2nd Exam: Fluid and Hemodynamic Derangements Flashcards by Tedman McMahon

This kills more than the top 3 cancers combined:

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Greatest to least prevalance: lung, breast, colorectal cancers, stroke, HD:

HD, stroke, lung, colorectal, breast

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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

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What happens to red blood cells that enter the air spaces?

degenerate, macros will come and ingest them

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most common blockage leading to hydrostatic pressure and fluid build up in lungs:

pulmonary vein to aorta blockage

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Pulmonary edema, fluid that contains:

protein

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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

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Inc p in sys caps leads to:

R sided CHF

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Inc p in pulm caps leads to:

L sided CHF

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Dec flow in pulm caps leads to:

hypoxemia

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Dec flow in sys caps leads to

hypoperfusion

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Dependent edema, chronic passive congestion: which type of heart failure?

R-sided CHF

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Weakness, drowsiness, cyanosis, clubbing (deformity of fingers and toes), polycythemia (inc hemoglobin): hypoxemia or hypoperfusion?

hypoxemia

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Dyspnea, orthopenia, hemoptysis: L or R-CHF?

L-sided CHF

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Dyspnea:

difficult, labored breathing

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orthopenia:

shortness of breath while laying down

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hemoptysis:

coughing up blood

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Syncope/coma, kidney failure, tissue necrosis: hypoxemia or hypoperfusion?

Hypoperfusion (shock)

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Structures involved in R-sided CHF:

vena cava, R atrium/ vent, tricuspid valve, pulm valve, pulm a., intrinsic lung disease, L-sided CHF

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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

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Structures involved in L-sided CHF:

pulm v., L atrium/ ven, mitral valve, aortic valve, systemic hypertension

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Causes of hypoperfusion:

low P (vasod) or V (blood loss) , MI, fibrilation, sepsis

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R-sided CHF leads to __ and L leads to __:

hypoxemia, hypoperfusion

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Clinical presentation of R-sided CHF:

swollen ankles and legs

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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:

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.

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