shock

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1.

2.

What is shock?

Why is shock
considered a
"syndrome"?

A widespread abnormal cellular

metabolism that occurs when the human
need for oxygenation and tissue
perfusion is not met to the level needed
to maintain cell function. It is the "wholebody" response that occurs when too
little oxygen is delivered to the tissues.
Because the cellular, tissue, and organ
events that occur in response to its
presence happen in a predictable
sequence.

3.

What can start the

syndrome of shock
and lead to a lifethreatening
emergency?

Any problem that impairs oxygen

delivery to tissue and organs

4.

What is shock
more often the
result of?

Cardiovascular problems and changes.

5.

What are older

patients in long
term care at risk
for?

Sepsis and shock related to UTI's

What occurs when

adaptive
adjustments
(compensation) or
health
careinterventions
are not effective
and shock
progresses?

Severe hypoxia can lead to cell loss,

multiple organ dysfunction syndrome
(MODS), and dath.

How is shock
usually classified?

By the functional impairment it cuases

(hypovolemic shock, cardiogenic shock,
distributive shock, and obtrusive shock)
or by the origin of the problem
(hypovolemic, cardiogenic, vasogenic
and septic shock).

6.

7.

8.

What do
oxygenation and
tissue perfusion
depend on?

How much oxygen and arterial blood

perfuses the tissue.

9.

What is tissue and

organ perfusion
related to?

Mean arterial pressure (MAP)

10.

Since the
cardiovascular
system is a closed
but continuous
circuit what
factors influence
MAP/

" Total blood volume

Cardiac output
Size of the vascular bed"

11.

Total blood volume and

cardiac output are
directly related to MAP
so what raises MAP?

" Increase in Total blood volume

Increase in Cardiac output"

12.

How is the size of the

vascular bed related to
MAP?

Any problem that impairs oxygen

delivery to tissue and organs
vasoconstriction or dialation

13.

What is sympathetic
tone?

The state of partial blood vessel

constriction.

14.

What happens when

blood vessels dilate by
relaxing smooth muscle
in the vessel walls and
total blood volume
remains the same?

Blood pressure decreases and

blood flow is slower. Decreases in
sympathetic tone relax blood
vessel smooth muscle, dilating
blood vessels and lowering MAP.

15.

What happens when

blood vessels constrict
and total blood volume
remains the same?

Blood pressure increases and

blood flow is faster. Incrases in
sympathetic stimulation constrict
blood vessel smooth muscle even
more than normal and raise MAP.

16.

What parts of the body

can tolerate low levels
of oxygenation for hours
without dying or being
damaged?

Some organs, such as the skin

and skeletal muscles.

17.

What parts of the body

tolerate hypoxic
conditions poorly?

Other organs such as the heart,

brain, liver and pancreas tolerate
hypoxic conditions poorly, and
even just a few minutes with
adquated oxygen results in serious
damage and cell death.

18.

How do we classify
Hypovolemic Shock with
relation to functional
impairment?

"Total body fluid decreased in all

compartments
Hemorrhage
Dehydration"

19.

How do we classify
Cardiogenic Shock by
functional impairment?

"Direct pump failure, fluid volume

not affected
Myocardial Infarction
Valvular problems such as
stenosis or incompetence
Myopathies Dysrhythmias
Cardiac Arrest"

20.

How do we classify
Obstructive Shock by
functional impairment?

"Cardiac function is decreased by

noncardiac factors, total fluid
volume not affected, central
volume decreased.
Pulmonary hypertension Tension
pneumothorax Pericarditis
Thoracic tumor Tamponade"

How do we
classify
Distributive
Shock by
functional
impairment?

"Fluid shifts from central central vascular

space, total body fluid volume normal or
increased.
Neural-induced loss of vascular tone (head
trauma, anesthesia, opioids, sedatives)
Chemical-induced loss of vascular tone from
sepsis, anaphylaxis, capillary leak"

22.

When does
Hypovolemic
Shock
occur?

