Hemodynamics and Shock Flashcards
edema in the living
too much interstitial fluid in the tissues and outside the individual cells for whatever reason
intracellular edema
cloudy swelling we see in injured (but not necessarily killed) cells
Anasarca
generalized, severe edema
effusion
liquid in the pericardial, pleural, peritoneal or joint cavities
Ascites
effusion in the peritoneal cavity
hydrothorax
watery fluid in the pleural space
empyema
pus/purulent effusion in the pleural cavity - less often “pyothorax” (Ringo Starr)
Hydropericardium
watery fluid in the pericardial cavity
Hydrocephalus
too much cerebral spinal fluid for whatever reason
Hydrocele
extra fluid within the membrane around the testis
hydrosalpinx
too much fluid in the fallopian tube (oviduct)
often follows gonorrheal or other salpingitis
ileus
too much fluid in the small bowel for whatever reason
seroma
non-infected fluid in the surgical incision
loculated effusion
more than one compartment, due to scarring. Harder to drain
blister
fluid in the epidermis, or between the epidermis and dermis
bulla
big blisters
vesicles
little blisters
edema spreads ______ and _____
collagen and smooth muscle
Five mechanisms by which edema can form
- excess body fluid
- increased pressure in the small veins of the body (“vascular problems/ edema”)
- Decreased total plasma protein/albuim content
- lymphatic vessel obstruction
THESE will give you a TRANSUDATE, salt water without very much protein in it. These can be interconnected. - Leaky vessels, usually from inflammation
THIS will give you an EXUDATE, with plenty of protein in it.
Excess total body water
iatrogenic fluid overloading kidney failure (heart failure, after shock, antihypertensive Rx/Cach blockers, kidney dz)
increased venous pressure
ALL SYSTEMIC VEINS - R CHF, pericardial dz
PULMONARY VEINS - L CHF
LEG VEINS - Pregnancy, valve failure, standing up a lot
PORTAL VEIN - certain liver diseases, famously cirrhosis
OBSTRUCTED/NARROWED VEIN - thrombus, pressure
Decreased blood protein content
malnourished, malabsorption, liver failure, nephrotics
lymphatic obstruction
filariasis, surgery, radiation, cancer
hard to place
BRAIN - trauma, lead poisoning
MICROCIRCULATION/ANGIOEDEMA (genes, ace inhib)
dependent edema seen in patients with failing heart pumps
excess total body water and increased venous hydrostatic pressure contribute
edema will pit if the cause is
something other than inflammation or obstructed lymph vessels
cardiac edema tends to be worse in the ____ in those who are
feet, sacral region
up and about, bedridden
the reason is that gravity adds to hydrostatic pressure
increaed pressure in veins can result from
inadequate valves, internal obstruction by a thrombus, external compression by a mass (even the pregnant uterus)
Medusas head (kaput)
distended veins over the abdomen in liver failure/ ascites
Edema in liver is often a combination of
increased portal venous pressure and low serum albumin levels –> ascites
edema around the eyes
when generalized edema is due only to total body water overload (renal failure/other sodium retention)
because this tissue is very loose
renal wasting of protein
blood volume drops and the kidneys retain Na to keep BP adequate, very severe edema often results
lymphedema is most often due to
cancer. surgery and radiation therapy are also important causes. there is a filarial disease that still causes epidemic elephantiasis in many tropical regions
original mastectomies
took far too much tissue for no reason, and left thousands of women with lifelong lymphedema
podoconiosis (dust foot)
dessert dwellers who do not have shoes. may develop this from sand getting into and plugging the lymphatics
Milroy’s dz
lymphatics are malformed, producing lifelong lymphedema. worst in the legs
orange peel skin “peau d’orange:
ominous sign in the breast, signifying cancer plugging the dermal lymphatics
chylous effusions
result from damaged lymphatics, usually the thoracic duct. turbid, lipid rich fluid
non inflammatory exudates occur in
neovascularization, as deep wounds heal (granulation tissue) or cancers grow
generalized edema can develop in
dengue, in burn patients, and patients with sepsis/ “systemic inflammatory response” (IL-1/a TNF) without any localized infection
edema appearing first in the feet after standing
consider heart failure
CARDIAC EDEMA
edema appearing first around the eyes
consider total body water overload and/ or low blood albumin
RENAL EDEMA
edema appearing first as excess fluid in the abdomen
consider low blood albumin plus increased resistance to the portal venous flow
consider primary LIVER DISEASE
Dilated arteries by themselves
DONT cause edema.
