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INTRODUCTION
m A physiologic state characterized by
Inadequate tissue perfusion

mClinically manifested by
hemodynamic disturbances
Organ dysfunction
§

Any condition in which the circulatory system is
unable to provide adequate circulation to the vital
body organs such as the brain, heart and lungs. As
a result of a decrease in the blood pressure.
It is reversible, but left untreated will rapidly
become irreversible and lead to death.
A reduction in blood flow to tissues, depriving
them of oxygen (ischemia).
Organs of vital importance, brain, heart, lung and
kidneys can suffer irreversible damage, eventually
leading to death.

§

phock is usually accompanied by renal
failure, as a normal compensatory
mechanism, because the blood flow to the
kidney is decreased to keep enough blood
for the vital organs.
Tissue ischaemic sensitivity:
- heart, brain, lung: 4-6 min
- GI tract, liver, kidney: 45-60 min
- muscle, skin: 2-3 hours
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|. Increase heart rate as a result of the baroreflex:
ͻ phock will decrease the volume of blood
pumped from the heart and the blood flow to
the brain. That will activate the baroreceptors in
the carotid bodies to increase HR trying to
supply enough blood to the vital organs.
2. Pale skin:
ͻ As a result of vasoconstriction of the peripheral
vessels, because the skin is the least priority
tissue for blood flow


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Cold and clammy skin : As a result of
vasoconstriction.
ͻ phock decreases the skin surface
temperature as a result of vasodilatation,
which will increase the internal body
temperature. Because the skin plays a
major role in controlling body
temperature, as it will help in exchanging
heat with the external environment.

 
m Unit of life = cell

m Cells get energy (ATP) from cellular respiration:

O2 + Glucose ATP + water + CO2

No O2 = no energy
4







m ›

 
Damage to Damage to Damage to
Cell Tissues Organ

Damage to Damage to
Body Organ System


m þnadequate tissue perfusion
m Anaerobic metabolism
Result in lactic acid production, circulated to the
liver and causes metabolic acidosis.
 6 CO2

6 O2
6 H2O
METABOLISM

GLUCOSE 36 ATP

HEAT (417 kcal)

 2 LACTIC ACID

GLUCOSE METABOLISM 2 ATP

HEAT (32 kcal)

Anaerobicetabolis
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m Requires proper functioning systems
Cardiovascular
Respiratory
Renal
m Tissue perfusion is depend on 3 components
of circulatory system
Pump
Fluid
Container
m þn other words CVS system consist 3 part
maintain the perfusion:
Heart as pump
Blood vessels as container
Blood an fluid as volume in the circulatory
m Blood as vehicle for carrying oxygen and
nutrient through blood vessels and
capillaries.
m Volume or fluid need to transport blood
throughout the body.
m Volume moving into body due to pressure
generated by contraction of the heart and
affecting by dilating and constricting of blood
vessels.
andcontainer
m Pressure generated/ Blood pressure is a
rough measurement of tissue perfusion.
m The pressure is depend on cardiac output
(CO) and systemic vascular resistance (SVR)
m BP= CO x SVR
m CO= HR x SV
m SV= Preload
Contractility
Afterload
onditioninlowp

m There are only a few causes of low SVR, the

all cause vasodilation
Sepsis
Acute spinal cord injury
Vasodilators (anesthetic)
Anaphylaxis- allergic
m Preload
m Contractile force
Frank-starling mechanism
m Afterload
m · Peripheral
vasoconstriction«
m · peripheral vascular
resistance«

m · afterload«

m · blood pressure.
m · Peripheral
vasodilation«
 peripheral vascular
resistance«

 afterload«

 blood pressure.
m · fluid volume«

· preload«

· contractility (Starling¶s
Law)«

· blood pressure. · cardiac output.

m  fluid volume«

 preload«

 contractility (Starling¶s
Law)«

 blood pressure.  cardiac output.

m Renin-Angiotensin-Aldosterone system.
Works through kidneys to regulate balance of Na+
and water.
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m þnadequate pump
þnadequate preload
Poor contractility
Excessive afterload
þnadequate heart rate
m þnadequate fluid volume
Hypovolemia
m þnadequate container
Excessive dilation
þnadequate systematic vascular resistance
m Compensatory stage - Defense mechanisms
are in maintaining perfusion
m Progressive stage- no longer compensate.
m þrreversible stage - Complete failure of
compensatory mechanisms
m Normal compensation includes:
Progressive vasoconstriction
þncreased blood flow to major organs
þncreased cardiac output
þncreased respiratory rate and volume
Decreased urine output
m When BP fall, the body responds by
activating the sympathetic nervous system.
m SNS secrete epinephrine and norepinephrine
to increase cardiac output by causing the
hearth to beat fast and stronger.
m Blood is shunted away from the skin, kidneys,
and intestines to preserve blood flow to the
brain, heart, liver and lung.
ontcoensate
m Epinephrine, cortisol and glucagon raise
blood glucose level to supply cell with
fuel.
m Stimulation of the renin- angiotensin
aldosterone system from decreased
cardiac output.
m The body metabolic rate and
temperature begin to fall as a result of
reduce energy production.
ontcoensate

