Transcript Vrodené poruchy metabolizmu

Shock
Definition
Failure of circulation, that leads to inadequate
tissue perfusion.
Despite the compensatory mechanisms tissue
hypoxia is developed.
Tissue hypoxia leads to functional and
morfological changes in organs.
The result of untreated shock is irreversible
organ failure and death.
Pathomechanisms
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different mechanisms
leading to:
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Decrease in return of blood to the heart (!)
Decrease in cardiac output
Hypotension
Hypoperfusion of peripheral tissues
General activation of different neural, humoral
response at systemic, organ, tissue and cellular
level
Stages of shock
1. stage – reversible, compensated
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Response of compensatory mechanisms
activation of SAS – peripheral vasoconstriction
(skin, kidneys), vasodilatation in „central“ organs
(brain, heart)
RAAS activation
increased ADH secretion
And pro- and antiinflammatory cytokines as
procalcitonin and many others
Stages of shock
2. stage – developed, decompensated
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Failure of compensatory mechanisms
Microcirculation failure
– increased blood viscosity, higher platelets agregation,
thrombosis
– higher concentration of vasoactive mediators (histamine,
bradykinin...) – higher permeability, the cytokines as a
double-edged sword
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Metabolic (lactate) acidosis
Stages of shock
3. stage - irreversible
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Cell damage, necrosis or apoptosis
MODS (multiple organ dysfunction syndrome)
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ARDS – „shock“ lungs
acute kidney failure
acute liver failure
loss of consciousness, coma,
DIC
ulcers, bleeding in GIT
...
Types of shock
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hypovolemic shock
– haemorrhagic - bleeding
– nonhaemorrhagic – GIT – diarhea, vomiting;
kidneys – treatment with diuretics, DM; skin - burns
cardiogenic shock
– inadequate contractility – acute MI, myocarditis,
cardiomyopathies
– arrhythmias
– mechanical obstruction – acute valves dysfunction,
rupture of ventricular septum, cardiac tamponade
(obstructive shock)
distributive shock
– septic – toxic
– anaphylactic
– neurogenic – CNS, spinal cord damage
Clinical signs
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low minute cardiac output
– hypotension
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SAS activation
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tachycardia
sweating
piloerection
cold, pale skin
inadequate peripheral perfusion
– cyanosis
– oliguria
– unconsciousness
– muscle weakness
Hypovolemic shock
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Deficiency in volume of extracelular fluid
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Most frequent form – haemorrhagic shock
– bleeding
– traumatic shock – bleeding + pain
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other – nonhaemorhagic shock
– GIT – diarhea, vomiting
– kidneys – treatment with diuretics, patient with
diabetes mellitus
– burns (burn shock)
Cardiogenic shock
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heart failure
reduced cardiac output
– inadequate contractility – acute MI, myocarditis,
cardiomyopathies
– arrhythmias – ventricular tachycardia, supraventricular
tachycardia, atrial fibrilation, AV block - bradycardia,
WPW syndrome
– mechanical obstruction – acute valves dysfunction,
acute rupture of ventricular septum in MI, cardiac
tamponade...
Anaphylactic shock
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accelerated allergic reaction
increase of vasoactive mediators – histamine –
marked vasodilatation
8 – 10% - lethal
signs
– itching, nausea, erythema, dyspnoe
– larynx oedema, bronchospasm
– circulation failure, unconsciousness, cramps
Septic shock
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bacterial, viral infection
release of vasoactive mediators – permeability,
vasodilatation
platelets adhesion and agregation
Neurogenic shock
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acute damage of brain or spinal cord
inflammation, trauma, bleeding, anaesthesia
loss of vasomotoric regulation  marked vasodilatation
irritation of n. vagus  bradycardia,
damage of respiratory centre  hypoventilation