Listening for pulmonary edema
warning of both heart failure and pneumonia - crackles, little bubbles of edema that pop
snap crackle pop
The reason for the snap crackle and pop of pulmonary edema is
the little bubbles air makes with the water and surfactant. surfactant has the physical properties of soap
crackles= rales
You might have experienced mild pulmonary edema
when you push yourself to your limit as a tuner, especially if you’re just getting into shape
Heroin and opiate overdose
froth from the mouth, typical gush of pulmonary edema
pulmonary edema only shows well on histology if its
an exudate
Cerebral edema is especially problematic because
it can push the brainstem out of the bottom of the skull
can get it from injury, poisoning, or a variety of other causes
Angioedema
poorly understood syndrome, blood vessels suddenly becoming extra-permeable
angioedema is best known in
hereditary C1-esterase deficiency
it’s also a rare but serious side effect of drugs like captopril (ace inhibitor)
in C1 esterase deficiency, edema of the larynx can kill
Hyperemia
increased blood flow to the organ. Hyperemia is generally RED and THROBS
Congestion
decreased bloos flow from the organ. congestion is typically PURPLE and doesn’t throb
both hyperemia and congestion increase
the amount of blood in the organ
what happens to your liver when you die?
unless your last few heartbeats are as strong as they are in health, or you bleed out, your blood will pool in you liver, causing congestion nearest the veins that drain it
NUTMEG LIVER
Describe blood flow and effects based on shape of liver lobule
blood pools around a hepatic central vein. The central liver cells die of lack of good blood flow over several hours.
liver cells die first in the central areas because they are furthest away from where thee fresh blood ethers.
Nutmeg liver with portal areas _____ and central areas_____
alive
dead
________ runs with hydrostatic lung edema, especially if
pulmonary congestion
the left ventricle can’t pump adequately
remember that in the lungs, the arteries and veins don’t run together
in pulmonar congestion, which runs with hydrostatic lung pressure, little bleed can leave behind
“heart failure cell”
little iron pigments of hemosiderin
Congestion can result form
any of the vascular problems that produce a transudate.
blood that is to viscous
(too much IgM, cyroglobulin, way high Hgb/Hct, sickles)
cryoglobulin precipitates
when you get too cold (it’s only marginally soluble)
hemorrhage
blodd cells that have escaped from a blood vessel. Can be trivial. Can be deadly
what determine whether a hemorrhage is serious
quantity and location
hematoma
enough blood in the tissues for you to be able to palpate it
cauliflower ear results from
the organization of a hematoma (transformation of mass of blood to mass of fibrous tissue, scar tissue)
Hemothorax
blood in pleural cavity
common, especially in trauma or thoracic aortic ruptruer, to bleed to heath iNTO your pleural cavities - each can hold maybe two quarts of fluid and you have only 5 quarts of loud.
fluid compressing the lungs also prevents people from taking deep breaths
Hemopericardium
blood in the pericardial sack
hard fro heart to pump bc it has pressure around it. hard for blood to get to the heart to supply it
hemoperitoneum
blood in the peritoneal cavity
hemarthrosis
bleed(s) into a joint
common in hemophilia
Petechiae
little bruiss
purpura
bigger than petechia, bruises
ecchymoses
largest bruises, might be defined to be over 10 mm, or due to injury, or either
suction contusions may be
petechiae or purpura
Tourniquet test
to see if a person has fragile blood vessels
(dengue)
appearance of many little petechiae confirms exaggerated capillary fragility
petechiae on lower eyelid warn of
endocarditis.
can also confirm the impression of strangulation in forensic cases
little bits of pieces of infection in the heart break off, will end up getting suck in places with small blood vessels. fiber and bacteria are more dense than blood, shot straightt up from heart to carotid, external carotid, lower eyelids–> get infected, neutrophils come in and tear up blood vessels leading to petechiae
purpura commonly seen in older folks results from
old sun exposure/loss of tissue support rendering the capillaries more fragile/likely to break.
no valves here as compared with legs.
