Hemodynamics Flashcards
1
Q
Circulatory disorders:
A
Edema Hyperemia and Congestion Hemorrhage Thrombosis Embolism Infarction Shock
2
Q
% of water from body weight
A
45-75% of body weight
Young, healthy men = 50-60%
Young, healthy women = 45-50%
* decreases with age
3
Q
Decreased Osmotic pressure
Or
Reduced plasma osmotic pressure
Causes
A
Hypoproteinemia: liver disease 1- Protein losing glomerulopathies (nephrotic syndrome) 2- Liver cirrhosis 3- Malnutrition 4- Protein losing gastroenteropathy
4
Q
~ 5% of total body fluid is in the…
A
vascular compartment
5
Q
The balance between vascular hydrostatic pressure and plasma colloid osmotic pressure is the driving force that maintains movement of fluids between vascular and interstitial spaces
A
Normal fluid balance
6
Q
may occur due to clotting disorders, or from trauma
A
Bleeding
7
Q
Normally, the exit of fluid into the interstitium at the arteriolar end is almost balanced by
A
inflow of fluid from the interstitium back into the vascular bed at the venular end
8
Q
In normal case
The blood net flow in arteriole is
A
Out
9
Q
A small amount of fluid stays in the interstitium because
A
of little higher hydrostatic pressure to push fluids out
10
Q
In acute inflammation the net flow changes are
A
Net flow out in arterioles and venules and capillaries
11
Q
increased fluid in the interstitial tissue spaces
A
Edema
12
Q
Distribution of Body Water
In intracellular and extracellular compartments
A
Intracellular compartment: 2/3 of body water (40% body weight) Extracellular compartment: 1/3 of body water (20% body weight) Plasma (water = 4% - 5% body weight) Interstitial fluid (water = 15% body weight)
13
Q
pleural effusion
A
hydrothorax
14
Q
Venous obstruction or compression
Causes of it
A
a- Thrombosis
b- External pressure (tumor)
c- Inactivity of lower limb
15
Q
pericardial effusion
A
hydropericardium
16
Q
A small amount of fluid stays in the interstitium because of little higher hydrostatic pressure to push fluids out
This little amount of fluid is drained back by…
A
Lymphatics
17
Q
ascites
A
hydroperitoneum
18
Q
Lymphatic obstruction
Causes
A
Elephantiasis
1-Inflammatory
2- Neoplastic
3- Post-surgical
4- Post-irradiation
19
Q
Leaky vessels
A
Inflammation
20
Q
Impaired venous return
Causes of it
A
1- Congestive heart failure
2- Constrictive pericarditis
3- Ascites (liver cirrhosis)
4- Venous obstruction or compression
21
Q
Arteriolar dilation
Causes of it
A
1- Heat
2- Neurohumoral disturbance
3- Inflammation
22
Q
Edema of the dependent parts of the body (e.g., the legs when standing) is a prominent feature of
A
cardiac failure, particularly of the right ventricle
23
Q
Myocardial cells die after
A
20-30 minutes
24
Q
is severe and generalized edema with profound subcutaneous tissue swelling
A
Anasarca
25
In............,diminished outflow leads to a capillary bed swollen with deoxygenated venous blood and resulting in cyanosis
Congestion
26
In capillaries normal case the blood net flow is
No net flow
27
It can be diffuse, or it may be more prominent in the regions with the highest hydrostatic pressures (the edema distribution is influenced by gravity and is termed dependent).
Finger pressure over significantly edematous subcutaneous tissue displaces the interstitial fluid and leaves a finger-shaped depression
I-Subcutaneous edema (pitting edema)
28
Inflammation
1- Acute inflammation
2- Chronic inflammation
3- Angiogenesis
29
II- Edema due to renal dysfunction or nephrotic syndrome
| It may be initially manifest in tissues with a loose connective tissue matrix, e.g. eyelids, causing....
periorbital edema
30
The surface of the brain with ...........demonstrates widened gyri with a flattened surface. The sulci are narrowed
Cerebral edema
31
Inflammatory edema has a high protein content and is associated with an inflammatory reaction.
