1 Management of clients with Shock and Multisystem Disorders (escalante-saac)

Shock

Hypovolemic, cardiogenic,
distributive
Hypovolemic shock

Cardiogenic shock
MI, valvular insufficiency
cause by disease or
trauma, cardiac
dysrhythmia, or
obstructive condition such
as pericardial tamponade,
pulmonary embolus
Cardiogenic shock
>Sustained hypotension
(systolic BP <90 mm hg for
at least 30 min)
>Reduced cardiac index
(<2.2 L/min/m2)
> presence of elevated
pulmonary capillary
occlusion pressure (>15
mm Hg)
Oliguria(<30 ml/hr), cool
extremities, and altered
mentation
40%
Obstructive shock
Cardiac tamponade
Pneumothorax
Pulmonary embolism
Distributive shock
Anaphylactic shock
Neurogenic shock
Spinal cord injury
Spinal anesthesia
Severe vaso-vagal
reactions caused by pain
or psychic trauma
Septic shock
15%, 40%-60%
Hemorrhage, burns and
dehydration
Hemorrrhage
15%-25%, 500-1500 ml
5 liters
Burns
Intravascular to interstitial
Myocardial depressant
factor (MDF)

Nephrotic syndrome,
severe crush injury,
starvation, surgery,
conditions that accumulate
in abdominal cavity (liver
cirrhosis, pancreatitis,
bowel obstruction)
Dehydration
sweating and insensible
fluid loss through
respiratory tract in hot
environment
excessive urine output
prolonged vomiting and
diarrhea
dehydration-induced
hypovolemic shock
inability to obtain fluids
diuretic induced
dehydration
Cardiogenic shock

>Life threatening condition often requiring team action by many health care provider, including
nurses, physicians, laboratory, technicians, pharmacists, and respi therapists
>potentially lethal, debilitating, and costly
>defined as failure of the circulatory system to maintain adequate perfusion of vital organs
Classifications of shock
It is due to inadequate circulating blood volume resulting from hemorrhage with actual blood loss,
burns with massive shifts of fluid due to movement of plasma proteins into the interstitial spaces,
and fluid shifts or dehydration, with or without loss of fluid volume.
>it is the most common type of shock and develops when the intravascular volume decreases to the
poinyt where the compensatory mechanism are unable to maintain organ and tissue perfusion
>is due to inadequate pumping action of the heart.
The heart muscle can be diseased as a result of primary cardiac dysfunction or mechanical
obstruction of blood flow caused by:

The clinical definition of_ is decreased cardiac output and evidence of tissue hypoxia in the presence
of adequate intravascular volume
Hemodynamic criteria for cardiogenic shock are:

Manifestation of tissue hypoperfusion

Cardiogenic shock after an MI usually occurs when_ or more of myocardium has been damaged
Used to condition that lead to sudden obstruction of blood flow examples are:

Also called vasogenic shock, is due to changes in blood vessels tone that increases the size of
vascular space without an increase in the circulating volume
Severe hypersensitivity reaction resulting in massive vasodilation (examples: penicillin, ceftriaxone,
cefuroxime)
Or interference with nervous system control of blood vessels, can occur with conditions such as:

Cause by release of vaso active substance

_in clients with sepsis, and_in client with septic shock
Conditions that may cause a reduction in circulating blood volume includes:
Loss of blood.
Clinical manifestations may begin to appear with a blood volume deficit of_or about_ml.
Shock fully develops if a previously healthy client lose about 1/3 of the normal circulating blood of_
Hypovolemic shock produced by_ occurs mostly in people with partial thickness/ full thickness burns.
It is caused by primarily by a shift of plasma from the_
Client may have cardiac dysfunction that is due to the presence of_. A polypeptide that affects the
contaction of the cardiac muscle by depressing the myocardial muscle function. The result is
impaired cardiac output
Other causes of hypovolemic shock that may produce fluid shifts similar to burns

Shock may also occur either from reduced oral fluid intake or from significant fluid losses like:

Inability of heart muscle to function adequately or from mechanical obstruction of blood flow to or
from the heart.

2 Management of clients with Shock and Multisystem Disorders (escalante-saac)

Ischemic heart disease of
the left or right ventricle
1. MI
2. Obstructive
conditions
a) large pulmonary
embolism
b) pericardial
tamponade
c)

tension
pneumothorax
3. Other causes of
cardiogenic shock
cardiac valvular
insufficiency
myocardia aneurysm
rupture of a valvular
papillary muscle
ventricular rupture
aortic stenosis
mitral regurgitation
cardiac dysrhythmias
infectious and
inflammatory processes
such as myocarditis and
endocarditis
pulmonary HPN
toxic drugs
Distributive (Vasogenic)
shock