Dengue
complex viral infection involving the microvasculature
the virus damages the vessels
in addition to hemorrhage, systemic edema is common
targets endothelial cells, carried by mosquitos - bug that has the fastest access to blood vessels. can have a lot of bleeding
After removal of IV lines, we should
apply pressure, especially in patients on anticoagulants
peticeiae on the epicardium
sever thrombocytopenia
hemoptysis
coughing up blood
hematemesis
throwing up blood
hematochezia
bright red blood from the rectum
melena
blood digested during passage through the gut (upper gut)
thrombus
blood that has solidified within a vascular lumen or cardiac chamber
clot
blood that has solidified anywhere else
The instant you’re hurt, hemostasis starts with
VASOCONSTRICTION. reflex vasoconstriction.
vaso constriction in injury is followed by
primary hemostasis
primary hemostasis is carried out by
platelets plugging up any little injuries in seconds
Platelet adhesion is followed by
aggregation and release of platelet granule contents
specific deficiencies in platelets (low numbers, poor function) may produce
petechiae at first. when severe, GI and brain bleeding are the most fears consequences
secondary hemostasis
the clotting cascade turning liquid blood solid. this takes minutes
Thrombin does a lot of things
thrombin bound to thrombomodulin on intact endothelium stops activating fibrinogen and starts activating protein C instead, preventing/stopping clotting
thrombi form when
over time
when pro-thrombotic factors overshadow antithrombotic mechanisms (which prevent their formation and or remove them afterwards)
it takes a few hours for factor XIII to
cross-link/polymerize the fibrin, making the thrombus more firm and crumbly
Virchow’s Triad
- injured endothelium
- altered blood flow (turbulance/stasis)
- hyper coagulable blood
need only to have one component to be at risk for a thrombus, often you have multiple
antemortem clot
lines of sahn.
all thrombi form chaotically, with some areas incorporating more red cells than others
The most thrombogenic thing that you can have in your circulatory system is
a thrombus. THROMBI PROPOGATE
in an organized thrombus,
the thrombus turns into a scar.
what breaks down thrombi
plasmin
recanalization
thrombi usually turn into granulation tissue, and contraction opens many little channels (scar contracts)
post mortem thrombus
red cells on bottom, liquid on the top.
chicken fat and currant jelly
rubbery rather than crumbly. don’t adhere to the wall, and are not propagated distally
the most common site for venous thrombi
the legs
problematic when it embolizes to lungs
mural thrombus
on the wall of a heart. can overlie an old MI. keeps chamber from filling, prone to embolize. one of the most dreaded side effects of MI
atheroclerotic plaques often often cause
overlying thrombi
Vegetations
thrombi on a valve (mitral valve)
thromboembolus
is both a thrombus and an embolus
Virchow’s triangle: INJURED ENDOTHELIUM causes
on top of a ruptured atherosclerotic plaque
myocardial infarcts/myocardidtis
cardiac jet lesion (abnormal flow)
inflamed heart valves/prosthetic heart valves
radiation injury
after an electrical injury (gangrene can result)
tumor in a vessel or cardiac chamber
sclerosing htrapy for varicose veins
indwelling lines in veins/heart
smoking
high blood pressure itself
Virchow’s triad: ALTERED BLOOD FLOW causes
myocardial infarcts (dead awl balloons out)
quivering/fibrillating cardiac atria
overruptured athererosclerotic plaques
in dilated heart chambers (valve or muscle disease)
in weakened arteries that have ballooned (aneurysms)
at arterial branch points (why there;s more plaques there)
over-viscous blood (more prone to stasis)
Sicklers, polycythemia (high RBC mass), IgM, cryoglobin
vascular malformations. why hemagiomas often regress
prolonged bed rest/immobilization
Virchow’s triad: HYPERCOAGULABLE BLOOD causes
GENETIC
common: factor V leiden, prothrombin G20210A
less common: deficiencies of AT-III, protein S, protein C
rare: very high homocysteine
Pregnancy/ after childbirth
after sever trauma, burns, surgery, maybe even tissue necrosis, as during heart attack
nephrotic syndrome (lose small anticoagulant proteins)
tumors making prothrombotic substances
antiphopholipid syndrome (lupis anticoagulant)
old age
smokers, obesity, lack of exercise
White thrombi
arterial thrombi. blood flow in arteries is faster and more laminar, thus fewer red cells are trapped in the fibrin.
