Shock

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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. - PowerPoint PPT Presentation

Transcript of Shock

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

different mechanisms

leading to:

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

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

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

Metabolic (lactate) acidosis

Stages of shock

3. stage - irreversible

Cell damage, necrosis or apoptosis MODS (multiple organ dysfunction syndrome)

– ARDS – „shock“ lungs– acute kidney failure– acute liver failure– loss of consciousness, coma, – DIC– ulcers, bleeding in GIT– ...

Types of shock 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

low minute cardiac output– hypotension

SAS activation– tachycardia

– sweating

– piloerection

– cold, pale skin inadequate peripheral perfusion

– cyanosis

– oliguria

– unconsciousness – muscle weakness

Hypovolemic shock Deficiency in volume of extracelular fluid

Most frequent form – haemorrhagic shock

– bleeding

– traumatic shock – bleeding + pain

other – nonhaemorhagic shock

– GIT – diarhea, vomiting

– kidneys – treatment with diuretics, patient with diabetes mellitus

– burns (burn shock)

Cardiogenic shock

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

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 bacterial, viral infection release of vasoactive mediators – permeability,

vasodilatation platelets adhesion and agregation

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

Neurogenic shock