It occurs when too little circulating blood

volume causes a MAP decrease, resulting in
the body's total need for oxygen not being
met.

23.

When does
Cardogenic
Shock
occur?

When the actual heart muscle is unhealhty and

pumping is directly impaired.

What is the
most
common
cause of
direct pump
failure?

Myocardial Infarction

What does
any type of
pump failure
cause?

Decreased cardiac output and MAP

26.

When does
Distributive
Shock
occur?

When blood volume is not lost from the body

but is distributed to the interstitial tissues
where it cannot circulate and delivery oxygen.

27.

What can
cause
Distributibe
Shock?

A loss of sympathetic tone, blood vessel

dilation, pooling of blood in venous and
capilalry beds, and increased blood vessel
permeability (capillary leak). All these can
decrease MAP and may be started by nerve
changes (neural induced) or the presence of
chemicals (chemical induced).

28.

What is
neuralinduced
distrbutive
shock?

It is a loss of MAP that occurs when

sympathetic nerve impulses controlling blood
vessel smooth muscle are decreased and the
smooth muscles of blood vessels relax,
causing vasodilation. This blood vessel dilatin
can be a normal local response to injury, but
shock results when the vasoldilation is
widespread or systemic.

21.

24.

25.

29.

30.

What are the

three
common
origins of
chemicalinduced
shock?

" Anaphylaxis
Sepsis
Capillary leak syndrome"

What is the
result of
Anaphylaxis?

Widespread loss of blood vessel tone and

decreased cardiac output.

31.

What is the
result of
Sepsis?

Sepsis is a widespread infection that triggers

a whole-body inflammation response which
leads to distributive shock when infectious
microorganisms are present in the blood.

32.

What is
capillary leak
syndrome?

It is the response of capillaries to the

presenc of biologic chemical (mediators) that
change blood vessel integrity and allow fluid
to shift from the blood in the vascular space
into the interstitial tissues. Once in the
interstitial tissue, these fluids are stagnant
and cannot deliver oxygen or remove tissue
waste products.

33.

What does the

fluid shift in
capillary leak
syndrome
result from?

They result from increased size of capillary

pores, loss of plasma osmolarity, and
increased hydrostatic pressure in the blood.

34.

What problems
cause fluid
shifts?

" Severe burns

Liver disorders, Ascites
Peritonitis, Paralytic ileus
Severe malnutrition, Trauma
Large wounds, Hyperglycemia
Kidney disease, Hypoproteinemia

35.

What is
obstructive
shock caused
by?

Problems that impair the ability of the normal

heart muscle to pump efectively. The heart
itself remains normal but conditions outside
the heart prevent either adequate filling of
the heart or adequate contraction of the
healthy heart muscle.

36.

What are the

cardiovascular
manifestations
of shock?

" Decreased cardiac output

Increased pulse rate,Thready pulse
Decreased blood pressure, Narrowed pulse
pressure
Postural hypotension, Low CVP
Flat neck and hand veins in dependent
positions
Slow cap refill, Diminished peripheral pulses

37.

What are the

most common
causes of
obstructive
shock?

" Pericarditis
Cardiac tamponade"

38.

What are the

respiratory
manifestations
of shock?

" Increased respiratory rate

Shallow depth of respirations
Decreased Paco2
Decreased Pao2
Cyanosis, especially around lips and nail
beds

39.

What are the

neuromuscular
manifestations
of shock?

"Early= Anxiety Restlessness Increased

thirst
Late= Decreased CSN activity (lethargy to
coma) Generalized muscle weakness
Diminished or absent deep tendon reflexes
Sluggish pupillary response to light

40.

What are the renal

manifestations of
shock?

" Decreased urine output

Increased specific gravity
Sugar and acetone present in urine"

51.

What happens if
the initiating
events continue
and MAP
decreases further?

Some tissues function under anaerboic

conditions which increases lactic acid
levels and other harmful metabolites
which lead to electrolyte and acid-base
imbalances with tissue-damaging effects
and depressed heart muscle activity.

41.

