Hemodynamics Flashcards
(158 cards)
1
Q
EDEMA, HYPEREMIA AND HEMORRHAGE
symptoms (5)
A
-Tumor
-Rubor
-Calor
- Dolar
- Loss of function
2
Q
Edema –
A
escape of fluid
3
Q
Congestion –
A
Abnormal accumulation of blood
4
Q
Infarction –
A
ischemic necrosis
5
Q
Shock –
A
tissue injury secondary to systemic hypotension
6
Q
Hemorrhage –
A
escape of whole blood
7
Q
Thrombosis –
A
undesired clotting of blood
8
Q
Embolism –
A
detached intravascular mass
9
Q
Water accounts for –% of the lean body weight
A
60
10
Q
Total body water is distributed between the
A
intracellular and extracellular compartments
11
Q
Extracellular compartment
(2)
A
• Intravascular 5%
• Interstitial 15%
12
Q
Hydrostatic Pressure
A
• Pressure exerted by volume of blood when confined
to a blood vessel
13
Q
Osmotic (Oncotic) Pressure
(2)
A
• Proteins in blood vessels
• Albumin
14
Q
Movement of Water Between the
A
Intravascular and Interstitial Spaces
15
Q
Opposing effects of
A
vascular
hydrostatic pressure and
plasma colloid osmotic
pressure
16
Q
Outflow at the arterial end
is nearly balanced by
A
inflow
at the venular end
17
Q
Residual fluid left in the
interstitium is drained by
A
lymphatic vessels
18
Q
— ml/min out
A
14
19
Q
— ml/min in
A
12
20
Q
— ml/min to
lymphatics
A
2
21
Q
Increased hydrostatic pressure or decreased plasma osmotic pressure will cause
A
interstitial fluid to increase
22
Q
If the capacity for lymphatic drainage is exceeded,
A
fluid accumulates (edema)
23
Q
Edema -
A
swelling of tissues that result from excessive accumulation of fluid
24
Q
Edema -
may be (3)
A
• May be highly localized as occurs in a small region of skin involved with an insect bite
• May be more regionalized, involving an entire limb or a specific organ, such as the lungs (e.g., pulmonary edema)
• May be generalized, involving the whole body
25
Hydrothorax
pleural effusion
26
Hydropericardium
pericardial effusion
27
Hydroperitoneum
ascites
28
Anasarca
generalized edema
29
Inflammatory causes of edema -
-inflammatory edema is caused by increased vascular permeability of a protein-rich exudate (exudate)
30
Non-inflammatory causes of edema -
edema caused by increased hydrostatic pressure or reduced oncotic pressure is usually protein-poor fluid (transudate)
31
Non-inflammatory causes of edema -
ex (4)
• Heart failure
• Renal failure
• Hepatic failure
• Malnutrition
32
Exudate –
high specific gravity – protein rich
• Inflammatory edema
33
Transudate –
low specific gravity – protein poor
• Volume or pressure overload
• Reduced plasma protein
34
Lymphangitis (2)
• Lymphatic spread of
bacterial infection
• Painful red streaks
and regional
lymphadenopathy
35
Lymphedema – (3)
a term used to describe an increase in
fluid in the interstitial space caused by an abnormality
in the lymphatic system
• Lymphatic fluid collects in tissues causing edema
• May be congenital or acquired
36
Acquired lymphedema
(2)
• Infection - filariasis
• Surgery, radiation therapy
37
Congenital Lymphedema - Aplasia
• Congenital malformation
of lymphatic system
38
Congenital Lymphedema - Aplasia
• Age 1 Week:
Lymphoscintigraphy exhibits
no migration of
radiopharmaceutical agent
from right foot to right
inguinal nodes
39
Congenital Lymphedema - Aplasia
• Diagnosis:
congenital aplasia
of the lymphatic system of
right leg
40
Congenital Lymphedema - Aplasia
Age 4.5 months:
debulked
41
Stewart-Treve Syndrome
(2)
• Angiosarcoma arising
from chronic
lymphedema
• Long-standing
lymphedema
secondary to surgical
lymph node dissection
and/or radiation
therapy
42
Anasarca in Renal Disease
(2)
• Severe
• Generalized edema
43
Edema Danger Zones (2)
• Lungs - Pulmonary edema
• Brain - Cerebral edema (central nervous system)
44
Cerebral Edema -
Cerebellar Tonsil Herniation (2)
• Increased intra-cranial pressure may result in herniation through the foramen magnum
• Compression of the medulla results in depression of the centers for respiration and cardiac rhythm control
45
Localized edema is usually caused by
(2)
• Increased vascular permeability (injury-inflammation)
• Obstruction of venous or lymphatic outflow
46
Generalized edema is generally caused by
decreased
plasma osmotic pressure