Exudate
32
Noninflammatory edema has a low protein content is caused by alterations in hemodynamic forces across the capillary wall (hemodynamic edema).
Transudate
33
Sodium Retention
| Causes
1- Excessive Na intake with renal insufficiency
2- Increased tubular absorption of Na
a- Renal hypoperfusion
b- Increased renin-angiotensin-
aldosterone secretion
34
..........is an active process that results from increased blood flow because of arteriolar dilation.
Tissues that have.............means that they have more oxygenated blood and will appear more red
Hyperemia
35
It’s a passive process, it may result from impaired venous return from the tissue involved
Tissues will have deoxygenated blood
The tissue has a blue-red color (cyanosis)
Causes may be local or systemic: cardiac or hepatic
Congestion
36
In ........, increased inflow leads to engorgement with oxygenated blood, resulting in erythema.
Hyperemia
37
In both cases there is an increased volume and pressure of blood in a given tissue with associated capillary dilation and a potential for fluid extravasation
Hyperemia and congestion
38
In chronic passive congestion, there will be:
1- Stasis of poorly oxygenated blood
2- Chronic hypoxia due to impaired circulation
3- Degeneration & Death of the parenchymal cells in that tissue
4- Persistent congestion of the capillaries will cause their rupture, resulting in foci of hemorrhage
5- Red cells fragments and necrotic tissue will be phagocytosed resulting in aggregates of hemosiderin macrophages
39
In normal case
| The blood net flow in venules is..
In
40
Increased capillary hydrostatic pressure
| Causes
Venous obstructions
Cardiac failure
Arteriolar dilation
41
Red cells fragments and necrotic tissue will be phagocytosed resulting in ....
aggregates of hemosiderin macrophages
42
Hemorrhage simply means
bleeding
43
Capillary bleeding can occur because of
congestion, trauma, or inflammation
44
Collection of blood within a tissue is called
Hematoma
45
Large hematomas can be
Fatal
46
More severe than cardiac edema and affects all parts of the body equally.
Edema due to renal dysfunction or nephrotic syndrome
47
........may be external or internal (within the tissues)
Bleeding
48
Significance of bleeding depends on:
the amount and the place where bleeding occurs.
Small amounts of bleeding in the cranial cavity may be fatal, whereas, 1.5 liters of blood in the stomach may pass unnoticed by the patient.
49
Rapid bleeding of up to 20% of total body blood may be
compensated for by the body and does not cause serious clinical manifestations
50
Slow bleeding may result in
iron deficiency anemia, particularly in elderly people
51
Small hemorrhages of 1-2 mm into the skin or mucous membranes .
Petechiae
52
Petechiae are caused because of:
1- increased intravascular pressure
2- low platelet count
3- defective platelet function
4- clotting factor deficiency
53
Petechial hemorrhages of the colonic mucosa, as a consequence of ...ll
thrombocytopenia.
54
larger hemorrhages: 3-5 mm
Purpuras
55
Anticoagulation mechanism (Antithrombotic counter regulation) is triggered after the formation of
permanent clot by polymerization of fibrin and aggregation of platelets
56
Purpuras causes
```
Causes:
1- Increased intravascular pressure
2- Low platelet count
3- Defective platelet function
4- Clotting factor deficiency
5. Vasculitis
6. Increased vascular fragility
7. Trauma
```
57
Ecchymosis:
are subcutaneous hematoma or bruise
| They are 1-2 cm in area
58
The erythrocytes in these hemorrhages are phagocytosed and degraded.
In Ecchymosis
59
```
After the phagocytosis of ecchymosis’ erythrocytes
Their hemoglobin (red-blue in color) will be converted to ..
