal cord injury above T6
What is SIRS?
Systemic Inflammatory Response Syndrome
Define "sepsis".
Systemic inflammatory response to a bacterial infection with bacteriemia.
What are the criteria for diagnosing SIRS?
TWO OR MORE OF THE FOLLOWING: 1) 36 > Temperature > 38 2) HR > 90 bpm 3) RR > 20 or PaCO2 < 32 mmHg 4) 12,000 < WBC < 4000
When is septic shock in its progressive phase?
When widespread tissue hypoxia results in anaerobic glycolysis and metabolic acidosis.
From what does anaphylactic shock result?
Widespread systemic allergic reaction to an antigen.
What activates mast cells?
- Tissue trauma - C3a and C5a - IgE cross linking of antigen on mast cell surface
What are three possible causes of neurogenic shock?
1. Traumatic spinal cord injury 2. Effects of epidural or spinal anesthetics 3. Reflex parasympathetic stimulation (e.g. gag reflex)
What are the effects of histamine in the four systems it works?
Cardiovascular: decreases BP, increases HR, edema Respiratory: bronchoconstriction Gastrointestinal: smooth muscle contraction, diarrhea Skin: urticaria
What is unique about the clinical presentation of septic shock?
There is a warm phase preceeding the colder phase.
How is anaphylactic shock treated "aggressively"?
- Airway support - IV epinephrine - Antihistamines, corticosteroids - Immediate withdrawal of the antigen if possible - JUDICIOUS CRYSTALLOID ADMINISTRATION - Positive inotropes
What happens during the initial phase of septic shock?
- Baroreceptor reflex - SANS response = catecholamines + vasoconstriction - RAA system - ADH release = vasoconstriction + fluid resorption
Where are H1 receptors found? How do they respond?
- Endothelium - Smooth muscle PIP2 -------> IP3 + DAG
Where are H2 receptors found? How do they respond?
- Gastric mucosa - Cardiac muscle - Mast cells INCREASES cAMP
What are the clinical manifestations of neurogenic shock?
- Hypotension - Bradycardia - Hypothermia + warm, dry skin (????!??!?!?!????????) - Decreased CO - Flaccid paralysis of body below level of spinal lesion
Where are H3 receptors found? How do they respond?
- Pre-synaptic brain DECREASES HISTAMINE RELEASE
What are the three types of distributive shock?
- Septic shock - Anaphylactic shock - Neurogenic shock
What is the anaphylactic response?
- Vasodilation - Increased vascular permeability - Bronchoconstriction - Increased mucus production - Increased inflammatory mediator recruitment to sites of antigen interaction
What are the clinical manifestations of anaphylactic shock?
1. An almost immediate response to inciting allergen 2. Cutaneous manifestations 3. Respiratory compromise 4. Circulatory collapse = tachycardia, vasodilation, hypotension
What is the result of complement, histamine, kinins and prostaglandins produced from the IgE response to an allergen?
1. Increased capillary permeability 2. Peripheral vasodilation 3. Constriction of extravascular smooth muscle (= bronchoconstriction, laryngospasm, GI crams)
What four things characterize septic shock?
1. Systemic vasodilation yielding hypotension 2. Diminished myocardial contractility = decreased CO (These two together lead to metabolic acidosis!) 3. ARDS 4. DIC
How many receptors does histamine have?
3
What characterizes "severe sepsis"? What is the mortality rate?
Additional end-organ dysfunction Mortality rate: 25-30%
How does antigen exposure lead to histamine release from mast cells and basophils?
Antigen exposure ---> the body is stimulated to produce IgE antibodies specific to the antigen ---> reexposure to the antigen ---> IgE binds to mast cells and basophils to release histamine
What stage is not included in the staging system for septic shock?
Compensatory phase
The IgE response to an antigen activates what immune systems?
Complement/kinins/histamine/prostaglandins
Why does anaphylaxis happen?
Due to previous sensitization to the allergen
What receptors are present on mast cells?
Fc receptors
How does anaphylaxis result in relative hypovolemia and impaired cellular metabolism?
Increased capillary permeability + peripheral vasodilation = fluids leave the intravascular space + there is decreased venous return = relative hypovolemia = decreased CO = decreased tissue perfusion = impaired cellular metabolism
What leads to neurogenic shock?
Loss or suppression of sympathetic tone