Advanced Concepts of Clinical Decision-Making: Unit VII: Shock

 Shock can be identified as early or late, depending on

the signs and symptoms and the overall severity of
organ dysfunction: stages: compensatory (stage 1),
progressive (stage 2), and irreversible (stage 3). The
window of opportunity that increases the likelihood of
patient survival occurs when aggressive therapy
begins within 6 hours of identifying a shock state,
especially septic shock.

 acute, widespread process of impaired tissue perfusion

 results in cellular, metabolic, and hemodynamic

malfunction

 in other words, all body systems are affected

from the cellular level all the way up to organ
systems.
 Eventually, if shock continues without being interrupted,
it causes cellular dysfunction, and multiple organ
dysfunction syndrome (MODS), and death.

 Etiology
 5 Classifications (according to most literature) based on
the underlying cause:
 Hypovolemic shock: loss of circulating volume

 From whatever shock including: gunshot

wound, postpartum hemorrhage, knifing.
 Cardiogenic shock: impaired pumping of the
heart

 You have enough volume but it’s just not

getting to where it’s supposed to go
 Septic shock: caused by infection

 Massive dilation that causes a drop in blood

pressure from not having enough pressure
in the system anymore
  Neurogenic shock: altered vascular tone caused
by CNS injury, medications, or anesthesia.
 Sympathetic vascular tone where you only
have unopposed parasympathetic impulses
left and the vascular bed doesn’t constrict,
just stays dilated of course then you lose
the pressure in your vasculature.
 Anaphylactic shock: hypersensitivity reaction.

 Caused by a histamine release as a

reaction to an allergen or multiple allergens
 Other Classifications seen in the literature where types of
shock are grouped according to “whats going on with the
blood supply” because a lot of the initial stages of shock
has to do with blood pressure:
 Distributive shock: mal-distribution of
circulating blood volume d/t massive vasodilation
(loss of symathetic tone); a.k.a. circulatory or
vasoactive shock
 Septic, Anaphylactic, or Neurogenic (mal-
distrubtion of blood volume)

 Again, there’s enough volume but it’s not

going where it’s supposed to go
 Obstructive shock: external forces are
compressing the heart or obstructing the outflow
of blood from the heart
 Can be caused by tension pneumothorax,
cardiac tamponade, a massive pulmonary
embolism, severe pulmonary hypertension,
severe aortic stenosis
 Traumatic shock: (usually from trauma) can
start with hypovolemia; ends with massive
cellular swelling causing obstruction to
microvascular blood flow (cause there is so much
pressure from all of this fluid being sequestered
everywhere in the tissues) even though
 macrovascular flow (large vessels) may be
normal. (When it gets to the capillary levels
where the exchange of oxygen and carbon
dioxide occurs) this is where the problem is and
this state of affairs causes MODS and death.

 Pathophysiology

 Cellular Changes
 Poor perfusion and as a consequence, there is
poor oxygenation of the cells causing:
 The cell to swell and cell membrane to
become more permeable so that different
electrolytes and fluids move in and out of the cell
much more easily than normal which causes big
fluid and electrolyte shifts and in the meantime,
these cellular changes create a demand for
glucose.

Cellular effects of shock. The cell swells and the cell

membrane becomes more permeable; fluids and electrolytes
seep from and into the cell. Mitochondria and lysosomes are
damaged, and the cell dies.

 Depletion of glycogen stores

 If the patient has been in a shock state for

more than 48 hours, all of their glycogen
 stores, what you store for energy in your
liver, gets all used up because the body
needs more and more energy to keep
going. Mainly one of the problems is that
there is not enough glucose so some of this
energy has to be put towards making
glucose out of other things like protein and
carbohydrates and that’s called
gluconeogenesis and in order to do that,
you have to expend energy and all of this
causes a buildup of metabolic waste.
 Build-up of metabolic waste in cells and
interstitial spaces
 Because there is poor perfusion to be able
to exchange waste products and get them
away from the cells and because of all the
cellular swelling and the fluid shifts causing
impaired cellular metabolism.
 Impaired cellular metabolism and cellular
death eventually if it keeps going on

 Vascular responses

 Release of biochemical mediators (cytokines)

 These trigger vasodilation and
vasoconstriction as part of the
compensatory mechanisms that the body
has to deal with shock and because these
cells keep putting out these chemical
mediators that basically say to the other
body systems, “give us oxygen, give us
blood flow because we are not getting
enough” so more and more cytokines get
produced and these are implicated in the
development of systemic inflammatory
response syndrome (one of the
mechanisms which causes MODS) which is
a massive generalized inflammation that
won’t stop and one of the things that is
highly implicated are the cytokines, these
 circulating cytokines seem to take a life of
their own and go do things that the body
doesn’t really need them to do.
 Regulation of blood pressure