47
Increased hydrostatic pressure -
def
ex (2)
impaired venous return
• Congestive heart failure
• Venous obstruction or compression
48
Decreased plasma osmotic pressure (hypoproteinemia)
(3)
• Protein-losing glomerulopathies (nephrotic syndrome)
• Liver cirrhosis (ascites)
• Protein malnutrition
49
Lymphatic obstruction
(4)
• Inflammatory
• Neoplastic
• Postsurgical
• Postirradiation
50
Sodium retention
(4)
• Excessive salt intake with renal insufficiency
• Increased tubular reabsorption of sodium
- Renal hypoperfusion
- Increased renin-angiotensin-aldosterone secretion
51
Inflammation
increased permeability
52
Hyperemia
An active process in which
arteriolar dilation leads to
increased blood flow
• Sites of inflammation
• Skeletal muscle during
exercise
53
Hyperemia
Affected tissues turn red
(erythema) because of
engorgement of vessels with
oxygenatged blood
54
Congestion –
Deep Venous Thrombosis
(3)
• A passive process resulting from
reduced outflow of blood from a tissue
(stasis)
• May be systemic (heart failure) or
local (isolated venous obstruction)
• Congested tissues take on a dusky,
reddish-blue color (cyanosis) due to
red cell stasis and accumulation of
deoxygenated hemoglobin
55
Nutmeg Liver
Chronic Passive Congestion of Liver
56
Superior Vena Cava Syndrome
Compression of
superior vena cava
by neoplasm
obstructing venous
return
57
Hemorrhage –
extravasation of blood into the extravascular space
58
Capillary bleeding
oozing
59
Venous hemorrhage
seeping
60
Arterial hemorrhage
pulsating
61
Severe hemorrhage
rupture of a large vessel secondary to injury
62
Severe hemorrhage
ex (3)
Trauma, atherosclerosis, erosion of a vessel wall (inflammation or neoplasia)
63
Hemorrhagic diathesis –
increased tendency to hemorrhage occurs in a
variety of clinical disorders collectively called hemorrhagic diatheses
64
Hemothorax
thoracic cavity
65
Hemopericardium
pericardial cavity - cardiac
tamponade
66
Hemoperitoneum
peritoneal cavity
67
Hemarthrosis
joints
68
Petechiae
pinpoint hemorrhages
69
Purpura
petechiae become
confluent
70
Ecchymosis
purpurae become
confluent
71
Hematoma
cavity
72
Hemoglobin
red-blue
73
Biliverdin
yellow-green
74
Bilirubin
green-brown
75
Hemosiderin
golden yellow
76
Site of hemorrhage
• Subcutaneous tissues vs brain
77
Volume and rate of hemorrhage
• Rapid loss of up to ---% of blood
volume, or slow losses of larger
amounts may have little impact on
healthy adults
• Greater losses may cause
20
hemorrhagic (hypovolemic) shock
78
Immune Thrombocytopenic Purpura (ITP) (2)
• Autoimmune disease–
antiplatelet
autoantibodies produce
thrombocytopenia
• Treatment with
steroids, splenectomy
79
Hemostasis –
a physiologic process that maintains blood in a fluid state in normal vessels, yet also permits the rapid formation of a hemostatic clot at the site of a vascular injury
80
Thrombosis –
pathologic counterpart of hemostasis that involves blood clot
81
Hemostasis and Thrombosis
Both involve three components
• Vascular wall (endothelium)
• Platelets
• Coagulation cascade
82
von Willebrand Disease (5)
Most common hereditary bleeding disorder
• Group of bleeding disorders
• Quantitative or qualitative abnormality of
the von Willebrand factor (vWF)
• vWFis required for normal platelet
adhesion
• vWF is the carrier protein for factor VIII
83
vWF has functions in both
primary and secondary hemostasis
84
Primary hemostasis – vWF:
(2)
• Attaches to platelets via a receptor for glycoprotein Ib on the platelet surface
• Acts as a bridge between the platelets and damaged subendothelium at the site of vascular injury
85
Secondary hemostasis – vWF:
(2)
• Protects factor VIII from degradation
• Delivers factor VIII to the site of injury
86
von Willebrand Disease (2)
• Normal platelet count with increased bleeding time
• Compound defect involving platelet function and coagulation pathway
87
Factors Favoring Thrombosis (Virchow’s Triad)
• Endothelial injury
• Stasis or turbulent blood flow
• Hypercoagulability of the blood
88
• Balance between antithrombotic and prothrombotic properties of endothelium determines
whether thrombus formation, propagation or dissolution occurs
89