What are the

integumentary
manifestations of
shock?

" Cool to cold

Pale to mottled cyanotic
Moist, clammy
Mouth dry; pastelike coating present"

52.

Are these effects

temporary and
reversible?

Yes, if the cause of shock is corrected

within 1 to 2 hours after onset.

What are the

gastrointestinal
manifestations of
shock?

" Decreased motility

Diminished or absent bowel sounds
Nausea and vomiting
Constipation"

53.

What happens if
the hypovolemic
shock continues
for longer periods
without help?

The resulting acid-base imbalance,

electrolyte imbalances, and increased
metabolites cause so much cell damage
in vital organs that multiple organ
dysfuncton syndrome (MODS) occurs
and full recovery from shock is no longer
possible.

43.

What is the basic

problem with
hypovolemic
shock?

A loss of blood volume from the vascular

space, resulting in a decreased MAP,
and a loss of oxygen-carrying capacity
from the loss of circulating red blood
cells.

44.

What does the

reduced MAP with
Hypovolemic
Shock result in?

Decreased tissue pefusion. The loss of

RBCs decreases the ability of the blood
oxygenate the tissue it does reach.

54.

What are the

stages of
hypovolemic
shock?

" Initial Stage

Nonprogressive Stage
Progressive Stage
Refractory Stage"

45.

What do the
oxygenation and
tissue perfusion
problems lead to ?

Cellular anaerobic (without oxygen)

conditions and abnormal cellular
metabolism.

55.

In the initial stage

of hypovolemic
shock what
occurs?

46.

What is the main

trigger leading to
hypovolemic
shock?

A sustained decreased in MAP that

results from decreased circulating blood
volume. A decrease in MAP of 5 to 10
mm Hg below the patient's normal
baseline value is detected by pressuresensitive nerve receptors (baroreceptors
in the aortic arch and carotid sinus. )

"A decrease in baseline MAP of 510mmHg results in increased

sympathetic stimulation
Mild vasoconstriction
Increase in heart rate"

56.

In the
nonprogressive
stage of
hypovolemic
shock what
occurs?

47.

What happens
when the
baroreceptors
sense a decrease
in MAP of 65 to 10
mm Hg below the
baseline n
hypovolemic
shock?

The information is transmitted to the

brain centers, which stimulate
adjustment (adaptive or compensatory
mechanisms).

"A decrease in MAP of 10-15mm Hg from

the patient's baseline value causes
continued sympathetic stimulation.
Moderate vasoconstriction
Increased heart rate, Decreased pulse
pressure
-chemical compensation RAAS, mild
acidosis and hyperkalemia

57.

And chemical
compensation
occurs, causing
secretion of renin
aldosterone, and
ADH secretion
resulting in:

Increased vasoconstriction
Decreased urine output
Stimulation of the thirst reflex

What do the
adaptive or
compensatory
mechanisms do in
hypovolemic
shock?

They ensure continued blood flow and

oxygen delivery to vital organs while
limiting blood flow to less vital areas.

58.

Some anaerobic
metabolism in
nonvital organs
lead to:

Mild acidosis
Mild hyperkalemia"

59.

49.

What causes the

manifestations of
hypovolemic
shock?

Moving oxygenated blood into slected

areas while bypassing others causes the
manifestations of shock.

In the progressive
stage of shock
what occurs?

50.

With hypovolemic
shock what occurs
if the events that
caused the initial
decrease in MAP
are halted at this
point?

The adaptive (compensatory)

mehcanisms can return the body tissues
to a normal perfused and oxygenated
state.

"A decrease in MAP of > 20mm Hg from

the patients' baseline value causes the
anoxia of nonvital organs, hypoxia of
vital organs and overall metabolism is
anaerobic resulting in:
Moderate acidosis
Moderate hyperkalemia
Tissue ischemia"

42.

48.

60.

In the refractory
stage of shock
what occurs?

" Severe tissue hypoxia and ischemia

and necrosis
Release of myocardial depressant
factor from the pancreas
Buildup of toxic metabolites
Multiple organ dysfunction syndrome
(MODS)
Death"

68.