 Catecholamine release

 Because the body knows that it is not

getting enough blood perfusion and enough
oxygenation so their signal is sent to the
brain which releases adrenal corticotropics
hormone (ACTH)from the pituitary which
tells the adrenal glands to release cortisol,
glucagon, and catecholamines like
glucocorticoids, epinephrine, and
norepinephrine.
 Activation of Renin-Angiotensin-Aldosterone
system (sensed by the kidneys very quickly that
the b/p is not being maintained by homeostasis.)
 When Renin is released, it goes to the lungs
and converted from Angiotensin I to
Angiotensin II which is the most potent
vasoconstrictor known so the body
attempts to raise the blood pressure with
Angiotensin by vasoconstriction
 Aldosterone is also released and this
basically tells the kidneys to conserve
Sodium and Water, so that you are not
losing anymore blood volume (if that’s the
problem) and this conservation also raises
the blood pressure
 Release of ADH (anti-diuretic hormone) from the
brain which also tells the kidneys to conserve
water

 Aerobic vs. Anaerobic metabolism

 Aerobic

 more efficient; produces more energy

  requires strong heart and effective circulation to
keep it going
 requires ability (at the cellular level) to exchange
O2 and CO2 through the capillary membranes
 meets typical body demands of typical ordinary
life
 by-products are CO2 and H2O

 Anaerobic (without oxygen)

 body switches to this pathway when energy

demands or O2 levels are low
 meant to be used for short periods

 when you need to run away from

something or exercising intensely and
when your muscle have used up the
available oxygen in the muscle tissue and
they switch to anaerobic metabolism. This
is why the muscles start hurting because
there is a build-up of lactic acid from
anaerobic metabolism.

 by-product is lactic acid

 requires healthy, well oxygenated muscle tissue
to clear lactic acid

 So if you are not healthy, and not well

oxygenated, the lactic acid will build-up in your
blood
 Compensatory (initial) Stage

 In the compensatory stage of shock, the BP

remains within normal limits. Vasoconstriction,
increased heart rate, and increased contractility of
the heart contribute to maintaining adequate
cardiac output. This results from stimulation of the
sympathetic nervous system and subsequent
release of catecholamines (epinephrine and
norepinephrine). Patients display the often-
described “fight or flight” response. The body
shunts blood from organs such as the skin, kidneys,
and gastrointestinal tract to the brain, heart, and
lungs to ensure adequate blood supply to these
vital organs. As a result, the skin is cool and
clammy, bowel sounds are hypoactive, and urine
output decreases in response to the release of
aldosterone and ADH.
 Homeostatic mechanisms attempt tissue perfusion in
response to insult: attempts to increase tissue perfusion
in response to all of this and attempt to compensate.
 neural (sympathetic): increases HR and
contractility, vasoconstriction- shunts blood to
vital organs. This is why people’s skin become
getting cool and clammy because the blood has
been shunted away from the periphery and go
into the core where all the vital organs are.
 hormonal: renin-angiotensin-aldosterone
mechanism activated; ADH secreted; ACTH
secreted → adrenals secrete glucocorticoids
(epinephrine, norepinephrine, cortisol, and
glucagon) and aldosterone (which tells the
kidneys to save Sodium and Water)
 chemical: hyperventilation- body attempts to
blow off CO2 to counteract the lactic acidosis
(which is the metabolic acidosis) and so the body
tries to compensate with the respiratory system.
 fluid shifts: are occurring in response to ↓
intravascular volume
 Progressive Stage

 In the second stage of shock, the mechanisms that

regulate BP can no longer compensate, and the MAP falls
below normal limits. Patients are clinically hypotensive;
 this is defined as a systolic BP of less than 90 mm Hg or a
decrease in systolic BP of 40 mm Hg from baseline

 Irreversible Stage
Clinical Findings in Stages of Shock

Stage
Compensator
Finding y Progressive Irreversible

Blood Normal Systolic <80–90 mm Requires mechanical or

pressure Hg pharmacologic support
Requires fluids
resuscitation to
support blood
pressure

Heart rate >100 bpm >150 bpm Erratic or asystole

Respirator >20 Rapid, shallow Requires intubation

y status breaths/min respirations; and mechanical
PaCO2 <32 crackles ventilation and
mm Hg PaO2 <80 mm Hg oxygenation
PaCO2 >45 mm Hg

Skin Cold, clammy Mottled, petechiae Jaundice

Urinary Decreased 0.5 mL/kg/h Anuric, requires

output dialysis

Mentation Confusion Lethargy Unconscious

Acid–base Respiratory Metabolic acidosis Profound acidosis

balance alkalosis

 Compensatory Stage: This are the s/sx that a pt. in

compensatory stage will be exhibiting:
 B/P: will usually be normal
  Cardiac output (CO) normal (however there may be
changes that are occurring to keep it that way)
 HR > 100 and RR > 20 bpm or both INCREASED
 aerobic → anaerobic metabolism and lactic acidosis has
started to occur.
 respiratory alkalosis (happens as a compensatory
mechanism to the lactic acidosis: blowing off a lot of
CO2) metabolic acidosis being compensated with
respiratory alkalosis.
 urine output drops (as the Renin Angiotensin
Aldosterone system and the ADH release from the brain
tells the kidneys to save H2O) so there wont be as much
urine excreted
 cool, clammy skin :as blood is shunted from the
periphery (which is the skin) and the extremities toward
the core where all the vital organs are.
 hypoactive bowel sounds (as blood is shunted away from
the peristalsis)
 mental status: confusion (may become confused and
combative) and is usually caused by the blowing off of a
lot of CO2 and respiratory alkalosis
 Medical Management of the Compensatory Stage