Normally, endothelial cells exhibit (3) properties
antiplatelet, anticoagulant and antifibrinolytic
90
Endothelial cells may be activated by (5)
trauma,
infectious agents,
hemodynamic forces,
plasma mediators and
cytokines
91
After activation, endothelial cells acquire
procoagulant activities
92
• Mural thrombi
• Occur in heart chambers or aortic lumen
93
• Arterial thrombi
(3)
• Frequently occlusive
• Coronary, cerebral, femoral arteries, most commonly
• Superimposed on ruptured, ulcerated atherosclerotic plaque
94
• Venous thrombi
(2)
• Usually occlusive – thrombus forms a long cast of the lumen
• Veins of lower extremities
95
• Vegetations –
thrombi on heart valves
96
Thrombi are focally
attached to the
underlying
vascular surface
97
Thrombi propagate from
the point of attachment in
the direction of blood flow
98
The propagating portion
of a thrombus is often
poorly attached and is
prone to
fragmentation
and embolization
99
Arterial or cardiac thrombi
(2)
• Begin at sites of turbulence or endothelial injury
• Propagate away from the heart
100
Venous thrombi
(2)
• Occur at site of stasis
• Propagate toward the heart
101
Lines of Zahn (4)
• Thrombi often have groosly and microscopically apparent laminations called lines of Zahn
• Pale platelet and fibrin deposits alternating with darker red cell-rich layers
• Laminations signify that a thrombus has formed in flowing blood
• Their presence can therefore distinguish antemortem thrombosis from the bland, non-laminated clots that occur postmortem
102
Fate of a Thrombus (4)
Dissolution
Propagation
Embolization
Organization and recannalization
103
• Dissolution –
fibrinolysis (plasmin)
104
• Propagation –
accumulate additional platelets and fibrin
105
• Embolization –
dislodge and travel to other sites in the vasculature
106
• Organization and recannalization
(2)
• Ingrowth of endothelial cells, smooth muscle cells and fibroblasts
• Capillary channels eventually form that re-establish the continuity of the original lumen to a variable degree
107
Clinical Consequences of Thrombi (2)
• Obstruct veins and arteries
• Embolize downstream
108
Venous thrombi (phlebothrombosis)
(2)
• Congestion and edema in vascular beds distal to the obstruction
• Embolize to lungs and cause death
109
Arterial thrombi
(2)
• Thrombotic occlusions at critical sites (stroke, myocardial infarct)
• Embolize and cause downstream infarctions
110
Most venous thrombi occur in
superficial or deep veins of lower extremity
111
Superficial venous thrombi
(2)
• Cause local congestion, swelling, pain and tenderness
• Rarely embolize
112
Deep venous thrombi (DVT)
(3)
• Cause local pain and edema – rapidly offset by collateral channels
• More often embolize to lungs
• Half are asymptomatic, recognized in retrospect after embolization
15
113
Risk Factors for Venous Thrombi (7)
• Hypercoagulable states
• Endothelial injury
• Bedrest, immobilization
• Congestive heart failure
• Trauma, surgery, burns
• Thrombotic diathesis of pregnancy
Neoplasia
114
Risk Factors for Arterial
and Cardiac Thrombi (3)
• Cardiac and aortic mural thrombi may embolize
peripherally and cause infarcts of brain, kidney and spleen
• Major cause of arterial thrombi is atherosclerosis
• Predisposition to cardiac thrombi associated with
• Myocardial infarct
• Rheumatic heart disease
• Atrial fibrillation
115
Disseminated Intravascular
Coagulation (DIC)
• Formation of widespread fibrin thrombi in the microcirculation
• Thrombi not grossly visible – can be seen microscopically
• May cause diffuse circulatory insufficiency, especially in brain,
heart, lungs and kidneys
• Widespread microvascular thrombosis results in platelet and
coagulation protein consumption (consumptive coagulopathy)
• Fibrinolytic mechanisms are activated
• The initially thrombotic disorder may evolve into a bleeding
disorder
• Not a primary disease but a potential complication of any
condition associated with widespread activation of thrombin
• Obstetric complication
• Advanced malignancy
116
Embolus
A detached intravascular solid, liquid or gaseous
mass that is carried by the blood to a site distant
from its point of origin
117
Embolus
Lodge in vessels...