```
bilirubin, which is blue green in color
60
bilirubin will be converted to
hemosiderin, a golden-brown colored material
61
is a kind of injury, usually caused by blunt impact, in which the capillaries are damaged, allowing blood to seep into the surrounding tissue.
A bruise or Ecchymosis
62
Larger accumulations of blood
1-hemothorax: blood in the ..... cavity
2- hemopericardium: blood in the pericardial cavity
3- hemoarthrosis: blood in the .....
4- hemoperitoneum: blood in the peritoneal cavity
Pleural
| Joints
63
is an areas of ischemic necrosis that is caused by occlusion of either the arterial supply or the venous drainage in a particular tissue.
Infarction
64
Infarction Examples:
```
Myocardial infarction
Cerebral infarction
Pulmonary infarction
Bowel infarction
Extremities necrosis (gangrene)
```
65
What vascular lesions lead to infarction?
[Thrombosis , Embolism ] 90%
66
Uncommon causes of infarction
Vasospasm of vessels: coronaries in Prinzmetal angina
Compression from outside by tumors or edema
Twisting of the vessels as in torsion of testis or intestinal intussusception or volvulus
Entrapment of vessels as in strangulated hernia
Traumatic rupture of the blood supply
67
occurs in arterial occlusions or in solid organs (such as heart, spleen, and kidney)
White infarcts (anemic)
68
Neurons undergo irreversible damage if they are deprived of their blood supply for
only 3-4 minutes
69
Infarcts are generally wedge shaped.
| The apex of the wedge is at the site of the occluded vessel, and the base points towards the periphery of the organ.
White infarcts
70
If the base of the infarcts is a serous surface, there will be ............on that surface
fibrinous exudate
71
Hemorrhagic infarcts
Red infarcts
72
Red infarcts occur in
Loose tissues like lung that permits collection of blood
Tissues with dual blood supply, lungs and intestine.
Venous occlusion (e.g. ovarian torsions)
Already congested tissues from impaired venous flow (e.g. liver congestion)
Reperfusion of tissues after arterial occlusion that has caused necrosis
73
Sequence of hemostasis
```
Vasoconstriction
Platelet activation
Platelet aggregation
Coagulation cascade
Stable clot formation
Clot dissolution
```
74
EMBOLIZATION TO SMALL DISTAL VESSELS IN LUNG MAY CAUSE ISCHEMIC NECROSIS OF TISSUE OR INFARCT
PULMONARY INFARCT
75
Factors that affect development of infarct
1. Nature of the vascular supply:
2. Rate of occlusion development:
3. Susceptibility of involved tissue to hypoxia:
4. Oxygen content of the blood:
76
have end-arterial blood supply
spleen, kidney, and the eye
77
Have radial and ulnar blood supply
Upper extremities
78
pulmonary and bronchial blood supply
Lung
79
Slowly developing occlusion may give time for
alternative pathway
80
.....Are more likely to develop infarction as compared to normal people
Cyanotic patients or anemic
81
the process by which the blood is maintained in a clot-free fluid state and produces a local hemostatic plug at sites of vascular injury
Normal hemostasis
82
inappropriate activation of the hemostatic process in uninjured vasculature or formation of thrombus in the setting of relatively minimal vascular injury
Thrombosis
83
Platelet activation
| Platelet aggregation
Primary hemostasis
84
Coagulation cascade
| Stable clot formation
Secondary hemostasis
85
initial vasoconstriction is stimulated by the release of..
endothelin from the endothelial cells. The endothelin is an important vasoconstrictor
86
results in diffuse opacification of the lung
Pulmonary edema
87
Activation & adherence of platelets: Platelets adhere to exposed........... via............ and are activated.
extracellular matrix (ECM) via von Willebrand factor (vWF)
88
Activated platelets undergo a ..........change and ..........release
Shape change and granule release
89
released........ and........... lead to further platelet aggregation, to form the primary hemostatic plug.
