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Pathophysiology of circulatory shock

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Title: Bez nadpisu Author: PATFYZ Last modified by: Tatar Created Date: 3/7/2002 1:21:49 PM Document presentation format: P edv d n na obrazovce – PowerPoint PPT presentation

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Title: Pathophysiology of circulatory shock


1
Pathophysiology of circulatory shock
  • Prof. MUDr. Miloš Tatár, CSc.
  • Dept of Pathophysiology

2
Clinical features of shock
- drop of systolic blood pressure (BP ? 90 torr)
in hypertonic patients decrease of 50 torr
- low cardiac output and tachycardia
- vasoconstriction skin and splanchnic areas
- oliguria (lt 20 ml/hour)
- cold wet skin
- constriction of superficial veins
- marked muscle weakness
- usualy ? body temperature (except septic shock)
- disorientation
- metabolic acidosis
3
Characteristics of circulatory shock
Complex clinical syndrome encompassing a group of
conditions with variable hemodynamic
manifestations
Common denominator is generalised inadequacy of
blood flow through the body hypoperfusion
compromises the delivery of oxygen and nutrients
and the removal of metabolites tissue hypoxia
shifts metabolism to anaerobic pathways with
production of lactic acid
if shock is not corrected it leads to
a) cell dysfunction
b) irreversible multiorgan insufficiency
d) death
4
Cardiovascular dysorders in shock
a) acute circulatory insufficiency
b) mismatching between blood volume and
volume of vascular bed
tissue hypoperfusion
5
Blood pressure
Tissue perfusion
Cardiac output
x
Vascular resistance
6
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7
Factors determining tissue perfusion
A. cardial cardiac output
B. vascular changes in vascular resistance
regulation of vascular tone
- tonic sympathetic activity
- systemic catecholamines
  • myogenic response - constant tissue blood
  • flow during changed perfusion pressure

- metabolic autoregulation - vasodilatory
substances
- endothelial NO
8
C. humoral renin, vazopresin, prostaglandins,
kinins, atrial natriuretic factor
Factors determining microcirculation
  • adhesion of leukocytes and platelets on
    epithelial
  • lesions

- intravascular coagulation
- constriction of precapillary and postcapillary
vessels
- intense hypoxia ? vasodilation of arteriols,
venoconstriction continues ? intravascular fluid
loss
- ? capillary permeability ? tissue edema
9
Etiology of circulatory shock
1. Hypovolemic - intravascular fluid volume
loss hemorrhage,
fluid depletion or sequestration
2. Cardiogenic - impairment of heart pump
myopathic lesions
myocardial infarction,
cardiomyopathies
dysrhythmias obstructive and
regurgitant lesions of intracardial
blood flow mechanics
10
3. Obstructive - factors extrinsic to cardiac
valves and myocardium
v. cava obstruction, pericardial tamponade,
pulmonary embolism, coarctation of aorta
4. Distributive - pathologic redistribution of
intravascular fluid volume septicaemia
endotoxic, secondary to specific infection
anaphylactic
11
NORMAL
2. CARDIOGENIC
1. HYPOVOLEMIC
3. DISTRIBUTIVE
4. OBSTRUCTIVE
High Resistance
Low Resistance
12
Pathogenesis of circulatory shock
Usually results from inadequate cardiac output
(CO)
Any factor reducing CO will likely lead to shock
  • Cardiac abnormalities
  • decreased ability of the heart to pump blood

- myocardial infarction - toxic states of
heart - severe heart valve dysfunction -
arrhythmias
2. Decreased venous return
- diminished blood volume - decreased vasomotor
tone - obstruction to blood flow at some
points in the circulation
13
Stages of shock
1. Nonprogressive stage (compensated)
Compensatory mechanisms (negative feedback) of
the circulation can return CO and BP to normal
levels
- baroreceptor reflexes ? sympathetic stimulation
? constrict arteriols in most parts of the body
and venous reservoirs ? protection of coronary
and cerebral blood flow
  • angiotensin-aldosteron, ADH ? vasoconstriction,
  • water and salt retention by the kidneys