 identify cause of shock and correct it as soon as possible

 support compensatory mechanisms because they will not

continue forever
 re-establish and maintain adequate tissue perfusion done
by:

 medications

 fluid resuscitation
 Nursing Management of the Compensatory Stage

 meticulous assessment for those at risk (because early

intervention is absolutely critical: by the time the blood
 pressure begins to fall, in other words, before the pt
starts going into the progressive stage, the
compensatory mechanisms fail, and damage has already
been done at the microcirculatory level so tissue damage
has already started. EARLY INTERVENTION AND
IDENTIFICATION IS CRITICAL.
 recognize early signs, particularly in the elderly because
they don’t have too much reserve and their
compensatory mechanisms tend to burn out quicker.
 monitor tissue perfusion:

 vital signs and neuro checks

 calculating pulse pressure (normal 30-40) and

 narrowing pulse pressure is an early indicator of

the onset of shock, monitoring pulse pressure is
important.
 monitoring labs in the early stages of shock. The
Sodium levels will increase and the Glucose levels
will increase. The base deficit of ABGs will fall and
that is related to lactic acidosis, the body is using
up as much bicarbonate as it can to buffer the
lactic acidosis.

 continuous central venous oximetry

 urine output

 sublingual capnometry: a sublingual probe (like a

temperature probe) used to measure tissue
carbon dioxide: increased levels of carbon dioxide
in the tissue indicate poor tissue perfusion (done
under the tongue)
 near infra-red spectroscopy (NIRS): uses light to
measure the oxygenation of skeletal muscle and
they use it on the palm of the hand, on the
muscle that is right below the thumb. The normal
is greater than 80% oxygenation and anything
less than that is an indicative of tissue hypoxia.
  reduce anxiety and promote patient safety:
particularly of the patient is confused or
combative.
 Progressive Stage:

 Compensatory mechanisms begin to fail- affects every

organ system

 Heart is overworked and begins to malfunction

 There may be arrhythmias and/or evidence of

myocardial ischemia on the EKG (ST segment
depression)
 Microcirculation fails d/t release cytokines and chemical
mediators: which cause increased capillary permeability
which leads to fluid leakage and microcirculatory failure
because the fluid leakage creates a lot of pressure at the
microcirculatory level. Fluids are supposed to stay within
the capillaries; they aren’t supposed to leak between/in
the interstitial spaces between the cells; and as this fluid
leakage gets bigger and bigger, more and more pressure
occurs on the microcirculation and eventually shuts off
microcirculatory blood flow.
 Inflammatory response to whatever injury begins which
affects coagulation

 Vicious cycle continues even if precipitating cause is

successfully treated.

 For example, even if hypovolemic shock is

corrected, the shock syndrome will continue and
becomes a self-perpetuating thing and the
underlying reasons for this are poorly understood.
 Neuro: SNS dysfunction (we need these mechanisms to
aid in the compensatory process), coma and or lethargic,
thermoregulation in the brain may fail, cardiac and
respiratory centers may become depressed in the brain
 Respiratory: acute respiratory failure and ARDS: there is
capillary damage and damage to the alveolar membrane:
and all this is getting traced to the inflammatory
 response, blame is on the cytokine releases and the
capillary leakage which occurs and causes an increase in
pressure at the microcirculatory level which eventually
shuts off the microcirculatory circulation.
 CV: lack of adequate perfusion → rapid HR which
eventually causes chest pain from myocardial ischemia,
cardiac enzymes may become elevated, dysrhythmias,
cardiac failure

 Hematologic: DIC
 GI: hepatic (liver), pancreatic and intestinal become
ischemia and stop functioning the way they’re supposed
to and particularly with the intestines and the liver: the
liver quits filtering bacteria out of the mesenteric
circulation and the intestinal wall, the capillaries, become
more permeable, and eventually they become so
permeable that they become damaged and it allows →
failure; bacterial toxins to translocate into the systemic
circulation → which can cause SEPSIS even if the initial
insult wasn’t sepsis.
 Renal: ARF occurs when MAP < 70 (if less than 70, the
brain starts becoming ischemic; oliguria
 Capillary permeability is increased- leads to “third
spacing” with massive swelling and further ↓ in
intravascular volume. So you as the nurse, find yourself
giving the pt more fluids because of this increased
capillary permeability; the fluid eventually leaks out into
the interstitial space as the pt becomes very swollen but
their intravascular space (inside of the pipes) is dry
 Skin: mottled; petichiae may show particularly if they are
having a problem with DIC
 Mental status: very lethargic, and/or difficult to arouse
leading to coma
 Metabolic acidosis continues: r/t switch from aerobic to
more anaerobic metabolism; the respiratory-blowing off
of CO2 to compensate-can’t keep up with the massive
amounts of lactic acid
 Medical Management of the Progressive Stage

 Use meds and IV fluids to:

 Restore tissue perfusion

 Support myocardial contractility

 Improve vascular tone (to get that sympathetic
tone back)
 Support the respiratory system (may get
intubated and mechanically ventilated at this
point)
 Nutritional support: start it early! Because the pt doesn’t
need any negative nitrogen imbalance on top of
everything else; in fact, the pt’s nutritional needs get
more and more demanding up to over 3000 calories/day
depending on their condition but also because of the
increased energy demands of anaerobic metabolism and
gluconeogenesis.
 Aggressive glycemic control may be attempted
with IV insulin because of the high glucose level
from all the stress hormones.
 Prevent GI bleeding (another priority): H2
blockers, PPI’s, and/or antacids

 Nursing Management of the Progressive Stage

 Careful, frequent assessments/monitoring

 Prevention of additional complications:

 VAP (Ventilator Associated Pneumonia)

 UTI (Urinary Tract Infection)

 Decubitus Ulcers

 Or any complication that the pt didn’t come

in the ICU with

 Promote rest and comfort

  Family support: provide information!

 Information is the families #1 need.

 Irreversible Stage of Shock

 Irreversible process: shock has gone on long enough,

patient doesn’t respond to treatment; severe organ
damage continues; patient cannot survive
 At this time, the pt has MODS: 2 or more organ systems
fail
 Only 10-20% of patients survive MODS

 Death

 B/P: maintained by mechanical or pharmacologic means

 Cardiac: Arrhythmias; terminal heart failure agonal
rhythms; asystole
 Respiratory: maintained on mechanical ventilation and
cannot breathe on their own anymore
 Skin: grey pallor; jaundice from liver damage

 Renal: oliguria; anuria; requires dialysis

 Neuro: pt is unconscious most of the time or may be in a
coma
 Profound metabolic acidosis which is refractory to
treatment
 Medical Management of Irreversible Shock

 Same as in Progressive stage

 Experimental therapies do exist

 Nursing Management

 Same as in Progressive stage

 But the FOCUS becomes palliative; making the pt
comfortable and giving support to the family.
  Explanation of prognosis to family AFTER they have been
given the prognosis from the physician; correct any
misconceptions including the fact that many families may
get a false hope as they see all those machines and you,
the nurse, working with their loved one, and they may
interpret that as if there may still be hope for this pt., but
at this stage, there really isn’t any hope

 Allow family to visit and participate in care whenever

they desire
 Ask about living wills, advance directives, durable power
of attorney for health care because the pt will not be in
any condition to make their own choices at this point.

 Encourage family to express their wishes

 General Management Strategies for ALL forms of
SHOCK

 Fluid Replacement

 Crystalloids vs. colloids

 Isotonic Crystalloid: fluid replacement for

shock: includes 0.9% NS and LR

 The disadvantage of Crystalloid

replacement is that they are easily third-
spaced (they third-space faster than
colloids)
 Hypertonic Crystalloid: 3% NS is sometimes
used that pulls fluid into the vascular space
from the interstitial space because of the
higher amount of Sodium.

 Colloids: have larger particles that are

harder to pass through the capillary
membranes so the effect of colloid fluid
replacement lasts longer; however, they’re
expensive and there is a danger of allergy
with some colloids particularly albumin and
plasmanate
  Other non-blood product colloids include
Dextran which is heavy sugar and its
contraindicated in people with bleeding
problems because Dextran interferes with
platelet aggregation. They may also use
Heterstartch and it’s a carbohydrate
molecule.

 Complications

 Cardiovascular overload

 Abdominal Compartment syndrome

 Vasoactive Medications (see chart)

Vasoactive Agents Used in Treating Shock

 Desired Action in
Medication Shock Disadvantages

Inotropic Agents

Dobutamine Improve contractility, Increase oxygen demand of

(Dobutrex) increase stroke the heart
Dopamine volume, increase
(Intropin) cardiac output
Epinephrine
(Adrenalin)
Milrinone
(Primacor)

Vasodilators

Nitroglycerin Reduce preload and Cause hypotension

(Tridil) afterload, reduce
Nitroprusside oxygen demand of
(Nipride) heart

Vasopressor Agents

Norepinephrin Increase blood Increase afterload, thereby

e (Levophed) pressure by increasing cardiac
Dopamine vasoconstriction workload; compromise
(Intropin) perfusion to skin, kidneys,
Phenylephrine lungs, gastrointestinal tract
(Neo-
Synephrine)
Vasopressin
(Pitressin)

 Inotropes

 Vasodilators
  Vasopressors
 Nutritional support: EARLY INTERVENTION

 Increased energy requirements

 Enteral feeding IS PREFFERED vs. parenteral
nutrition: unless the pt has some difficulty with
their GI system either from ischemia or necrosis
that precludes from giving enteral feedings.
 Stress ulcers (Curling’s Ulcer)

 Hypovolemic Shock
 Absolute: e.g. blood loss from the vascular space, non-
blood fluid loss (massive diarrhea: CHOLERA: can kill in
less than 24 hrs if fluid is replenished)
 Relative: e.g. “third spacing” : fluid that should be in the
vascular space that isn’t because it is third spaced, so
the intravascular space has become very dehydrated.
 Pathophysiology of Hypovolemic Shock