In the
nonprogressive
state of hypovolemic
shock what occurs
when ADH is
secreted by the
posterior pituitary
gland.

ADH incereases wter reabsorption in

the kidney, further reducing urine
output, and also causes blood vessel
constriction in the skin and other less
vital tissue areas.

61.

In the initial stage

of hypovolemic
shock what do the
compensatory
mechanisms do?

They are very effective at returning MAP

to normal lvels that oxygenated blood
flow to all vital organs is maintained.

69.

Tissue hypoxia occurs, but it is not

great enough to cause permanent
damage.

62.

What is the
cellular change
during the initial
stage of
hypovolemic
shock.

The change is increased anaerobic

metabolism with production of lactic
acid, although overall cellular metabolism
is still aerobic. The adaptive responses
of vascular cconstriction and increased
heart rate are effective, and both
cardiac output and MAP are maintained
within the normal range.

What occurs in the

skin, GI tract and
kidney during the
nonprogressive
stage of
hypovolemic shock?

70.

What occurs due to

anaerobic
metabolism during
the nonprogressive
stage of
hypovolemic shock?

Acid-base and electolyte changes

occur in response to the buildup of
metabolites. Changes include acidosis
(low blood pH) and hyperkalemia
(increased blood potassium level).

71.

63.

Why is shock so
difficult to detect
in the initial stage
of hypovolemic
shock?

Because vital organ function is not

disrupted.

64.

What may be the

only
manifestations of
the initial stage of
hypovolemic
shock.

A heart and respiratory rate increase

from the patient's baseline level or a
slight increase in diastolic blood
pressure .

What are the

manifestations of
the nonprogressive
stage of hypvolemic
shock resulting from
decreased tissue
perfusion?

"Subjective changes include:

Thirst sensation, Anxiety
Objective changes include:
Restlessness,Tachycardia, Increased
respiratory rate, Decreased urine
output, Falling systolic blood pressure,
Rising diastolic blood pressure,
Narrowing pulse pressure, Cool
extremities, 2% to 5% decrease in
oxygen saturation"

72.

What occurs during

the nonprogressive
state of
hypovolemic shock
when the MAP
decreases by 10 to
15 mm Hg from
baseline?

Kidney and hormonal adaptive

(compensatory) mechanisms are
activated because cardiovascular
adjustments alone are not enough to
maintain MAP and supply needed
oxygen to the vital organs.

How long can a

person remain in the
nonprogressive
stage of
hypovolemic shock?

They can remain in ths nonprogressive

stage for hours without having
permanent damage.

73.

Stopping the conditons that started the

shock at this stage and providing
supportive interventions can prevent it
from progressing.

In the
nonprogressive
stage of
hypovolemic shock
what occurs when
the baroreceptors
in the kidney sense
an ongoing
decrease in MAP?

The kidneys begin to compensate by

releasing of renin, AdH, aldosterone,
epinephrine, norepinephrine is triggered.

What can prevent

hypovolemic shock
from progressing
beyond the
nonprogressive
stage?

74.

When does the

progressive stage of
shock occur?

When there is a sustained decrease in

MAP of more than 20mm HG from
baseline.

75.

What occurse in the

progressive stage of
hypovolemic shock?

Adaptive or compensatory mechanisms

are functioning but can no longer
deliver sufficent oxygen, even to the
vital organs.

In the
nonprogressive
stage of
hypovolemic shock
what oocurs when
renin is secreted
from the kidney?

Renin starts the reactions to decrease

urine ouptut, increase sodium
reabosorption and cause widespread
blood vessel constriction.

76.

What worsens the

problem?

The fact that the adaptive mechanisms

require large amounts of oxygen in
some tissues (e.g., the heart).

65.

66.

67.

What happens
to vital organs
during the
progressive
stage of
hypovolemic
shock?

