Hemodynamic Basis of Disease Flashcards
Extravasation of fluid into tissue –>
edema
Extravasation of fluid into spaces?
effusion
What results from increased hydrostatic pressure and reduced oncotic pressure?
transudate
what results from increased vascular permeability (inflammation –> endothelial cell contraction creates small gaps / direct damage to endothelial cells)
exudate
etiology of transudate
ultrafiltrate of plasma: incrased hydrostatic pressure and/or reduced oncotic pressure
etiology of exudate
increased vessel permeability due to inflammation
if our fluid has low specific gravity
transudate
low density
if our fluid has low LDH:serum
transudate
if our fluid has high specific gravity >1.020
exudate
if our fluid has high LDH:serum
exudate
if our fluid has many white blood cells
exudate
if our fluid has high glucose fluid:serum >0.5?
transudate
if our fluid has low protein?
transudate
if our fluid has high protein fluid:serum?
exudate
if our fluid has low glucose fluid:serum?
exudate
if our fluid has few white blood cells
transudate
this type of fluid usually results from inflammation / toxins / burns
exudate
this type of fluid usually results from heart failure / liver disease / venous obstruction / fluid overload
transudate
transudate sg? tp? p f:s? LDH f:s? glucose f:s? wbc? examples?
sg 0.5
WBC non or few
e.g. hf / ld / venous obs / fluid overload
exudate sg? tp? p f:s? LDH f:s? glucose f:s? wbc? examples?
sg >1.02 tp > 3 p f:s >0.5 LDH f:s >0.6 Glucose f:s
Types of increased blood volume (2)
hyperemia (physiologic)
congestion (pathologic)
hyperemia?
physiologic (active) increase in blood volume
due to arterial dilation
oxygenated blood: red
congestion?
pathologic (passive) increase in blood volume
impaired venous outflow
deoxygenated blood: pale or red/blue
liver congestion
side of hf?
right
gi tract varices
side of hf?
right
ascites
side of hf?
right
what is ascites
accumulation of fluid in the peritoneal cavity causing abdonminal swelling
splenic congestion
side of hf?
right
peripheral edema?
side of hf?
left?
pulmonary edema results from
side of hf?
left
pleural effusion
side of hf?
left
renal consequence of left hf?
decreased renal blood flow –> retention of na+ and water –> increased blood volume –> peripheral edema
hemorrhage
blood outside of the vasculature, due to vessel damage
causes of hemorrhage (3)
impaired integrity of vessel walls
low level / function of platelets
low level / function of coagulation factors
petechiae
1-2 mm blood dots from hemorrhage
purpura
> 3mm blood dots from hemorrhage
ecchymoses
1-2cm blood dots from hemorrhage
hematoma
blood accumulation from hemorrhage within tissue
thrombosis: virchow triad
endothelial injury
abnormal blood flow
hypercoagulability
virchow triad
cause of endothelial injury?
hypercholesterolemia
inflammation
virchow triad
cause of abnormal blood flow? (2)
stasis (e.g. a-fib, bed rest)
turbulence (e.g. atherosclerotic vessel narrowing)
virchow triad
cause of hypercogulability (2)
inherited
(e.g. factor V leiden)
acquired
(e.g. disseminated cancer)
most common type of embolus?
thromboembolus (DVT)
Risk factors for DVT (7)
Immobility / recent surgery estrogen pregnancy / post-partum previous or current cancer coagulation anomalies limb and/or orthopedic trauma obesity
thromboemboli - venous
source/cause
organ affected
clinical
source - deep leg veins / arm veins
organs - lungs
clinical - respiratory insufficiency / chest pain
fat/bone marrow emboli
source
organ
clinical
source - long bone fracture - vein damage
organ - lung
clinical - resp insufficiency
amniotic fluid emboli
source
organ
clinical
source - torn placental membranes / uterine vein rupture
organ - lungs/brain/vasculature
clinical - resp insufficiency / shock / seizures / DIC 10% maternal deaths
tumor emboli
source
organ
clinical
source - mucin secreting adenocarcinomas / liver / kidney
organ - lungs
clinical - resp insuff / chest pain
thromboemboli - arterial
source
organ
clincal
source - heart / aorta / carotid
organs - legs (75%) brain (10%)
clinical - stroke / tissue necrosis in leg
atheroemboli
source
organ
clinical
source - atherosclerotic plaque of aorta / iliac / carotid
organ - legs / brain / GI / kidney
clinical - stroke / tissue necrosis / GI pain or bleeding / acute kidney injury
gas bubble emboli
source
organ
clinical
source - diving or IV
organ - muscle / joints / lungs / heart
clinical - bends (skeletal / joint pain) - chokes (lung edema and hemmorhage) - respiratory insufficiency / myocardial infarction
disseminated intravascular coagulation
thrombosis and hemorrhage can occur simultaneously
DIC underlying condition?
tissue factor release, endothelial damage
DIC we see systemic activation of ?
coagulation
systemic activation of coagulation in DIC leads to (2)
widespread fibrin deposition –> thrombosis
consumption of platelets and clotting factors (bleeding)
DIC
symptoms?
from multiple organ systems - resp insufficiency - mental status changes / convulsions - acute renal failure - petechiae / purpura - GI / oral hemorrhage Shock
DIC blood work?
hemolytic anemia thrombocytopenia low fibrinogen elevated D-dimer other fibrin degradation products
infarction
tissue death (necrosis) caused by vessel occlusion
type of necrosis in infarction?
typically coagulative but liquefactive in brain
infarction: white insufficiency? blood supply? reperfusion? tissue type? organs?
insufficiency: arterial blood supply: single reperfusion: no tissue type: dense organs: heart / kidney / spleen
infarction: red insufficiency? blood supply? reperfusion? tissue type? organs?
insufficiency: venous blood supply: dual reperfusion: yes tissue type: loose organs: lung / liver / intestine
what is shock?
circulating blood volume or blood pressure is not adquate to perfuse body tissues –> multi-organ dysfunction / damage
cardiogenic shock -
myocardial pump failure
- myocardial damage, extrinsic compression, outflow obstruction
hypovolemic shock
low blood volume
- severe dehydration (vomiting / diarrhea), hemorrhage, burns
clinical manifestations of cardiogenic and hypovolemic shock?
low c.o and low b.p –>
vasoconstriction
increased heart rate
renal conservation of fluid –>
coolness and pallor of skin / tachycardia / low urine output
Systemic inflammatory response syndrome is seen in?
septic shock (microbial infection - bacteria/fungi)
what happens in SIRS
Immensely elevated inflammatory mediators –> fever / DIC / ARDS
Arterial vasodilation –> hypotension / warm / flush
vascular leakage –> hypotension / edema
venous blood pooling –> reduced c.o. / increased H.R.
If someone is in shock and is cool and has pallor, think?
hypovolemic or cardiogenic
if someone is in shock and warm and flush think?
septic
does septic shock respond to IV fluids?
often not