white clot syndrome/ “heparin induced thromocytopenia”
this is a dread illness caused by antibodies against a complex of heparin and platelet factor 4.
masses of platelets become the white clots existing thrombi extend, and moderate thrombocytopenia occurs
Fibrinolysis
thrombi begin breaking down as soon as they are made. –> balance
violin strings
thrombi that embolize to the lung and organize over months, leaving the lumen almost fully patent
DIC results whenever
blood clotting is activated through the circulating bloodstream
In DIC
platelets and clotting factors are consumed - consumption coagulopathy - then plasmin is activated
see schistocytes and thrombocytopenia. little fibrin thrombi
progression to bleeding from many places, including mucosal surfaces
DIC is both
“too much clotting” and “too much bleeding”
Death Is Coming
Fragmented red cells
=schistocytes
schistocytes and thrombocytopenia (too few platelets)
consider DIC
black plague got its nickname from
the DIC that’s often seen, producing gangrene
meningococcemia
DIC is part (not all) of the picture in meningococcemia
if this morning’s venipuntrue site/ your current IV site starts to bleed, consider
DIC
the mechanism is that plasmin has destroyed the fibrin holding the “injury” together
Tests for DIC
D-dimer, fibrin spli products
Causes of DIC:
thromboplastin gets into the blood
various obstetrical catastrophes disseminated cancers acute promyelocytic leukemia large infarcts really bad intravascular hemolysis (think of bad malaria) snakebite
Causes of DIC:
damaged endothelim
reickettsial disease
meningococcemia
vasculitis
toxemia of pregnancy
Causes of DIC
thromboplastin in blood AND damaged endothelium
bad trauma, big infarcts shock gram negative sepsis burns heat stroke ebola, marburg, and probably other emerging infections
pulmonary thromboembolus
thrombus–> embolizes and gets stuck in the lungs can be fatal
paradoxical embolus
from venous side, through foramen oval and out to systemic circulation
amniotic fluid embolus
from placenta–> lungs see keratin from unborn child in lungs
air embolus
about 100 ml of air is sufficient to kill
gas emboli have many causes
decompression sickness (most feared hazard of scuba diving)
fat embolization
most often follow fracture of a long bone
from broken ribs during CPR
in the brain with massive fat emolisation,
petechia occur throughout the with matter, no body knows why.
bone marrow embolus
from broken ribs during CPR
atheroembolie
choleterol embolic from an atherosclerotic plaque. spindle like.
trash foot
Heroin is often cut with other substances such as
talc
Intravenous heroin users may have ______ in lungs.
talc granulomas. the talc is inside the vessels, hence injected, not inhaled
what can embolize
lots of things. silicone. peanut butter. fat. air. thrombi
White infarcts
arterial insufficiency and not reperfused and single blood supply
Red infarcts
venous insufficiency
or
Reperfused
or Dual blood supply
infarct
area of ischemic necrosis caused by loss of the blood supply
arterial infects can result form
thromboemboli thromb formin in situ atheroemboli hemorrhage into an atherosclerotic plaque (small artery) tumor in an artery (rare)
venous infarcts can result from
any cause of congestion
remember twisting of a vascular supply
lung infants are always _____ . Why
red
dual blood supply
Bowel infarct always ____ because
red
usually venous, and always reperfused
strangulated hernia
compromise of the venous return causes bowel infarction
_____ and _____ have dual blood supplies. If you aren’t in shock already, it’s practically impossible to infarct them
lung and liver
brainstem infarcts are mostly ____
pale
are kidneys easy or hard to infarct
easy. only have one blood supply
testicular torsion leads to a
venous infarct
decubitus pressure ulcers are
basically infarcts, since the tissue dies because of ischemia. infection and other factors keep the process going
weight of the person keepl the blood from getting to the area, occluding the veins.