ADP and thromboxane A2 (TXA2)
90
Local activation of the coagulation cascade (involving ...........and ..........) results in .........polymerization, reinforcing the platelets into a definitive secondary hemostatic plug.
(involving tissue factor and platelet phospholipids) results in fibrin polymerization
91
The tissue factor (cellular lipoprotein) has the following characteristics:
is a pro-coagulant factor
synthesized by endothelium
is released at the site of injury
92
Tissue plasminogen activator (t-PA, a fibrinolytic product) and thrombomodulin (interfering with the coagulation cascade)
Counter-regulatory mechanisms activated to prevent further expansion of the clot and limit the hemostatic process to the site of injury.
93
Both hemostasis and thrombosis are dependent on
The vascular wall (Endothelium)
Platelets
The coagulation cascade
94
The endothelial cells normally posses ..... properties
Antiplatelet, Anticoagulation, and fibrinolytic properties
95
If the endothelial cells are injured or activated,
| They develop
pro-coagulant functions
These activators increase procoagulant activity, and decrease anticoagulant activity
results in a procoagulant phenotype that contributes to localized clot formation
96
Thromboplastin
Tissue factor
97
endothelial cells activators
1- Cytokines: IL-1 and TNF
2- Plasma mediators
3- Infectious agents
98
Endothelial cells synthesize
```
Endothelin
Tissue factor
PGI2 ,NO
Adenosine diphosphatase
Heparin like molecules
Thrombomodulin
T-PA
vWF
```
99
VWF helps in?
Platelets bind to collagen (and ECM)
100
t-PA: promotes
fibrinolysis of the fibrin clot
101
convert thrombin from procoagulant to anticoagulant
Thrombomodulin
102
allow antithrombin to inactivate thrombin, factor Xa, and other caogulation factors
Heparin like molecules
103
Dysfunctional endothelium may elaborate greater amounts of .....and smaller amounts of...
greater amounts of procoagulant factors (e.g., adhesion molecules to bind platelets, tissue factor) and smaller amounts of anticoagulant effectors (e.g., thrombomodulin, PGI2, t-PA).
104
activate the coagulation cascade, the extrinsic pathway
Tissue factor
105
PGI2 & NO
vasodilators and inhibit platelet aggregation
106
Adenosine diphosphatase
degrades ADP and inhibits platelet aggregation
107
Prothrombotic properties of endothelium
Platelets adhere to the exposed sub-endothelial collagen. This is facilitated by vWF secreted by endothelial cells
Endothelial cells secrete tissue factor which activates the extrinsic clotting pathway
Endothelium secretes plasminogen activator inhibitors which depress fibrinolysis
108
At injury site, platelets come in contact with ECM and they undergo three general reactions
Adhesion and shape change
2- Secretion
3- Aggregation
109
Genetic deficiencies of vWF (von Willebrand disease) or its receptors result
in serious bleeding disorders.
110
thromboxane A2 (TXA2)
Vasoconstrictor
Secreted by platelets for platelet aggregation
In the primamry hemostatic plug nd is reversible
111
formed in the coagulation cascade.
binds to platelet surface and with ADP and TXA2 causes further platelet aggregation, followed by platelet contraction and becoming irreversible (secondary hemostatic plug)
Thrombin
112
Loss of endothelium leads to
Exposure of ECM
Adherence of platelets, release of tissue factor, local depletion of PGI2 and t-PA particularly important in thrombus formation in the heart and arterial circulation
113
convert fribrinogen to fibrin that adds to cementing of the platelet plug
Thrombin
114
(a cyclooxygenase inhibitor) in patients at risk for coronary thrombosis is related to its ability to inhibit the synthesis of TXA2.
