Shock Flashcards
Shock
clinical manifestation of failure Of cellular function due to inadequate tissue perfusion and consequent cellular hypoxia resuiling from a reduction in the effective circulating blood volume
Oxygen consumption in the body
is 3m1/kg/min (200-250 ml for the average adult)
Respiratory dysfunction: Mediators 2
1.TNF-a, 2. Neutrophils
Respiratory dysfunction: TNF-a
basement membrane destruction and in- creased permeability ofllie pulmonary capillary endothelium leading 10 exudation of protein-rich fluid into the interstitium and alveoli
Respiratory dysfunction: Neutrophils
Sequestrated into the lungs and the oxygen free radicals they produce damage the alveoli still further.
Respiratory dysfunction: signs
The patient is tachypnocic, hypoxaemic and has respiratory alkalosis from the rapid breathing. ARDS may ensue.
Cardiovascular Dysfunction: Mediators 3
TNF-a and endotoxin activate the production and release of nitric oxide (NO) from the vascular endothelium, cardiac and smoolh muscles
Cardiovascular Dysfunction: NO
NO reduces the contractility crthe myocardium, already affected by reduced coronary perfusion and its reponsiveness 108- adrenergic agents.
Cardiovascular Dysfunction: signs
- Myocardial function is depressed 2. Hypotensions is worsened.
Renal Dysfunction
The hypovolaemia, vasoconstriction, thromboxane and leukotrienes lead to decreased renal output - oliguria - and later damage to thecclls - anuria.
Haemotological Dysfunction
DIC occurs and causes bleeding and microvascular thrombi in tissues reducing perfusion still further. Activation ofcoagulation by TNF- a is via the tissue factor extrinsic pathway. AT III , thrombomodulin and proteins C and S are reduced in sepsis thereby depres sing anti-coagulation
Hepatic Dysfunction: late or early
Early
Hepatic Dysfunction: cause
hypoperfusion from nitricoxide and DIC
Hepatic Dysfunction: effects
Damage of the parenchymal cell and consequent hyperbiJirubinaemia and elevated liver enzymes. Kupffer cell activity is impaired and so bacteria and toxic products e.g. lactic acid , cannot be readily eliminated.
Neurological Dysfunction
Septic encephalopathy and polyneuropathy
Gut Dysfunction
The gut barrier is impaired following hypotension and hypovolaemi a. Micro-organisms and toxic products can there- fore be translocated into the lymphatic, ponal and systemic circulation thereby causing further sepsis
Scoring of MODS: range
0-4
Scoring of MODS: Respiratory
Fraction of inspircd oxygen
Partial pressure ofoxygen
> 400-< 101
Scoring of MODS: Coagulation (platelet count x 109/l)
> 120 - < 21
Scoring of MODS: Renal (Creatinine;umollL)
> 134-<439
Scoring of MODS: Glasgow Coma Score
15 - < 6
Septic shock: 2 types
- Following hypovolaemia brought about by trauma or sequestration of extracellular fluid as in peritonitis, intestinal obstruction, acute pancreatitis, septic abonion or gangrene
- associated with bacteraemia from the urinary Iract- infcction, obstruction, instrumentation or operation - biliary tract operation or infcction, bowel surgery. and less commonly from lung, skin or soft tissue infections .