They develop hypoxia, and less vital organs

become anoxic (no oxygen) and ischemic
(cell dysfunction or death from lack of
oxygen. As the result of poor oxygenation
and a buildup of toxic metabolites some
tissue have severe cell damage and die.

What do the
manifestations
of the
progressive
stage of
hypovolemic
shock
include?

"It includes a worsening of subjective

changes:
Severe thirst sensation, Severe anxiety
A sense of impending doom
Worsening objective changes include:
Rapid, weak pulse, Low blood pressure
Pallor to Cyanosis of oral mucous
membranes and nail beds
Cool and moist skin, Anuria
5% to 20% decrease in oxygen saturation"

What may lab

values show
during the
progressive
stage of
hypovolemic
shock?

" Low pH
Rising lactic acid level
Rising potassium level."

How long can

vital organs
tolerate the
progressive
stage of
hypovolemic
shock?

Only a short time before they are damaged

permanently. The patient's life usually can be
saved if the conditions causing shock are
corrected within 1 hour or less of onset of the
progressive stage.

When does the

refractory
stage of
hypovolemic
shock occur?

When too much cell death and tissue damage

result from too little oxygen reaching the
tissues. Vital organs have overwhelming
damage.

82.

Why is this
stage of
hypovolemic
shock termed
refractory?

Because the body can no longer respond

effectively to interventions and shock
continues. The remaining cells metabolize
anaerobically.

83.

Is therapy
effective
during the
refractory
stage of
hypovolemic
shock?

Therapy is not effective in saving the

patient's life, even if the cause of shock is
corrected and MAP temporarily returns to
normal. So much tissue damage has ocurred
with widespread release of toxic metabolites
and detructive enzymes that cell damage to
vital organs continues despite agrressive
interventions.

What re the
manifestations
of the
refractory
stage of
hypovolemic
shock?

77.

78.

79.

80.

81.

84.

Rapid loss of consciousness

Nonpalpable pulse
Cold, mottled or dusky extremities
Slow, shallow respirations
Unmeasurable oxygen saturation

85.

What is multiple
organ dysfunction
syndrome?

The sequence of cell damdage caused by

the massive release of tox metabolites
and enzymes.

86.

What occurrs
with MODS?

Once the damage has started, the

sequence bcomes a vicious cycle as
more dead cells break open and release
harmful metabolites..

87.

What do the
metabolites
trigger?

They trigger small clots (microthrombi) to

form

88.

What do the
microthrombi do?

They block tissue oxygenation and

damage more cells, thus continuing the
devastating cycle.

89.

Where does
MODS occur
first?

First in the liver, heart, brain, and kidney.

90.

What is the most

profound change
with MODS?

It is damdage to the heart muscle.

91.

What is one
cause of this
damage to the the
heart muscle?

The release of myocardial depressant

factor (MdF) form the ischemic pancreas.

92.

What type of
shock is more
common in
younger adults?

Hypovolemic shock from trauma

93.

Where are signs

of shock first
evident?

Changes in the cardiovascular function.

94.

What changes do
we see as shock
progresses?

Changes in the renal, respiratory,

integumentary, musculoskeletal, and
central nervous systems becom evident.

95.

What oxygen
saturation level
is considered a
life-threatening
emergency?

Any value below 70% and may signal the

reftractory stage of shock.

96.

What happens
when anoxia or
hypoxia persists
beyond one hour?

Patients are at risk for acute tubular

necrosis and kidney failure.

97.

What skeletal
muscle changes
occur in
hypovolemic
shock?

Cahnge inlcude muscle weakness and

pain response to tissue hypoxia and
anaerobic metabolism (later
manifestations). Weakness is generalized
and has no specific pattern.

98.

What do nursing
interventions for
hypovolemic
shock focus on?

They focus on reversing the shock,

restoring fluid volume to the normal range,
and preventing complications through
supportive and drug therapies.

99.

What are the two

types of fluids
used to increase
fluid volume?

Crystaolloids and colloids

100.

What do
crystalloids
contain?

Nonprotein substances (e.g., minerals,

salts, sugars)

101.