Aspirin
115
The intrinsic pathway initiated by
Activation of Hageman factor
116
The extrinsic pathway is initiated by
Tissue factor
117
It’s a series of reactions in which inactive proenzymes are converted into active enzymes
This results in the formation of thrombin, that converts the soluble fibrinogen into insoluble fibrin
Coagulation cascade
119
HMWK: high-molecular-weight kininogen.
| Activates
Hageman factor to XIIa
120
Intrinsic pathway factors
12, 11, 9, 8
121
is triggered after the formation of permanent clot by polymerization of fibrin and aggregation of platelets
Anticoagulation mechanism Antithrombotic counter regulation
122
Extrinsic Pathway
| Factors
Tissue factor, (7)
123
Clotting is regulated in a way to be confined to the site of injury by two natural anticoagulants
1. Antithrombins: (e.g., antithrombin III)
| 2. Protein C and S:
124
It inhibits the activity of thrombin, factor IXa, Xa, XIa, & XIIa
Antithrombins
125
Antithrombin is activated by
binding to heparin like molecules on endothelial cells
126
They are two vitamin K dependent proteins
| They inactivate cofactors Va and VIIIa
Protein C and S
127
fibrinolytic cascade
| limits the size of the final clot by activation of
Plasmin
128
Plasmin is obtained from the precursor plasminogen either by .... or by....
XIIa or by plasminogen activators (mainly t-PA)
129
Plasmin breaks down fibrin producing
fibrin split products (also called fibrin degradation products)
130
Fibrinolysis is blocked by
Plasminogen activator inhibitors
131
Causes of Thrombosis
Endothelial injury
Blood hypercoagulability
Stasis or turbulence of blood flow
132
Common pathway factors
10
| 5,2
133
Causes of endothelial cell injury:
```
§ Physical disruption
§ Hypertension
§ Turbulent f low over scarred valves
§ Bacterial endotoxins
§ Radiation
§ Hypercholesterolemia
§ Toxic substances (e.g., cigarette smoke)
```
134
Flow of platelets in the blood is
Laminar
135
Turbulence or stasis will result in:
1) Bring platelets into contact with the endothelium
2) Prevent dilution of activated clotting factors by fresh- flowing blood
3) Promote endothelial cell activation, predisposing to local thrombosis and leukocyte adhesion
4) Delay the inflow of clotting factor inhibitors and permit the build-up of thrombi
136
Hypercoagulability Conditions associated with an increased risk of thrombosis
Primary (Genetic) causes
1- Factor V mutations
2- Prothrombin mutations
3- Antithrombin III deficiency 4- Protein C and S deficiency
137
Hypercoagulability
| Secondary (Acquired) causes:
1. Prolonged bed rest or immobilization
2. Myocardial infarction , (MI)
3. Tissue damage (surgery, fracture, burns)
4. Cancer
5. Prosthetic cardiac valves
6. Disseminated intravascular coagulation (DIC)
7. Lupus anticoagulant
138
They cause obstruction of arteries and veins. They are possible sources of emboli
Thrombi
139
.......may develop anywhere in the cardiovascular system
....... are of variable size and shape
An area of attachment to the underlying vessel or heart wall, frequently firmest at the point of origin, is characteristic of all .......
Thrombi
140
are those thrombi that form on the walls of the heart chambers and aorta
Mural thrombi
141
Causes of Mural thrombi
arrhythmias, dilated cardiomyopathy, MI, myocarditis, catheter trauma
142
Lines of Zahn
```
produced due to alternating
pale layers of platelets and
fibrin with dark layers of
RBC in thrombi formed in
the heart or aorta
```
143
Thrombi in coronary arteries are almost always due to
endothelial damage resulting from atherosclerosis.
144
Venous thrombosis (Phlebothrombosis)
Characteristically occur in
Sites of stasis
145
.....May not be well attached and are prone to emboli
| They contain more RBCs, therefore known as red, or stasis, thrombi
Venous thrombosis (Phlebothrombosis)
146
Venous thrombosis (Phlebothrombosis)
90% of cases involve the veins of
Lower extremities
147
Superficial venous thrombi usually occur in the..... particularly in....
the saphenous system, particularly in varicosities
148
Superficial thrombi may cause swelling and pain but seldom...