too small to permit further
passage and cause partial or complete occlusion
118
Embolus
Major consequence is
ischemic necrosis (infarction) of
the downstream tissue
119
Thromboembolus –
almost all emboli represent
some detached part of a thrombus
120
Venous emboli –
tend to lodge in one vascular bed (lung)
121
• Arterial emboli –
can travel to a wide variety of sites
122
Arterial emboli
Point of arrest depends on (2)
source and relative amount of blood flow
123
Arterial emboli
Major sites are
Major sites are lower extremities and brain
124
Arterial emboli
Consequences depend on
vulnerability of tissue to ischemia, caliber of occluded vessel and collateral blood supply
125
Paradoxical Embolus
An embolus that originates on the right
side venous circulation and lodges in
the left side systemic arterial
circulation
126
• Thromboemboli –
most emboli are thromboembolic in origin
127
• Fat -
bone fractures
128
• Bone marrow -
bone fractures
129
• Air -
---
130
• Nitrogen bubbles –
decompression sickness in divers caisson disease
131
• Atherosclerotic debris (cholesterol emboli) -
---
132
• Tumor fragments -
---
133
• Amniotic fluid –
obstetric complication
134
• Foreign bodies –
catheters, etc.
135
• Infarct -
an area of ischemic necrosis caused by occlusion the
vasculature
136
• Most infarcts occur from
thrombotic or embolic arterial
occlusions
137
• Venous thrombosis may cause
infarction, but usually just
congestion
138
• Atherosclerotic vascular disease causes
40% of all deaths in the
United States – mostly myocardial infarction or cerebral
infarction
139
Ischemia
(2)
• Restriction in blood supply, usually due to factors in
the blood vessels
• Oxygen, glucose and other blood-borne materials
140
• Infarct
(2)
• Complete loss of blood supply, resulting in necrosis
• An area of ischemic necrosis
141
• Hypoxia
(2)
• More general term denoting a shortage of oxygen
• Usually a result of lack of oxygen in the air being
breathed
142
Factors that Influence Development of an Infarct
(4)
Nature of the vascular supply – single vs double
Rate of occlusion development
Vulnerability of individual tissue to hypoxia
Amount of oxygen in the blood – anemia or cyanosis
143
Nature of the vascular supply – single vs double
(3)
• Lungs – dual pulmonary artery and bronchial artery
blood supply
• Liver – dual hepatic artery and portal vein circulation
• Kidney and spleen circulations are end-arterial
144
Rate of occlusion development
• Slowly-developing occlusions provide time to develop
alternate perfusion pathways – collateral circulation
145
Vulnerability of individual tissue to hypoxia
• Neurons –
• Cardiac myocytes –
• Fibroblasts -
3 to 4 minutes
20 to 30 minutes
hours
146
Insufficient blood supply is the most common cause of
gangrene
147
types of gangrene
• Ischemic gangrene (dry gangrene)
• Infectious gangrene (wet gangrene)
148
gangrene
Often associated with
peripheral vascular disease secondary to diabetes and long-term smoking
149
Thrombophlebitis -
Phlebothrombosis (2)
• Superficial veins
• Deep leg veins – high risk
of pulmonary embolus
150
Trousseau Syndrome (4)
• Migratory thrombophlebitis
• Paraneoplastic syndrome
• Hypercoagulability
• Adenocarcinoma
• Pancreas
• Colon
• Lung
151
Shock
Systemic hypotension due to either reduced
cardiac output or to reduced effective
circulating blood volume
152
shock leads to
impaired tissue perfusion and
cellular hypoxia
153
shock
Initially --- cellular injury
reversible
154
Prolonged shock leads to
irreversible cellular
injury
155
Cardiogenic shock –
low cardiac output due to pump
failure
156
Causes of Shock (4)
• Myocardial infarct
• Ventricular arrythmias
• Extrinsic compression (cardiac tamponade)
• Outflow obstruction (pulmonary embolism)
157
Hypovolemic shock –
def
ex (2)
low cardiac output due to loss of
blood or plasma volume
• Massive hemorrhage
• Fluid loss from severe burns
158
Septic shock –
vasodilation and peripheral pooling of blood
as part of a systemic immune reaction to a bacterial or
fungal infection