What do colloid
solutions contain?

Large molecules, ususually starches.

102.

Why are
crystalloid fluids
given?

103.

104.

105.

115.

How do
vasoconstricing
drugs stimulate
venous return?

By constricing the blood vessels and

decreasing venous pooling of blood
thereby increasing cardiac output and
MAP, which help improve tissue perfusion
and oxygenation.

To help maintain an adequate fluid and

electrolyte balance.

116.

What
vasoconstricting
drugs are used?

Dopamine and norepinephrine

What are two

common
crystalloids?

Normal saline and Ringer's lactate.

117.

What is the fluid

replacement
solution of choice
to increase
plasma volume?

Normal saline, it can also be given with

blood

What do
inotropic drugs
directly
stimulate?

Adrenergic receptor sites on the heart

muscle and improve heart muscle cell
contraction resuling in greater recolil and
more blood leving the left ventricle during
contraction.

118.

What inotropic
drugs are used?

Dobutamine and milrinone

119.

What does
Ringer's contain?

" Sodium
Chloride
Calcium
Potassium
Lactate
All dissolved in water

What do the
drugs enhancing
myocardial
perfusion
ensure?

That the heart is well perfused, especially

when giving drugs to impprove cardiac
contraction, so that aerobic metabolisms
is maintained in the heart cells and
maximum contractility occurs.

120.

What drugs are

used to enhance
myocardial
perfusion?

Drugs that dilate coronary blood vessels

while minimally dilating systemic vessels
such as sodium nitroprusside.

121.

Why must care

be taken when
we administer
drugs that
enchance
myocardial
perfusion?

Because they can cause systemic

vasodilation and increase shock if the
patient is volume depleted.

122.

How often
should you
assess vital
signs in a
patient with
shock?

Every 15 minutes until the shock is

controlled and the patient's conditon
improves.

123.

What do
changes in CVP
reflect?

Hypovolemic shock.

124.

What surgical
interventions
may be need to
correct the
cause of shock
after a cause
has been
established?

" Vascular repair or revision

Surgical hemostasis of major wounds
Closure of bleeding ulcers, and chemical
scarring (chemosclerosis) of varicosities

125.

What is sepsis
or septic shock?

It is a complex type of distrbutive shock

that usually begins as a bacterial or fungal
infection and progresses to a dangerous
condition over a period of days. It is
widespread and couple with a more general
inflammatory response known as systemic
inflammatory response syndrome.

Why should you

not hang Ringer's
with blood?

The calcium induces clotting of the

infusing blood

107.

What helps restore

osmotic pressure
and fluid volume?

Protein containing colloids such as

blood and blood products when shock is
caused by blood loss.

108.

What do whole
blood and prbc's
do?

They increase hematocrit and

hemoglobing along with fluid volume.

109.

Why is whole
blood used?

To replace large columes of blood loss

because it increase colume and
imporves the oxygen-carrying capacity
of the blood.

110.

Why are PRBC's

used?

They are given for moderate blood loss

because they resotre the red blood cell
deficit and improve oxygen carrying
capacity without adding excessive fluid
colume.

111.

Why is plasma
given?

To restore osmotic pressure when

hematocrit and hemoglobin levels are
within normal ranges.

112.

What do plasma
protein factors and
synthetic plasma
do?

They increase plasma volume and are

used as early treatment for hypovolemic
shock before a cause can be
established.

113.

Why might drug

therapy be used?

If the volume deficit is sever and the

patient does not respond sufficiently to
the replacement of fluid volume and
blood products.

114.

What are the

actions for drugs
for shock?

They increase venous return, improve

cardiac contractility, or improve cardiac
perfusion by dilating the coronary
vessels.

106.

126.

Whem is
SIRS
triggered?

When an infection escapes local control. The

organisms and the toxins or endotoxins in the
bloodstream enter other body areas and the
inflammatory response becomes an enemy
leading to extensive tissue and vascular
changes that furtehr impair oxygenaton and
tissue perfusion.

135.