Embolize
149
........thrombi in the large veins particularly those above the knee joint in the popliteal, femoral, & iliac veins are more serious as they may embolize
Deep
150
....... thromboses are asymptomatic in 50% of cases. Advanced age, bed rest, and immobilization increase the risk of .......thrombosis
Deep vein
151
Fate of Thrombus
1. Propagation: thrombi may accumulate more fibrin & platelets causing obstruction
2. Embolization: thrombi may detached and be transported to other sites in the vasculature
3. Dissolution: thrombi may be removed by fibrinolytic activity
4. Organization and Recanalization: Thrombi may induce inflammation and fibrosis (organization) and may become recanalized (re-establish vascular flow), or they may be incorporated into a thickened vascular wall. (in old thrombi)
152
Abnormal solid mass carried in blood.
Embolus
153
```
Embolism types with example
Thromboembolism - .....
Fat - .....
Gas – ....
Liquid – ......l
```
Thromboembolism - atherosclerosis
Fat - Fractures
Gas – ‘Caisson disease’
Liquid – Amniotic fluid
154
Outcome of Embolism
– Collateral circulation
– Infarction
– Hemorrhage
155
When embolus lodges within a vessel and blocks blood supply its called
Embolism
156
99% of all emboli represent part of thrombus, hence the commonly used term
Thromboembolism
157
Rare forms of emboli include:
Droplets of fat, bubbles of air or nitrogen,
atherosclerotic (cholesterol emboli), tumor fragments,
bits of bone marrow, or foreign bodies such as bullets.
158
Thromboembolism common in hospitalized patients
Pulmonary thromboembolism
159
Pulmonary thromboembolism originates mainly in
Deep veins of lower extremities
160
Emboli travel to the right side of the heart to the pulmonary arteries.
Pulmonary thromboembolism
161
Pulmonary thromboembolism May be so large to block the main pulmonary artery at the site of bifurcation, called.....
Or it may be small and pass into smaller branches
saddle embolus
162
Fate of pulmonary embolism
- Sudden death, right ventricular failure, or cardiovascular collapse occur when 60% or more of the pulmonary circulation is obstructed with emboli.
- 60-80% are clinically silent because they are small, undergo dissolution or recanalization
- Embolic obstruction of medium-sized arteries may result in pulmonary hemorrhage
- Multiple emboli over time may cause pulmonary hypertension with right ventricular failure
163
Refers to emboli traveling within the arterial circulation
Systemic thromboembolism
164
Systemic thromboembolism
80% arise from intra-cardiac mural thrombi associated with
left ventricular wall infarcts (2/3),with dilated left atria (1/3)
The rest originates from:
Atherosclerosis in aorta or from aortic aneurysms
• Paradoxical embolism: rarely, emboli may travel from venous to arterial circulation via a communication between arterial & venous circulation
165
Major sites for lodging of systemic emboli:
the lower extremities (75%) and the brain (10%)
166
.....emboli cause infarction of tissues in the distribution of the obstructed vessel
Arterial
167
mainly after fractures of long
| bones or, rarely, in the setting of soft tissue trauma and burns
Fat embolism
168
Fat embolism symptoms
Fatal in about 10% of cases
Respiratory: tachypnea, dyspnea
Neurological: irritability, restlessness, and coma
Thrombocytopenia with characteristic petechiae
It generally develops 1 to 3 days after injury
The pathogenesis involves both mechanical obstruction and toxic injury to endothelium by FFA
169
Enters the circulation from marrow after rupture of bone vascular sinusoids, or from adipose tissue through rupture of tissue venules
Fat embolism
170
may enter the circulation during surgical obstetric procedures or as a consequence of chest wall injury
Generally, > 100 mL of ....is required to produce a clinical effect
May cause focal ischemia in the brain and heart
May cause edema, hemorrhages, and focal atelectasis or emphysema, leading to respiratory distress in the lungs
Air/Air embolism
171
Amniotic Fluid Embolism
| The underlying cause is
the leakage of amniotic fluid (and its contents) into the maternal circulation via a tear in the placental membranes and rupture of uterine veins.