Major cause of cardiogenic shock`

Impaired heart muscle action caused by_. The area of dying or dead tissue that occurs with
infraction impairs contractility of the myocardium and cardiac output decreases.
Several typed of mechanical obstructions of blood flow may cause cardiogenic shock:
>an embolus is usually the result of blood clot that breaks loose in the person with DVT. Inhibits
perfusion
>accumulation of blood or fluid in the pericardial space that compresses the myocardium and
interferes with the ability of myocardium to expand
>significant amount of air in the pleural space that compresses the heat and great vessels thus
interfering with venous return to the heart
`

Results from inadequate vascular tone. Blood volume remains normal but the size of the vascular
spaces increases dramatically because of massive vasodilation. Result is maldistribution of the blood
because of decreased BP and lack of blood returning to the heart referred to as relative hypovolemia
Major cause
Occurs as a result of an acute allergic reaction from exposure to a substance to which the client has
been sensitized like:

Massive vasodilation
1. Acute allergic
reaction (anaphylactic
shock)
bee stings
chemotherapy
latex
chocolate
strawberries
peanuts
snake venom
iodine based contrast for
x-ray
NSAIDs
IgE
Reexposure to foreign substance results in the offending antigen binding immunoglobulin_ on the
Massive vasodilation
mast cell
Urticaria
Manifestations includes:
Laryngeal edema
Bronchial constriction
Epinephrine injection
Prevent onset of anaphylactic shock
2. Spinal cord injury
With injury to cervical spine, commonly with injuries around the T6 level, the autonomic nervous
(neurogenic shock)
system is affected
Triad of hypotension,
Manifestations of Spinal cord injury (neurogenic shock)
bradycardia, hypothermia
Maintain airway breathing,
Safety measures to prevent neurogenic shock and Spinal cord injury
provide circulatory
support, provide
thermoregulation
3. Septic shock
Presence of infection and activation of inflammatory cascade. SIRS (systemic inflammatory
(infection)
response syndrome) is a term used to define this clinical condition, and is considered present if
a) Body temperature
abnormalities exist in two of the following 4 clinical parameters:
b) Heart rate
c) Respiratory rate
d) Peripheral
leukocyte
Sepsis
Defined as presence of SIRS in the setting of infection
Severe sepsis
Sepsis with evidence of end organ dysfunction as a result of hypoperfusion
PATHOPHYSIOLOGY OF SHOCK
Dec. pumping action of the heartdec. cardiac output--- dec. circulating blood volume(hypotension)--- vasoconstriction and dec.
cardiac output to compensate dec. volume---releass of catecholamines---epinephrine and norepinephrine--- inc. HR---inc. vascular
resistance--- inc. venous return
Cardiogenic shock
When cardiac output fails, the body compensate by releasing catecholamines (epi and norepi) to
increase HR and systemic vascular resistance to inc. venous blood return
Dec. CO, hypotension,
The diseased heart cannot maintain its own myocardial tissue oxygenation which results in_
further myocardial
ischemia
Anaphylactic shock
Anaphylaxis is a systemic type 1 hypersensitivity reaction from the sudden release of inflammatory
mediators from mast cells and basophils
IgE is stimulated and the mast cell and basophils release large amount of histamine that leads to
vasodilation, bronchial constriction, broncorrhea, pruritus, laryngeal edema, and angioedema that
obstructs the airway
Septic Shock
Have bacteremia, with gram negative rods and gram positive organisms being most common

3 Management of clients with Shock and Multisystem Disorders (escalante-saac)

Non progressive

Progressive

Irreversible

agents. Endotoxins are produced by gram negative organisms. Gram positive cocci produce
exotoxins. There is an overwhelming inflammatory response to the microbes regulated by tumor
necrosis factor (TNF), interferon and interleukin.
Mediators and vasodilatory and endotoxic property are released systemically includes
prostaglandin, thromboxane A2, and nitic oxide. This results in vasodilation and
endothelial damage which leads to hypo perfusion and leakage. Cytokines activated the
coagulation pathway, result in capillary micro thrombi and end-organ ischemia
Stages of shock
>during the initial of non progressive stage of shock, cardiac output is slightly decreased because of
loss of actual relative blood volume, bodys compensatory mechanism can maintain BP within
normal to low normal range and can maintain perfusion of organs. During the compensatory PHASE,
the systemic circulation and microcirculation work together in a hyperdynamic state that leads to
increased lactic acid.
>if shock and compensatory vasoconstriction persists, the body begins to decompensate and the
systemic circulation and microcirculation no longer work in unison. As vasoconstriction continues,
the supply of oxygenated blood to the tissue is reduced. The result is anaerobic metabolism and
further lactic acidosis. Acidosis and increasing PaCo2 cause microcirculation to dilate that cause
decrease venous return and decrease circulation of reoxygenated blood. Result is low CVP central
venous pressure, and inadequate venous return to the right side of the heart. Decrease in circulating
volume and capillary flow does not allow to adequate perfusion and oxygenation of vital organs. The
tissue becomes hypoxic
>occurs if cycle of inadequate tissue perfusion is not interrupted. The shock becomes progressively
more severe, cellular ischemia and necrosis leads to organ failure and death