In additon
what does the
amplified
sirys and
cytokine
release result
in?

Capillary leakiness, injured cells, and

increased metabolism.

127.

What occurs
at the tissue
level with
sepsis?

The WBCs are producing many proinflammatory cytokines and as a result, there
is a widespread vasodilation and pooling of
blood in some tissues.

136.

What does
damage to the
endothelial
cells do?

It reduces anticlotting actions and triggers

the formation of even more small clots.

128.

What are
some of the
signs of
sepsis?

Mild hypotension
Increased respiratory rate
These actions result in a hypodynamic state
with decreased cardiac output.
Temperature can vary (low, low-grade or
high)
Reduced urine output
Elevated WBC's

137.

What does the

continued
anaerobic
metabolism
result in?

Poor oxygen uptake and the continued

stress response triggers the continued
release of glucose form the liver and the
patient also has hyperglycemia. The more
severe the response the higher the blood
sugar.

138.

Why is the
sepsis often
missed in the
second stage?

Because cardiac function is hyperdynamic in

this phase. The pooling of blood and the
widespread capillary leaking stimulatse the
heart, and cardiac output is increasee with a
more rapid heart rare and an elevated
systolic blood pressure.

139.

What may the

patient's
extremities
feel like at
this time?

They may feel warm and there is little or no

cyanosis.

140.

By this time
what changes
are occuring
at the cellular
level?

WBC count may no longer be elevated.

Oxygen sats are lower, respiratory rate is
rapid, urine output is decreased or absent
and there is a change in the patient's
cognition and affect.

141.

What is septic
shock?

It is the stage of sepsis and SIRS when

multiple organ failure is evident and
uncontrolled bleeding occurs.

142.

Even with
intervention
what is the
death rate of
patients in
this stage of
sepsis?

60^

129.

What
symptoms
result
directly from
SIRS?

Fever and hypotension

130.

What
symptoms
are a result
of the
adaptive
mechanisms?

" Reduced urine output

Increased respiratory rate

What causes
cell hypoxia
and reduced
organ
function with
sepsis?

Microthrombi begin to form within the

capillaries of some organs.

132.

Is the
damage at
this point
reversible?

Yes, if if it is stopped at this point but it is

very hard to detect.

133.

What do the
microthrombi
do?

They increase the number of cells that are

operating under anaerobic conditions, which
results in the generation of more toxic
metabolites. These cause more cell damage
and increase the production of proinflammatory cytokines, leading to an
intensifying or amplification of the SIRS and a
vicious repeating cycle of poor oxygenation
and tissue perfusion.

134.

What is
severe
sepsis?

It is the progression of sepsis with an

amplified inflammatory response. All tissues
are involved and all have some degree of
hypoxia, although some organs are
experienceing cell death and dysfunction at
this time. Microthrombi formation is
widespread using much of the available
platelets and clotting factors (DIC)

131.

143.

What is
present in
this stage
of septic
shock?

Hypovolemic shock is present with

hypodynamic cardiac function. This is the result
of an inability of the blood to clot because the
platelets and clotting factors were consumed
eariler, capillary laek continus as a resulf ofo
the presense of pro-inflammatory cyotkines and
cardiat contractility is poor from cellurlar
ischemia and the presence of myocardial
depressant factor. This resembles the late
stages of hypovolemic shock.

152.

How is
increased
cardaic output
reflected?

" Tachycardia
Stroke Volume increased
Normal to elevated systolic BP
Normal CVP
Skin color appears normal with pink mucous
membranes
Skin may be warm to touch"

153.

As sepsis
progresses
what may
occur?

DIC with the formation of thousands of small

clots in the tiny capillaries of the liver,
kidney, brain, spleen, and heart, reducing
oxygenation in those organs.

154.

When does
hemorrhage
occur with
sepsis?

In the septic shock stage.

155.

What
respiratory
changes may
occur in
septic shock?

As tissue hypoxia becomes more profound

and metabolic acidosis is present, the depth
of the respiration also increases. The lungs
are susceptible to damage and the life
thrreatening lung complication of ARDS may
occur in septic shock.

