Download Ischemic Anoxia Phase

Li Ke
Depart. of Pathophysiology
School of Basic Medical Sciences
Shock
the state in which profound and wide
spread reduction of effective perfusion
leads first to reversible, and then, if
prolonged, to irreversible cellular injury
Clinical Manifestation

Dulled sensorium / anxious / Coma

Pale face and cyanosis

Cold and clammy skin

Oliguria / anuria

Rapid, weak pulse

Narrowed pulse pressure
Hypotension
Etiology

Loss of blood and/or fluid

Burn

Infection

Trauma

Acute Heart failure

Anaphylaxis

severe mental stimulation or
nerve disorders/diseases
Classification
Adequate
effective Perfusion
Sufficient
Hypovolemic
blood
volume
shock
Pumping
cardiogenic
ability of
the
shock
heart
Normal
Vasogenic
vasomoter
function
shock
Burn
Trauma
Loss of blood
and/or fluid
Infection
Heart failure
⌒
⌒
Blood volume↓
Anaphylaxis
nerve disorders
/diseases
Vascular bed ↑
Decreased
Effective
perfusion ↓
Microcirculation
dysfunction
shock
Heart pump ↓
 直捷通路
 动--静脉短
路
 迂回通路 (真毛细血管通路)
调节：
神经因素--交感，受体、
体液因素（收缩，舒张）
代谢因素（腺苷、K+、H+等）----舒张
Cap灌流的局部反馈调节
局部代谢
产物聚积
真Cap网
血流↓
平滑肌对缩血管
物质反应性↓
Cap前括约肌
与后微A舒张
Cap前括约肌
与后微A收缩
平滑肌对缩血管
物质反应性↑
真Cap网
血流↑
局部代谢产物
被稀释或冲走
Pathogenesis
Micro-circulation
Micro-circulation
Micro-circulation
Pathogenesis
Ischemic Anoxia stage
Stagnant Anoxia stage
Refractory Stage
Ischemic Anoxia Phase
Ischemic Anoxia Phase
Sympathetic-adrenal system activation


Sympathetic nerve activation
Vasoconstriction factors
CA
 Ang II
 VP
 ET
 TXA2
 LTs

Ischemic Anoxia Phase
Sympathetic-adrenal
system activation
Ischemic Anoxia Phase
Autotransfusion
Autotransfusion
 first-line defensive response
 which results from constriction of
the capacitance vessel by disgorging
stores red blood cells and plasma.
Autoperfusion
 second-line defensive response
 which results from the decreased
capillary hydrostatic pressure by
promoting tissue fluid circumfluence.
Ischemic Anoxia Phase
precapillary resistance > postcapillary resistance
Hydrostatic
Autoperfusion
pressure↓
Blood volume↓
Venous return ↓
CO↓
BP↓
Sympathetic excitation
Blood redistribution
CA、RAA、VP、TXA2、LTs etc
Peripheral vasoconstiction（A＞V）
Capillary perfusion deficiency
Tissue ischemia
Autotransfusion
Autoperfusion
Ischemic Anoxia Phase
---Clinical Manifestation
Question 1: BP↓↓？
the force of the pump
the amount of blood pumped
the arteries (size & flexibility)
Ischemic Anoxia Phase
---Clinical Manifestation
Question 1: BP↓↓？

Autotransfusion

Autoperfusion

Reninangiotensionaldosterone system

ADH
Ischemic Anoxia Phase
---Clinical Manifestation
Question 1: BP↓↓？
Question 2:
Is BP the most
important index in
diagnosis and
management of
shock？
NO！
Ischemic Anoxia Phase
---Clinical Manifestation
Hemorrhage, infection, trauma
Sympathetic-adrenal system activation
HR↑
Increase in small blood
vessel resistance and
redistribution of blood
Rapid, weak pulse
Urine output ↓
Narrowed PP
Activation of the
sweat glands
cool and moist skin
Ischemic Anoxia Phase
---Clinical Manifestation
Sympathetic-adrenal
system activation
Autotransfusion
Autoperfusion
Blood redistribution
Ischemic Anoxia Phase
---Clinical Manifestation
Pulse Pressure = Systolic Pressure - Diastolic
Pressure
Ischemic Anoxia Phase
---Clinical Manifestation





Arterial pressure: normal or mildly reduced
Skin: cool and moist
Heart rate: increased
Weak and thready pulse
Oliguria
Sympathetic-adrenal system activation
autoregulation
60-70mmHg
Pathogenesis
Ischemic Anoxia stage
Stagnant Anoxia stage
Refractory Stage
Stagnant anoxia phrase
Sympathetic adrenal system
Ischemic
anoxia
Lactic acid
Histamine
Adenosine NO
precapillary
resistance
Sympexis
Leucocyte
conglutination
Platelet adhesion
Venule contract ？
permeability
Congestion
Plasmexhidrosis
Venous return
BP
postcapillary
resistance
Sympathetic adrenal system
precapillary
resistance
< postcapillary
resistance
Hydrostatic
pressure
↑
Manifestation
Stasis in microcirculation
congestion
of kidneys
Returned
blood volume
CO
Renal blood flow
BP
Congestion
hemagglutination
Cyanosis
Piebaldism
Cerebral ischemia
Oliguria
anuria
Dulled sensorium / coma
Pathogenesis
Ischemic Anoxia stage
Stagnant Anoxia stage
Refractory Stage
Refractory Stage
Refractory Stage
Mechanism

Toxins from the sepsis-producing organisms incite an
immune reaction which leads to decreased vascular
tone and increased permeability.