172
Amniotic fluid embolism
| The presence of the followings in the pulmonary circulation will confirm the diagnosis:
Squamous cells from fetal skin
Lanugo hair
Mucin derived from fetal respiratory or GI tracts
173
Systemic hypoperfusion due to a reduction either in cardiac output or in the effective circulating blood volume
Shock (cardiovascular collapse)
174
Types of shock:
```
Cardiogenic shock
Pump failure
Hemorrhagic (hypovolemic) shock
Decrease in blood volume
Septic shock
Failure of microcirculation to retain pressure leading to wide spread peripheral vasodilatation
```
175
Failure of myocardial pump owing to intrinsic myocardial damage, extrinsic pressure, or obstruction to outflow
Cardiogenic shock
176
Causes of Cardiogenic shock
1. myocardial infarction
2. cardiac tamponade
3. outflow obstruction in pulmonary embolism 4. ventricular arrhrythmia
177
Signs and symptoms: Cardiogenic shock
```
Tachycardia
• Hypotension
• Tachypnea
• Restlessness, agitation
• Pallor & sweating
```
178
Results from loss of blood or plasma volume
Hypovolemic shock
179
Causes of Hypovolemic shock
1. Hemorrhage
| 2. Fluid loss from severe vomiting, diarrhea, burns, or trauma
180
Hypovolemic shock Signs and symptoms:
same as in cardiogenic shock
* Tachycardia
* Hypotension
* Tachypnea
* Restlessness, agitation
* Pallor & sweating
181
Results from spread of an initially localized infection (e.g., abscess, peritonitis, pneumonia) into the bloodstream.
Septic shock
182
Occurs when an overwhelming infection leads to low blood pressure, and vital organs may not function properly
Septic shock
183
Has 25% to 50% mortality rate
| One of the most common causes of death in intensive care units
Septic shock
184
Causes of Septic shock
Caused by systemic microbial infection:
Most commonly (~ 70%), gram-negative infections (endotoxic shock)
Can also occur with gram-positive and fungal infections.
185
Pathogenesis of Septic Shock
Endotoxins are bacterial wall lipopolysaccharides (LPSs)
LPS activate mononuclear cell with production of chemical
mediators
The collective effect of these mediators result in:
Fever, acute-phase reaction, neutrophilia
Vasodilation: hypotension
Widespread endothelial cell injury
Activation of the coagulation system
Multiorgan system failure
186
Hemodynamic shock due to loss of vascular tone and peripheral pooling of blood resulting in vasodialtion
Neurogenic shock
187
Initiated by a generalized immunoglobulin E-mediated hypersensitivity response
Associated with systemic vasodilatation and increased vascular permeability
Anaphylactic shock
188
Neurogenic shock:causes of it
spinal cord injury or trauma
189
Causes a sudden increase in the capacity of the vascular bed, which cannot be filled adequately by the normal circulating blood volume. Thus, tissue hypoperfusion and cellular anoxia result.
Anaphylactic shock
190
Stages of Shock
Initial nonprogressive stage
Progressive stage
Irreversible stage
191
the causative factors of shock are contained and perfusion of vital organs is maintained (adequate compensatory mechanism)
Initial nonprogressive stage
192
tissue hypoperfusion continues, resulting in tissue hypoxia, and metabolic disturbances (e.g., anaerobic glycolysis produced lactic acidosis).
Compensatory mechanism is no longer adequate
Progressive stage
193
the patient has multiple organ failure, and death becomes inevitable
Irreversible stage