 Loss of circulating blood volume

 Risk Factors of Hypovolemic Shock are listed in CH. 15

THIS IS HOW HYPOVOLEMIC SHOCK WORKS:

 There is decreased blood volume from whatever reason

 Which causes a decreased venous return which basically

causes decreased preload
 Decrease preload means decreased stroke volume

 A decreased stroke volume means a decreased cardiac output

 A decreased cardiac output causes due to not enough blood

circulating around you get decreased tissue perfusion
 Assessment and Diagnosis of Hypovolemic Shock

 Initial stage: signs may go undetected unless looked for

 Especially pts that are at high risk

 Later stages:
 significant fall in BP, (very obvious) narrowing
pulse pressure, urine flow of < 30 mL/h, and a
progressive increase in the arterial lactic acid
concentration (metabolic acidosis)
 Signs related to compensatory mechanisms that
the body uses to keep the vital organs perfused
such as:

 Tachycardia, tachypnea, and thirst

 Signs related to organ hypo-perfusion

 Decreased/altered mental status, cool-
clammy skin, renal failure, hepatic failure,
respiratory failure.
 Hemodynamic Assessment
 Normal or reduced ventricular filling pressure with a low
cardiac output in a patient with shock is diagnostic. A
right ventricular filling pressure or central venous
pressure (CVP) < 7 cm H2O (< 5 mmHg) suggests
hypovolemia.

 <7 cm H2O (of water): Water manometer: are

hardly used

 <5 mmHg (of mercury): Electronic monitors

 Medical Management of Hypovolemic Shock

 Correcting the hypovolemia with crystalloids (0.9% NS or

LR) and/or colloids (blood products and/or plasmanate,
albumin, fresh frozen plasma) replacement; depending
on what the loss is. If its blood and what the pts labs are
like.

 Restore tissue perfusion

 Complications of receiving blood products:

 Hypothermia: pts may need blood warmed

if they are going to get massive
transfusions because of the danger of
hypothermia from large amount of cold
bank blood.
 Hyperkalemia: from large amounts of
banked blood is high in K+, it has 4 mEq/L

 Hypocalcemia: because the citrate

preservative in banked blood bind calcium.
 Acidosis may worsen because banked blood
is acidotic to begin with and/or Alkalosis
from citrate and Lactate which are used are
used as preservatives and those are
converted to bicarb in the liver when the
pt’s blood volume is restored. So they may
be acidotic for a while, and then all of a
sudden their hypovolemia is corrected with
a metabolic alkalosis.
  Clotting disorders may occur because
banked blood, particularly packed red blood
cells, don’t have any clotting factors in it;
those you have to get by getting fresh
frozen plasma; the plasma has been taken
away.
 Cellular debris is always present in banked
blood and after 4 units of blood the pt
needs to have a blood filter (an extra
microfilter) that is used to remove this
debris because it has been postulated that
pts with hypovolemic shock who have had
massive blood transfusions may develop
such problems as: DIC and ARDS: because
of the presence of cellular debris in their
circulation and it sets up more
inflammatory processes.
 Infectious agents that can be transmitted
by blood transfusions include (although
incidences have gone down since testing
has been initiated): hepatitis, risk of
contracting HIV (very low), CMV
(cytomegalovirus), and ebola virus
(hemorrhagic fever) can be passed to blood
recipients by asymptomatic carriers
(although in the US, it doesn’t seem to be a
big of a problem as it is in other parts of the
world.
 Nursing Management of Hypovolemic Shock

 Prevention of hypovolemic shock to begin with

 Prompt detection and identification of at risk pts

 Minimize and/or preventing further fluid losses

 Enhance volume replacement by keeping the pt warm,

monitoring their I&O’s, monitoring their hemodynamic
values by monitoring their vital signs, and monitoring
and managing CVP lines and pulmonary artery catheters-
monitor those readings, monitoring for dysrhythmias,
 and making sure that the pt has at least 2 IV large bore
sites at all times during the acute phase.

Above: MODIFIED TRENDELENGBURG POSITION: will help in

HYPOVOLEMIC SHOCK!

 This will help to shunt blood that has pooled in the lower
extremities up into the core and it’s a temporary
measure so YOU the nurse, still have to replace the fluid
volume that has been lost. It is called MODIFIED
TRENDELENGBURG because the pts head and shoulder
are flat on the bed. COMPLETE TRENDELENBURG- head
will be lowered and not flat.

 Complications of massive blood transfusion:

 Hypothermia

 Hyperkalemia

 Hypocalcemia

 Acidosis

 Alkalosis

 Clotting disorders

 Cellular debris

 Infectious agents

 CARDIOGENIC SHOCK
  Failure of the heart to pump blood around the body
effectively.

 The cardiac output becomes inadequate for the

metabolic and oxygen needs of the body and
shock ensues.