Watershed infarcts
necrosis at the places that are farthest from the arterial supply
after shock (systemic hypo perfusion)
Shock
whenever there is widespread under perfusion of the body, for whatever reason.
our bodies have a limited ability to deal with a damaged heart, loss of blood/ water, or loss of vascular tone.
if the underlying problem is not or cannot be fixed, shock is self perpetuating, further damaging the body until death results.
Three main categories of the causes of shock
hypovolemic
cardiogenic
loss of vascular tone
Causes of shock - cardiac
big MI, rupture, diphtheria, some poisons, tamponade, PULMONARY EMBOLI
causes of shot - hypovolemic
hemorrhage (internal, external) other fluid (sweat, vomiting, diarrhea, burns, 3rd space)
causes of shock - lost vascular tone
septic/total body inflammation/ Toxic shock syndrome (superantigens, etc)
anaphylacitic (capillaries relax and leak)
neurogenic (poisons, war gas, cord injury, vasovagal)
meds (especially some anesthetic agents)
other leaky capillary syndromes (dengue, ebola, more)
lactic acidosis
poor perfusion, too little oxygen to tissue
a host of poorly understood chemical mediators, there have been attempts to target some of these molecules, but so far there has been little success
Compensated shock
you are shunting blood.
the body sends what blood is available to brain and heart first. measured blood pressure is maintained, but the kidneys, gut liver, skin are probably under perfused
pale, cold
don’t look that bad. might have a fast pulse and or respirations, and you’ll die soon unless the underlying problem is corrected
progressive shock/ decompensated shock
you are going anaerobic
kidney and liver cells are probably mostly dead, the anaerobic metabolism has shot the lactate levels up and the pH down, and other things are being released into blood from oxygen deprived tissues
the acidity in much of your body DILATES arteries that would better be constricted, and blood pools in them. and pH drop interferes with heart function and much more.
look horrible, vital signs are bad. If and only if, we fix the cause of shock can we still save you
irreversible shock
you will be dead soon
there has been sufficient damage to your body from lack of perfusion that NO intervention can save you
lysosomes are digesting your cells, and your gut mucosa is probably permeable to bacterial products
you can still make your will ,make decisions involving your care, etc, but you WILL die within a few hours
shock not only _______ but ______
stops the machine, but wrecks the machinery
after a few hours in shock, expect to see
diffuse hypoxic brain injury
subendocardial necrosis
contraction bnd necrosis in the myocardium
acute tubular necrosis in the kidneys
“stress lesions” in the adrenal cortex (thick, lost lipid)
“stress ulcers”/ bleeds in the stomach and duodenum
Necrosis of the small intestine (if dopamine used)
fatty change/ necrosis in the centers of liver lobules
congested liver (unless much hemorrhage)
days later :shock lung” often develops - hyaline membranes
Sepsis
bacteria actually flourishing in the blood stream
is rapidly fatal if not Rx’d quickly and successfully
Gram ____ _____ are the most common causes of sepsis, but _________ can also cause sepsis
gram positive cocci
gram negatives, fungi, and viruses
Most shock patients feel _____
septic patients may feel _______ because
cold
warm, widespread arterialdilation
Watershed infarction of ______ is part of the downward spiral of shock
subendocardium
some people will survive shock. One sign of a previous bad episode of shock is
widespread scarring of the subendocardium, where the infarcts have healed. scarring can provide long survival, even if only a few cells didn’t die
Late lung changes that follow shock ar probably caused by
cytokines and neutrophil products.
late lung changes following shock
fibrin leaking from vessels, plastered over the air space
cyanosis
blue color. when theres >5gm of unoxygenated hemoglobin in the blood it’ll look bluish. This could be because of poor oxygenation (lung disease), poor systemic perfusion (shock - all the oxygen’s being taken), or just a part of your body surface bing cold (no need to send extra blood to cold area)
____ is basic to caring for the patient in shock, and provides support while we are preparing for definitive treatment of whatever’s the underlying cause
proper fluid management
