Shock

Question 1

Shock

Answer 1

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

Question 2

Oxygen consumption in the body

Answer 2

is 3m1/kg/min (200-250 ml for the average adult)

Question 3

Respiratory dysfunction: Mediators 2

Answer 3

1.TNF-a, 2. Neutrophils

Question 4

Respiratory dysfunction: TNF-a

Answer 4

basement membrane destruction and in- creased permeability ofllie pulmonary capillary endothelium leading 10 exudation of protein-rich fluid into the interstitium and alveoli

Question 5

Respiratory dysfunction: Neutrophils

Answer 5

Sequestrated into the lungs and the oxygen free radicals they produce damage the alveoli still further.

Question 6

Respiratory dysfunction: signs

Answer 6

The patient is tachypnocic, hypoxaemic and has respiratory alkalosis from the rapid breathing. ARDS may ensue.

Question 7

Cardiovascular Dysfunction: Mediators 3

Answer 7

TNF-a and endotoxin activate the production and release of nitric oxide (NO) from the vascular endothelium, cardiac and smoolh muscles

Question 8

Cardiovascular Dysfunction: NO

Answer 8

NO reduces the contractility crthe myocardium, already affected by reduced coronary perfusion and its reponsiveness 108- adrenergic agents.

Question 9

Cardiovascular Dysfunction: signs

Answer 9

1. Myocardial function is depressed 2. Hypotensions is worsened.

Question 10

Renal Dysfunction

Answer 10

The hypovolaemia, vasoconstriction, thromboxane and leukotrienes lead to decreased renal output - oliguria - and later damage to thecclls - anuria.

Question 11

Haemotological Dysfunction

Answer 11

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

Question 12

Hepatic Dysfunction: late or early

Answer 12

Early

Question 13

Hepatic Dysfunction: cause

Answer 13

hypoperfusion from nitricoxide and DIC

Question 14

Hepatic Dysfunction: effects

Answer 14

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.

Question 15

Neurological Dysfunction

Answer 15

Septic encephalopathy and polyneuropathy

Question 16

Gut Dysfunction

Answer 16

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

Question 17

Scoring of MODS: range

Answer 17

0-4

Question 18

Scoring of MODS: Respiratory

Answer 18

Fraction of inspircd oxygen

Question 19

Partial pressure ofoxygen

Answer 19

> 400-< 101

Question 20

Scoring of MODS: Coagulation (platelet count x 109/l)

Answer 20

> 120 - < 21

Question 21

Scoring of MODS: Renal (Creatinine;umollL)

Answer 21

> 134-<439

Question 22

Scoring of MODS: Glasgow Coma Score

Answer 22

15 - < 6

Question 23

Septic shock: 2 types

Answer 23

1. Following hypovolaemia brought about by trauma or sequestration of extracellular fluid as in peritonitis, intestinal obstruction, acute pancreatitis, septic abonion or gangrene
2. 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 .