 Etiology
 Usually caused by Primary ventricular ischemia, e.g. MI:
and it does not have to be a HUGE MI, although it seems
like pts that have a large area of heart muscle affected
are more likely to go into cardiogenic shock. Sometimes
people with a smaller MI; just because of their own
physical makeup, their heart is unable to pump
effectively for a period of time and they will go into
cardiogenic shock.
 Structural problems: e.g. penetrating trauma, myocardial
rupture, valve disorders particularly acute mitral
regurgitation, which is an emergency, is usually caused
by papillary muscle rupture (from a very large MI or an
infarction that involves the papillary muscles that control
the opening and the closing of the mitral valve and when
it happens it’s been known to be uniformly fatal. Survival
is very low.
 Dysrhythmias may cause cardiogenic shock: e.g.
profound bradycardia (down to 30bpm caused by A-V-
blocks: third degree heart block), VT & VF (where no
blood is moving at all).

 Pathophysiology
 Characterized by an impaired ability of the ventricle to
pump blood
 The shock syndrome is caused by a “heart” problem
NOT by blood volume, not by sepsis, not by a problem
with the neurologic system, then the “dominoes effect”
takes place and everything else begins to fall.
 Assessment and Diagnosis of Cardiogenic Shock

 Low CO and low BP

  Compensatory mechanisms develop

 Hemodynamic Assessment
 Diagnosis usually requires demonstration of reduced
cardiac output with increased ventricular filling pressures
where there is increased preload and increased afterload
and reduced cardiac output.

CARDIOGENIC SHOCK
 First there is a decreased cardiac contractility that
starts everything and is caused by ischemia, infarction or
arrhythmia.
 Then causes decreased stroke volume and cardiac
output
 Which then causes pulmonary congestion (blood/fluid
gets backed up in the lungs which starts to leak out from
the higher pressures into the alveoli), decreased
systemic tissue perfusion (because not enough blood
is being pumped out to the body), and decreased
coronary artery perfusion (the heart has its own
needs for blood and that alone makes the myocardial
contractility problem worse.
 Medical Management of Cardiogenic Shock

 Correcting the underlying cause of pump failure if possible

 By using anti-dysrythmics, inserting a pacemaker, by

doing percutanous coronary interventions like PTCA
(Percutaneous Transluminal Coronary Angioplasty)
and stent placement, coronary bypass surgery, an
emergency replacement of a cardiac valve, and
thrombolytic therapy.
 Increasing myocardial oxygen supply by supporting
respiration and usually intubation and mechanical
ventilation is required.
 Decrease cardiac workload by promoting rest, giving
nitroglycerin (will decrease preload and afterload),
morphine (will decrease preload and afterload), sometimes
beta-blockers to slow the heart but you have to be careful
with beta-blockers because they tend to depress myocardial
contractility, and diuretics to decrease preload and
afterload.
  Improve contractility with the use of inotropic agents

 IABP or VAD

 Intra-aortic balloon pump (IABP) is a mechanical

device that decreases myocardial oxygen demand
while at the same time increasing cardiac output.
Increasing cardiac output increases coronary blood
flow and therefore myocardial oxygen delivery)
 Ventricular assist device, or VAD, is a mechanical
circulatory device that is used to partially or
completely replace the function of a failing heart.
Some VADs are intended for short term use, typically
for patients recovering from heart attacks or heart
surgery, while others are intended for long term use
(months to years and in some cases for life), typically
for patients suffering from congestive heart failure).
 Restore tissue perfusion by doing all of the above

 Nursing Management of Cardiogenic Shock

 Preventing cardiogenic shock by identifying at risk patients

early so that appropriate interventions can be done for pts
that need: a pacemaker, a PTCA, bypass surgery (because
they are having so much pain), or pts that have very
hemodynamicly significant arrhythmias.
 Limit myocardial oxygen consumption by decreasing the pts
activity by making sure that they have adequate pain
control and decreasing their anxiety.
 Enhancing their oxygen supply by proper positioning and by
administering oxygen and/or maintaining them on
mechanical ventilation.
 Knowledge of usage and side effects of medications
because almost all of them are titratables.
 Inotropes, Vasodilators, Thrombolytics (need to know
how to give them and how to take care of the pt while
they are on this therapy: for example: if they are
having an MI and need to have thrombolytic therapy
to restore circulation into their heart)
  IABP, VAD (knowing how to use these)

DISTRIBUTIVE SHOCK:
Anaphylaxis Shock, Sepsis Shock, and Neurogenic Shock
All of which have the same mechanism
 Massive vasodilation which then causes

 Maldistribution of blood volume: a lot of plasma fluid (not the

cells but the fluid) crosses into the interstitial spaces that causes
swelling, edema, which then causes
 Decreased venous return to the heart so preload is down and
that causes
 Decreased stroke volume which causes

 Decreased cardiac output a low cardiac output will give you a

 Decreased tissue perfusion!