Cytokines incite neutrophil activation, result in
capillary leak syndrome and DIC.

Abnormal oxygen delivery or the ability of cells to use
oxygen effectively.
Refractory Stage
DIC
Diffuse Intravascular Coagulation

MSOF
Multiple System Organ Failure
Tissue anoxia
Cell injury
Collagen exposure
Blood coagulation
factors activation
+
Acidosis
+
Blood rheology
+
TXA2/PGI2
Phagocyte
activation
IL-1 TNF
MODS
IL-6 etc
Cell necrosis
Apoptosis
DIC
MODS
Bleeding
MODS
MODS is the progressive dysfunction of
two or more organ systems resulting from
an uncontrolled inflammatory response to a
severe illness or injury.
General and Specific Character of Shock
Generality
Sympathetic
excitation
Ischemia
Individuality
Without ischemic anoxia phase
Without DIC
Cardiac output
Cell injury
Congestion
Failure
hemorrhagic shock :
caused by
insufficient circulating volume
the most common type
15min
20％
pressure (% of normal)
Cardiac output and arterial
BP=CO×SVR
% of total blood removed
Septic shock:
Tissue hypoperfusion as a
result of systemic response to
overwhelming infection.
Endotoxin
Inflammatory
Sympathomimetic
factors
nerve effect
α-R
Vasoconstriction
Cold shock
β-R
Vasodilation
Warm shock
Septic shock:
Hypodynamic shock (Cold Shock):
an inadequate or falling cardiac output,
vasoconstriction (increased SVR).
Septic shock
Hyperdynamic shock (Warm shock):
a normal to high cardiac output,
systemic vasodilation (decreased SVR).
Hemodynamic
Parameter
Hyperdynamic
"Warm" Shock
Hypodynamic
"Cold" Shock
SVR
↓
↑
CO
↑
↓
Opening of arteriovenous shunt
Neurogenic shock :
decreased sympathetic control of
blood vessel tone caused by a defect
in vasomotor center in the brain stem
or sympathetic outflow to the blood
vessels.
Anaphylactic shock:
a widespread hypersensitivity reaction
known as anaphylaxis.
-- vasodilation, peripheral pooling, and
relative hypovolemia, leading to
decreased tissue perfusion and impaired
cellular metabolism.
infection
anaphylaxis
Capacity of
blood vessel
bleeding
Myocardial
infarction
Wound
Blood volume
Returned blood volume
CO
BP
Sympathetico-adrenomedullary system
Perfusion of microcirculation
Tisssue anoxia
Metabolic acidosis
Stasis in microcirculation
DIC
MODS
Plasmexhidrosis
BP
Functional and Metabolic Changes
Impaired cellular metabolism
↓Tissue
perfusion
Impaired oxygen use
Anaerobic
metabolism
↓ATP
↓Na+,K+ pump
↓O2 affinity
for HB
↑Serum
glucose
↑Lactate
Metabolic acidosis
↓Circulatory volume
CAs, cortisol. etc
↑Pyruvate ↑Lipolysis
↑Intracellular Na+ and water
Clotting cascade
Impaired glucose use
Cellular
edema
Inflammatory
response
Serum
↑Gluconeogenesis
triglycerides,
free fatty
↑Glucogenolysis
acids
↓Energy stores
Release of lysosomal enzymes
Disturbances of cell metabolism
Organ Dysfunction
Shock lung

Rapid and labored
respiration

PaO2
Diffusion impairment
Ventilation-perfusion imbalance
1st
Renal failure
 Oliguria
Functional
renal failure
 Azotemia
Parenchymal renal failure
 Hyperkalemia

Metabolic acidosis
2nd
Heart failure

Discrepancy between
myocardial oxygen
availability and
consumption

Decreased PO2

Acidosis

Hyperkalemia

DIC

Endotoxin
Hepatic insufficiency
gastrointestinal
system
dysfunction
Treatment Measures
Don’t ever wait for symptoms to
develop before beginning the treatment
for shock.
shock is
easier to prevent than to cure.
Treatment Measures


Blood and plasma transfusion
Vasoactive drugs
Blood and Plasma transfusion
lose
The amount is based on how much patients need
Hydrostatic pressure↑
Volume indicators: CVP and
PAWP
Volume Indicators
Central Venous Pressure (CVP)
-- Circulating blood volume
-- Venous tone
-- Right ventricular function
Pulmonary artery wedge pressure (PAWP)
-- left ventricular function
CVP
(6~12H2O)
High ( > 10cm water):
Low (< 3cm water):
Fluid overload
hypovolaemia
Right ventricular failure
haemorrhage
Superior vena caval obstruction
septicaemia
Tricuspid regurgitation
regional anaesthesia
Cardiac tamponade
polyuria
Pulmonary stenosis
gastrointestinal fluid sequestration
Pulmonary hypertension
Addisonian crisis
Left ventricular failure
sympathetic dysfunction
Glomerulonephritis
peripheral vasodilatation
PAWP (8~12 mmHg)
Low (< 8mmHg):
High ( > 20mmHg):
High ( > 30mmHg):
hypovolaemia
Left ventricular failure
lung edema
Treatment Measures


Blood and plasma transfusion
Vasoactive drugs
Vasodilator substance
(after the correction of acidosis)
neurogenic shock
anaphylactic shock
Vasoconstrictive substance
Hemorrhagic shock
Treatment Measures




Blood and plasma transfusion
Vasoactive drugs
Oxygen therapy
Other therapy
- acidosis
- glucocorticoids
Goal: correct or control the underlying
causes and improve tissue perfusion