What is the
major
cuase of
sepsis?

Bacterial infection that escapes local control,

although inimmunocompromised patients, fungal
infections can also lead to sepsis.

What are
some
common
organisms
that cause
sepsis?

Escherichia coli and Klebsiella pneumoniae as

well as Staph and Strep.

What is the
hallmark of
sepsis?

An increasing serum lactate level, a normal or

low total WBC count, and a decreasing
segmented neuthrophil level with a rising band
neutrophil level. (left shift)

156.

Blood is shunted away from the skin by

vasoconstriction and pallor, cyanosis , or
mottling may be present.

How does
sepsis and
septic
shock
differ form
other tpes
of shock?

Then entire syndrome may occur over many

hours to days
Manifestations usually are less obvious
The chance for recover is good when sepsis is
caught early and appropriate interventions are
started.
The cause of sepsis is often less obvious
than for other types of shock.

What happens
to the skin in
the
hypodynamic
stage of
sepsis?

157.

The skin is warm and no cyanosis is evident.

What are
the normal
levels in
the healthy
patient?

" Cardiac output - 3 to 5 L/min

Stroke volume - 60 to 80 mL
Serum lactate - < 2 mmol/L
Blood glucose - < 110
Oxygen saturation - 95%-100%

What happens
to the skin in
the
hyperdynamic
stage of
sepsis?

158.

What happens
to the skin
with septic
shock?

Circulation is severely compromised and the

skin is cool and clammy, and pallor, mottling,
or cyanosis is present.

149.

What are
the
parameters
for early
sepsis?

" Cardiac Output - decreased

Stroke Volume - decreased
Serum lactate - normal to slightly increased
Blood glucose - 110- 120 mg/dL
Oxygen Saturation - < 95%

159.

What happens
with patients
in DIC?

Petechiae and ecchymoses can occur

anywhere. Bood may ooze from the gums,
other mucous membranse, and venipuncture
sites, as well as around IV catheters.

150.

What are
the
parameters
for late
sepsis?

" Cardiac output - Increased

Stroke volume - Increased
Serum lactate - 2-4 mmol/L
Blood glucose - 110 - 120
Oxygen saturation - < 85%

160.

Urine output that is less than expected.

151.

What are
the
parameters
for Septic
Shock?

" Cardiac output - greatly decreased

Stroke volume - greatly decreased
Serum lactate - > 4 mmol/L
Blood glucose - > 150
Oxygen saturation - < 80%

What renal
urinary
change
indicates any
type of sepsis
or shock
problem?

161.

What is the
indicator that
patients may
be in the
beginning of
severe
sepsis?

Often a change in affect or behavior.

144.

145.

146.

147.

148.

162.

What is an indicator of sepsis and septic shock?

A low blood level of activated protein C.

163.

What are some other biologic indicators of

sepsis and septic shock?

Plasma D-dimer levels rise during sepsis as the fibrin in clots is broken down.

164.

What is the Systemic Inflammatory Response

Syndrome (SIRS) Criteria?

" Temp > than 100.4 or less than 96.8

Heart rate > 90 bpm
Repspiratory rate of > 20 breaths or a Paco2 level < than 32 mm Hg
Abnormal WBC count

165.

When is sepsis considered to be present?

"When two or more SIRS criteria are present along with any now infection and one
or more of these clinical manifestations:
Hypotension, Urine output less than expected
Positive fluid balance, Decreased cap refill
Hyperglycemia > than 120mg/dL in the absence of diabetes
Unexplained change in mental status

166.

What is a common collaborative problem for

patients with septic shock?

MODS

167.

What are the most common agents for septic

shock?

Gram- negative bacteria.

168.

What can the stress of severe sepsis cause?

Adrenal insufficiency in many patients. May need to suppor with low-dose

corticosteroids (hydrocortisone or fludrocortisone)

169.

What does the current therapy for clotting?

Activated protein C to stop the inflammatory response.