2nd Exam: Fluid and Hemodynamic Derangements Flashcards
This kills more than the top 3 cancers combined:
HD
Greatest to least prevalance: lung, breast, colorectal cancers, stroke, HD:
HD, stroke, lung, colorectal, breast
2 ways to get too much blood in vascular bed:
- active hyperemia: excessive inflow (dilation of precapillary arterioles, autonomic stimulation, blushing, inflammatory process, 2: passive hyperemia/ congestion: something blocking flow out of bed, obstruction of vein, most common is congestive heart failure
What happens to red blood cells that enter the air spaces?
degenerate, macros will come and ingest them
most common blockage leading to hydrostatic pressure and fluid build up in lungs:
pulmonary vein to aorta blockage
Pulmonary edema, fluid that contains:
protein
What happens to the hemoglobin of RBCs that enter the alveolar space after RBC is degraded?
converted to hemosiderin, ingested by macs, these “heart failure cells” impart rusty color to lungs and spit
Inc p in sys caps leads to:
R sided CHF
Inc p in pulm caps leads to:
L sided CHF
Dec flow in pulm caps leads to:
hypoxemia
Dec flow in sys caps leads to
hypoperfusion
Dependent edema, chronic passive congestion: which type of heart failure?
R-sided CHF
Weakness, drowsiness, cyanosis, clubbing (deformity of fingers and toes), polycythemia (inc hemoglobin): hypoxemia or hypoperfusion?
hypoxemia
Dyspnea, orthopenia, hemoptysis: L or R-CHF?
L-sided CHF
Dyspnea:
difficult, labored breathing
orthopenia:
shortness of breath while laying down
hemoptysis:
coughing up blood
Syncope/coma, kidney failure, tissue necrosis: hypoxemia or hypoperfusion?
Hypoperfusion (shock)
Structures involved in R-sided CHF:
vena cava, R atrium/ vent, tricuspid valve, pulm valve, pulm a., intrinsic lung disease, L-sided CHF
causes of hypoxemia (low o2 concentration in blood)
heart malformations w R to L shunt, pulm arterial hypertension, Lung d. w inc resistance to blood flow
Structures involved in L-sided CHF:
pulm v., L atrium/ ven, mitral valve, aortic valve, systemic hypertension
Causes of hypoperfusion:
low P (vasod) or V (blood loss) , MI, fibrilation, sepsis
R-sided CHF leads to __ and L leads to __:
hypoxemia, hypoperfusion
Clinical presentation of R-sided CHF:
swollen ankles and legs
How can pregnancy lead to R-sided CHF?
compression of vena cava
mark of R sided CHF:
depressed area due to pressure, pitting edema, interference of blood flow
_-sided CHF will impede drainage of liver sinusoids to vena cava.
R, sinusoids will dilate, grossly dilated resembles cut nutmeg
First liver sinusoids to dilate with R-sided CHF:
those around centrilobular veins of liver
A clear image of this is not seen in liver slides with R-sided CHF:
portal triad
Nutmeg liver is indicative of:
R-sided CHF
Valve more likely to suffer from age related problems:
aortic, 2 cusps, L sided CHF
Age related stenosis presents with same symptoms as:
bicupsid (aortic) valve stenosis
Age related stenosis:
lumps on aortic valves, rigid, harder to open, inc P, arteriosclerosis, more work for L ven, may fail
Age related stenosis and aortic valve stenosis are both assoc w __-sided CHF:
L
Blood supply to posterior L vent and posterior papillary of L vent:
L and R coronaries
Diagonal cross hatching, diseased or normal heart?
normal
Pathogenesis of L-CHF, acute MI:
One region of L-ven thinner, discolored, the rest hypertrophied, aortic valve may not be functioning
determines the amount of force required to pump the blood:
Pressure of the blood
Key finding in people with high BP:
hypertrophy of L ventricle
Which came first in L-CHF, acute MI, thckening or thinning of L-vent?
thickening
Greater L coronary artery supply is indicative of:
L-CHF, acute MI, needs more blood flow bc L-ven is working harder
This surrounds the heart and is not of concern to us:
epicardial fat
TF? Blood escapes because of congestion.
F.
Virchow’s triad:
endo injury, hypercoagulability, abnormal blood flow - any can lead to thrombosis
Factors that can lead to thrombosis:
endo injury, abnormal blood flow, hypercoagulability
These are responsible for hypercoagulability:
coagulation factors
__ occurs within the blood system, __ occurs when blood leaves system.
thrombosis, hematoma
Demarcations of thrombi in aa. and vv.:
aa.: Lines of Zahn, vv.: valve markings
TF? Thrombus formation can occur in living and dead.
F. living only
How to tell if a clot occured in death or life by looking at it:
Lines of Zahn or Valve markings (stratified pattern formation) = living
This type of thrombus,forms quickly, cylindrical, shiny, smooth bc it just formed:
artery (Lines of Zahn)
Describe veinous thrombus:
grainy areas, while ago (1-2d), body tried to reorganize it
post-mortem clots:
white head and a red tail, no Lines of Zahn, “currant jelly portion” (red tail) mostly RBCs, “chicken fat” upper portion (white head), shape of vessel, but does not fill vessel
Fate of thrombi:
resolution, embolization to lungs, organized and incorporated into vessel wall, organized and recanalized
What aides in thrombus organization?
adjacent, living tissue, tries to recanalize it
This can lead to multi-channeled lumen:
recanalization of thrombi via macs
embolus is likely to plug up
pulmonary system
____ agents can lead to resolution of a thrombus.
thrombolytic
mural thrombus:
thrombus in wall of atrium
Factors that help thrombus attach to wall of atrium:
turbulence, stasis of flow, endo damage, hypercoagulability
Failure to tx mural thrombus in L atrium results in:
stroke, after leaving L atrium
Mural thrombi can form here:
wall of any vessel
atrial fibrillation:
twitching movement, doesn’t propel blood, stasis, common rhythm promblem, 20% of 85yo have
classic location for thrombus in L ventricle:
site of previous MI, bc of blood stasis in region of dead tissue from MI
Most common reason for atrial fibrillation with a thrombus in the L atrium:
2 infarcts: 2 emboli (check)
How to id leg thrombi:
indentations from venous valves
Clot dislodged in location different from where it was formed:
embolus
hemorrhagic lung infarct:
L sided CHF, block pulmonary artery, can’t infarct normal lung
How can you tell if a thrombus has been there a while?
if attached to the wall
Granulation tissue surrounding embolus indicates:
been there at least 1wk, GT trying to reorganize thrombus
Main indication that an embolus has been there a while:
organization
How to remove thrombus?
Merci thrombus removal device (catheter)
Reopening of blood supply to an infarcted area can lead to:
hemorrhagic infart
Common cause of BM emboli:
CPR
BM emboli may lodge here:
lung
How to tell how long a BM embolus has been lodged in lung:
you can’t
Fat emboli may lodge:
kidney, lung
edema of ankles and legs, affected by gravity and position, lower limbs affected if standing, butt affected if supine.
dependent edema