- absorption of fluid from ISF and GIT, increased
thirst
14
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15
2. Progressive shock
  • circulatory system themselves begin to
    deteriorate,
  • without therapy shock becomes steadily worse
    until death
  • positive feedback mechanisms are developed and
    can
  • cause vicious circle of progressively
    decreasing CO

Cardiac depression - ? coronary blood flow, ?
contractility
Vasomotor failure - ? cerebral blood flow
Release of toxins by ischemic tissues histamine,
serotonin, tissue enzymes
Intestines hypoperfusion ? mucosal barrier
disturbance ? endotoxin formation and
absorption ? vasodilatation, cardiac
depression
Vasodilation in precapillary bed
Generalised cellular deterioration ? K , ? ATP,
release of hydrolases first signs of multiorgan
failure
16
3. Irreversible shock
  • despite therapy circulatory system continues to
  • deteriorate and death ensues

- marked hypoxic tissue damage
  • endothelial dysfunction ? adhesive molecules,
  • neutrophils, macrophages ? inflammation

- progressive acidosis
  • microcirculation failure ? plasma proteins leak
  • to interstitium

- advanced disseminated intravascular coagulation
17
Cardiogenic shock
  • infarction process (45 loss of functional mass
    of
  • left ventricle)

- ventricle fails as a pump
  • BP ? 90 torr for at least 30 min,
  • ? pulmonary capillary pressure ? lung edema

- self-perpetuing cycle then ensues (vicious
circle) metabolic acidosis and reduced coronary
perfusion further impairing ventricular function
and predisposing to the development of
dysrhythmias
Progression of myocardial dysfunction
- hypotension, tachycardia, fluid retention,
hypoxemia
18
Septic shock
Typical causes peritonitis, gangrenous
infection, pyelonephritis
Special features
1. high fever
2. marked vasodilatation (inflammation)
3. ? or normal CO vazodilatation, ? metabolic
rate
4. disseminated intravascular coagulation ?
clotting factors to be used up ? hemorrhages
occur into many tissue (GIT)
IL-1 and TNF PGE2, leukotrienes and NO -
vascular relaxation - ? endothelial permeability
(deficit of intravascular volume) - ? myocardial
contractility
19
Early stage no signs of circulatory insufficiency
Progression of infection circulatory disorders
becomes
Bacterial toxins ? deterioration of circulation ?
end-stage is not greatly different from the
end-stage of hemorrhagic shock (hypodynamic stage)
Death - hypotension - multiorgan failure
20
Cell dysfunction
prolong tissue hypoperfusion ? cell membrane
lesion, lysosomal enzymes ? cell death
mechanisms hypoxia, inflammatory mediators,
free radicals
21
Multiorgan failure
Kidney
- ? blood flow (to 10) ? ? GF ? oliguria
- ischemia ? acute tubular necrosis
- countercurrent mechanism failure ? izostenuria
- marked lesions ? acute renal failure
22
Lungs
  • disturbances of pneumocytes and
  • endothelium
  • accumulation of Tr, Neu in pulmonary
  • circulation ? release of proteases
  • ? leukotriens and free radicals

- ? permeability - ? surfactant, edema and
hemorrhagies
? respiratory insufficiency (ARDS)
23
100
SURVIVAL ( 142 Pts)
75
50
25
0-1 1-2 2-3 3-4 4-6 6-11
11-16 gt 16
LACTATE mM/l
24
EXTRACARDIAC Obstruction
CARDIOGENIC
DISTRIBUTIVE
HYPOVOLEMIC
Decreased systemic vascular resistance
Fluid loss, hemorrhage
e.g., Pericardial tamponade
Myocardial injury or necrosis
Reduced filling
Reduced systolic performance
Reduced preload
Low cardiac output
Myocardiac dysfunction
Decreased arterial pressure
High or normal cardiac output
Shock
Maldistribution of blood flow in microcirculation
Multiple organ system failure
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