外科休克(surgical+shock)

aqtocytolysis and to damage other cells DIC Cell damage, organ failure occur death occur
no perfusion and no fluid
16
Late Shock
Heart Rate: bradycardia; severe dysrhythmias
fluid and no perfusion
11
Compensatory significance
Keeping blood pressure normal
Perfusion to vital organs
12
Clinical manifestation of Shock
Early Stage (compensated shock):
multiple system organ failure, MSOF
17
2. Metabolic responses
Anaerobic metabolism
Decreased metabolic capability in the liver
lactic acid accumulates
decreased catecholamine responce
SURGICAL SHOCK
Qiangsong Tong, M.D. Ph.D.
Department of Pediatric Surgery Union Hospital of Huazhong University of Science and Technology
1
Objectives
• • • • Understand what is shock ？ Define types of shock Understand pathophysiology of shock Understand how to treat shock
arteriovenous shunt, direct passage way to open tissue hypoperfusion anaerobic metabolism lactic acid builds up metabolic acidosis
Pre- CRV to dilate Post- CRV to contract capillary hydrostatic pressure to increase
Skin:
Blood Pressure: Respirations:
delayed capillary refill; cool and clammy
normal or slightly elevated rapid and shallow
13
Compensatory mechanisms （ Progressive shock）
8
1. Microcirculation
• Precapillary resistance vessel： arteriole、metarteriole、precapillary sphincter
• Postcapillary resistance vessel：veinule
• Microcirculation perfusion：
The body attempts to compensate and restore perfusion by: Increasing cardiac output Stimulation of the sympathetic nervous system causes an increase in heart rate, stroke volume, and PVR (peripheral vessel resistance). Redistributing the circulating blood volume to vital organs
4
What is effective circulatory blood volume? Various types of shock result from failure in one or more of the 3 major components of the circulatory system：
9
Compensatory mechanisms (early shock)
A decrease in blood volume Stretch receptors in heart baroreceptors in aorta and carotid arteries
The HPA and neuroendocrine axes are triggered
• Myocardial infarction
• Anaphylaxis
• Extreme heat or cold
6
Types of Shock
• Hypovolemic Shock:
– haemorrhagic
– traumatic – dehydration
• Other causes of shock
• Circulatory level： blood pressure • Microcirculatory level： inadequate tissue perfusion • Cellular level and molecular level：
Frontier Exploratory stage，experimental therapies
Blood Pressure: decreased
Respirations: rapid and shallow Urine output: oliguria
15
Irreversible shock
Hypercoagulable character
erythrocyte and thrombocyte to aggregate Cellular hypoxia，lysosome rupture hydrolytic enzyme releasing
Increased catecholamine release
Increase glucocorticoid and mineralcorticoid release Activation of Renin-angiotensin system
10
Compensatory echanisms
•
• • • • • •
A breakdown of effective circulation
Inadequate tissue perfusion Decreased oxygen supply Anaerobic metabolism Accumulation of metabolic waste Multiple organ failure A clinical syndrome
plasma shift to interstitual spaces pachyemia and increasing blood viscidity
perfusion and no fluid
14
Middle Stage (uncompensated shock): Compensatory mechanisms are unable to maintain perfusion
Compensatory mechanisms are able to maintain perfusion of vital organs
Heart Rate:
mild tachycardia; bounding pulse
Level of Consciousness: lethargy, confusion, combativeness
3
WHAT IS SHOCK?
Shock results from poor tissue perfusion and tissue hypoxia from inadequate circulatory compensations needed to sustain acutely increased body metabolism.
– Septic Shock – Cardiogenic Shock – Neurogenic Shock – Hypersensitive Shock
7
Pathophysiology
1. Microcirculatory changes 2. The changes of body fluid metabolism 3. Mediators of inflammation release and ischemical reperfusion injury 4. Secondary lesion
18
3. Ischemical reperfusion injury
• An acute restoration of oxygen delivery can also amplify the initial ischemic insult, leading to further cell injury • During this phase of shock resuscitation, leukocytes adhere to postcapillary venular endothelium that is followed by the generation of reactive oxygen species. • The latter response damages proteins and membrane structures, and activates signal transduction pathways that can ultimately lead to apoptosis (programmed cell death).