 Distributive Shock: Anaphylaxis

 Etiology
  Antigen-antibody reaction where the immune system is
stimulated for poorly understood reasons by a release of
histamine and bradykinin (causes a massive peripheral
dilation and constriction of the airways)

 Pathophysiology

 Immunologic stimulation

 Peripheral vasodilation

 Assessment and Diagnosis

 CV: tachycardic, hypotension, and may have chest pain

 Respiratory: wheezing; stridor (if they have edema of the

larynx: VERY ALARMING); may have edema of the lips and
tongue; bronchospasm (because of narrowing of the larger
airways); and may end up with complete airway obstruction.
 Cutaneous on the skin: urticaria (hives), erythema (pt
turns pink or red), pruritus (very common because the hives
itch), or angioedema (edema of the eyes and face); eye
itching and conjunctival injection (where you can see all the
blood vessels and the eye (conjunctiva) turns red.
 Neurologic: makes them really anxious, tremors, sense of
being cold; behavior changes may occur if the pt is having
breathing difficulties and they will become very anxious and
upset, altered LOC (with worsening hypoxia or hypotension)
 GI, GU: will have cramplike abdominal pain with nausea,
vomiting, or diarrhea (more common w/food allergies)
 Medical Management of Anaphylactic Shock

 Remove antigen if you can and/or possible depending on

the antigen.

 If it’s a bee stinger/stinger from an insect, REMOVE IT.

 If it’s an atopical substance, REMOVE IT.

 Reversing the effects of biochemical mediators like
histamine and bradykinin with antihistamine medication for
 example Benadryl IV, Hydramine, and Epinephrine for
increasing the blood pressure with vasoconstriction.
 Fluid replacement is indicated particularly if the pt is
hypotensive.
 Oxygen may be needed for hypoxia.

 Epinephrine for vascular tone by causing vasoconstriction

so you increase the sympathetic tone.
 Corticosteriods may be used to decrease inflammation
which seem to be helpful.
 Nebulized bronchodilators (like Albuterol) may be used to
reverse some of the effects of histamine and bradykinin on
the large airways.
Nursing Management
 Prevention of anaphylactic shock by assessing for allergies
and teaching patients how to manage their allergies and
prevent exposure to allergens.
 Note all allergies whenever they are admitted to the
hospital and whenever they come in contact with the
healthcare system.
 Facilitate ventilation by giving oxygen, by intubation if
necessary: but if the pts throat is completely closed, they
may not be able to be intubated if the swelling is that bad
and they may need a cricotomy (incision of the cricoid
cartilage) and assisting them in HIGH FOWLERS to help
them breathe better.
 Enhance volume replacement by insuring IV access.

 Promote comfort such as helping them to deal with itching

and usually the Benadryl will help the itching go away.
Patients might have scratches on themselves from
scratching the hives.
 Assessing their Hemodynamics: Vital Signs: B/P, CVP, PA
(pulmonary artery) pressures; bio-impendance
cardiography; trans-thoracic or trans-esophageal
ultrasound; FloTrac which is CO and SVR via A-line.
 Hemodynamic monitoring will only be used if patients are
REALLY REALLY shocky and doesn’t respond to the
treatments.

 Patient teaching
 Distributive Shock: Neurogenic Shock

 Etiology
 Disruption of SNS: spinal anesthesia, certain drugs,
emotional stress, severe pain, and CNS dysfunction, e.g.
spinal cord injury.
 Most common of neurogenic shock IS spinal cord injury
above the level of T-6: and you NEED to KNOW that!

 Pathophysiology

 Loss of sympathetic tone

 Assessment and Diagnosis

 Hypotension
 Bradycardia: because the sympathetic nervous system is
not working; the parasympathetic is the only thing working
and it slows the heart rate.

 Hypothermia
 Warm dry skin: meaning that they are not going to be cold
and clammy.
 Hemodynamic Assessment: B/P, CVP, PA pressures; bio-
impendance cardiography; trans-thoracic or trans-esophageal
ultrasound; FloTrac: CO and SVR via A-line: SAME AS THE
ANAPHYLACTIC SHOCK: used if patients are REALLY REALLY
shocky and doesn’t respond to the treatments.

 Medical Management
 Removing the cause of the neurogenic shock if possible.

 Correct positioning after spinal anesthesia or

eliminating/decreasing the drugs that can cause this
 such as barbiturates (can highly cause neurogenic
problems).
 Restore tissue oxygenation and perfusion by intubation or
mechanical ventilation, giving oxygen, vasopressor agents.

 Nursing Management
 Basic Life Support (ABC’s)

 Immobilizing spinal cord injuries

 Vasoactive medications
 Particularly vasopressors like: epinephrine, dopamine,
neosynephrine, or norepinephrine.

 Fluid resuscitation
 Hemodynamic monitoring: B/P, CVP, PA pressures; bio-
impendance cardiography; trans-thoracic or trans-
esophageal ultrasound; FloTrac: CO and SVR via A-line.
SAME AS THE OTHER FORMS OF DISTRIBUTIVE SHOCK: used
if patients are REALLY REALLY shocky and doesn’t respond
to the treatments.

 DVT prevention

 Nutritional support
 Keeping the pt ALIVE to survive medical treatment.

 Distributive Shock: Septic Shock

 Etiology
 Septic origin(caused by organisms or the body’s responsed
organisms): most common cause of circulatory shock.

 Risk Factors of Septic Shock include:

 Intrinsic factors: e.g. immunosuppression,
malnutrition, age, & diabetes
 Extrinsic factors: e.g. invasive lines, catheters, surgical
incisions, & intubation.

 Pathophysiology
  Stimulation of the immune and inflammatory system of
biochemical mediators
 Causes a Systemic Response

 activation of plasma enzyme cascades

 activation of platelets, neutrophils, macrophages

 damage to endothelial cells in the blood vessels

 immune system becomes overwhelmedveither by

organisms themselves or organisms killing cells
outright and/or toxins being produced by the
organisms killing cells outright and the immune
system gets overwhelmed and can’t keep up with it.
 massive peripheral vasodilation in response to all of
the above
 causing increased capillary permeability

 formation of microemboli

 hyper-metabolic state

 activation of sympathetic nervous system (SNS)

 mal-distribution of circulating blood volume d/t all of
the above so now this pt becomes MASSIVELY third-
spaced (very swollen).

 Assessment and Diagnosis

 Phase 1: hyperdynamic state “warm”

 Massive vasodilation occurs

 Widening pulse pressure

 HR and CO increased because of the hyperdynamic
state that doesn’t last.

 Febrile; warm flushed skin

 Bounding pulses: label better than 4+ because the
pulse is lifting your finger off the pt’s skin.
  Increased respiratory rate to get rid of CO2 because of
metabolic acidosis d/t an anaerobic metabolism has
started because the aerobic metabolism can’t keep up
with the oxygen demands of the body.
 GI: n/v, diarrhea may occur

 Urine output: normal or somewhat decreased

 Neuro: restlessness and confused

 Assessment and Diagnosis

 Phase 2: hypodynamic state “cold”

 Vasoconstriction as the SNS tries to compensating

 B/P and CO falling

 Temp normal or ↓ (becomes normal); cold, pale,
clammy skin
 weak, thready pulses as the CO and B/P continue to
drop
 respiratory rate, HR continue to rise and pt may need
to be put on the ventilator as this phase progresses
 Renal Failure will ensue as CO drops

 Neuro: ↓ LOC, coma

 MODS may start to develop.

 Medical Management
 Aimed at Controlling/Identifying (the pathogen) and
eliminate infection
 Reverse pathophysiologic responses to the organism(s)

 Support CV system with drugs usually vasopressors to keep

the pts blood pressure up.
 Fluid administration to keep the pts circulating volume
adequate

 Provide oxygenation and ventilation

  Initiate nutrition (must be aggressive)

 Enteral nutrition is preferred

 Pharmacologic therapy
 Recombinant human activated protein C- dotrecogin
alfa (Xigris): has been used with some success for pts
with Septic Shock.

 Nursing Management
 Prevention of septic shock

 Hand-washing, strict asepsis with any invasives that

we do with pts, strict asepsis with wound care,
preventing vulnerable pts from nosocomial infections
from the hospital setting, if we can’t prevent sepsis
then we need to identify it early and start treatment
before the pt becomes so SICK that they end up in the
terminally stages of shock before we get things going.
 Maintain patent airway and adequate ventilation by
maintaining the patient on the ventilator, making sure that
their airway is open, analyzing their ABGs, and making sure
that the appropriate ventilator changes are made.
 Promote restoration of circulating blood volume by
administering IV crystalloids and colloids as ordered and
keeping STRICT I&Os and DAILY WEIGHTS.

 Administer vasoactives, antibiotics, and other drugs as

ordered
 Maintaining continuous, careful assessment of client (these
will be some of the physically demanding patients that you
will take care of because they are very sick and they will
require a lot of assessment and care.
 Provide psychological support: reassure client to
minimize anxiety; keep family informed and supported.

 Provide nutritional support

 The nurse will be the one that will need to suggest a

nutritional consult early.
  Prevent secondary complications such as skin breakdowns,
malnutrition, DVT, and the toxic effects of antibiotics, and
that everyone is kept informed of drug levels.

 Obstructive Shock
 pump failure caused by forces that compress heart: outflow
obstruction or increased resistance to ventricular filling

 Etiology
 resistance to ventricular filling, e.g. tension pneumothorax,
cardiac tamponade

 outflow obstruction: e.g. massive pulmonary embolism,

aortic stenosis

 Pathophysiology

 forces external to the heart prevent ventricular filling or

obstruct outflow
 Obstructive Shock

 Medical Management

 identify and correct source of obstruction/resistance

 support organ function

 ABC’s
 O2 and intubation/mechanical intubation

 IV access and IV fluid replacement

 Specific interventions depending on the cause for

example:
 Massive pulmonary embolism: may use
trithrombolytics and/or surgery
 Aortic stenois: may try surgery and valve
replacement, and/or commissurotomy (is a
surgical incision of a commissure in the body, as
one made in the heart at the edges of the
commissure formed by cardiac valves, or one
 made in the brain to treat certain psychiatric
disorders.

 Cardiac tamponade: relieving the fluid around

the heart

 Tension pnuemothorax: by quickly relieving the

pneumothorax

 Nursing Management

 same as other forms of shock

 specifics depend on the cause of what caused the
obstruction.

AND THIS IS THE END OF THIS PRESENTATION!! HAHA!!

STUDY!! STUDY!! STUDY!!