m Respiratory rate increase to deliver more oxygen

to the tissue.
m Decrease blood flow to hypothalamus
m Release of antidiuretic hormone (ADH)
from posterior pituitary.
Retention of salt, water
Peripheral vasoconstriction
signandsytos
m These compensation responses produce the
classic sign and symptoms of the initial phase
of shock:
Tachycardia
Tachypnea
Oliguria
Restlesness
Anxiety
Cool and clammy skin with pallor.
Nausea, vomiting and thirst.
rsinganagent

m Correct the causes, for example:

Stop bleeding.
m Monitor tissue perfusion and vital signs.
m Administer þV fluid and ordered medication.
m Promote safety.
m Progressive dysfunction of two or more organ
systems
m Defense mechanisms begin to fail
m Presentation
Hypotension
Prolonged Cap refill
Marked increase in heart rate
Rapid, thready pulse
Agitation, restlessness, confusion

edicalanageent

m Depends on type of shock and underlying

causes.
m Use of þVF and medication to restore tissue
perfusion by following method:
Optimizing intravascular volume
Supporting pumping action
þmproving the vascular system
Support the respiratory system
rsinganageent
m Help establish immediate status of airway,
breathing and circulatory.
m Requires expertise in assessing and
understanding of shock and significant
changes.
m Close monitoring vital sign (ECG, ABG, Serum
electrolyte, physical and mental changes).
m Rapid administration of þVF and drug, promote
rest and comfort, prevent complication and
support family members.
m ÷nd Organ Dysfunction
m Presentation
Oliguria or anuria
Progressive acidosis
Agitation,and coma
m Complete failure of compensatory mechanisms
m ÷nd point stage where there is severe organ
damage that patients do not respond anymore to
treatment, survival is impossible to maintain

edicalandnrsinganageent

m Mx same like progressive

management.
m þnformed family or relative about
patient condition.
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m Neurogenic
m Anaphylactic
m Septic
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m ovluid failure͟
m Decreased intravascular volume
m Causes?
m ͞Third spacing͟
m Hypovolemic shock is caused by low blood volume.
Reduced circulating blood volume with secondary
decreased cardiac output Results from decreased
preload
Normal blood volume is 5 L and by losing |-2 L it
can lead to shock.
The Decrease in blood volume is caused by:
m ÷xternal blood loss: ex. Hemorrhage

m Internal blood loss: ex. Ruptured spleen

caused by blunt trauma. ruptured aneurysm
m pevere dehydration as a result of:

Vomiting
Diarrhea (This is a typical condition in
cholera)
m Burns

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m Hypotensive
m flat neck veins
m clear lungs
m cool, cyanotic extremities
m evidence of bleeding?
trauma, bruising
m oliguria
m Correct bleeding abnormality þf PT or PTT
elevated then FFP
m Aggressive Fluid replacement with 2 large
bore þV¶s or central line.
m Pressors are last line, but commonly
required.
m Gram negative or other overwhelming
infection.
m Vasodilator causes decreased Peripheral
Vascular Resistance.
   







  




toxin reactions or allergic ± drugs, transfusions.
m The Peripheral Vasodilation secondary to
disruption of cellular metabolism by the
effects of inflammatory mediators.




 

  



 





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m Febrile
m Tachycardic
m warm extremities
m flat neck veins
m oliguria
m Decreased Peripheral Vascular Resistance
m oContainer failure´
m Massive & systemic allergic reaction
m Caused by a hypersensitivity reaction to an
allergen in a previously sensitised patient
m Large release of histamine
m þncreases membrane permeability &
vasodilation

anageentofana ylactics ock

m Ensure Airway is adequate

m Oxygen
m þV access early
m þV fluids
m Bronchodilators
m Steroids
m oContainer failure´
m Systemic infection
m Caused by uncontrolled inflammatory
response to injury or illness.
m infection/sepsis: G(-/+ ) speticemia,
pneumonia, peritonitis, meningitis,
cholangitis, pyelonephritis, necrotic tissue,
pancreatitis, wet gangrene, toxic shock
syndrome, etc.
pigns

m Early± warm w/ vasodilation, often adequate

urineoutput, febrile, tachypneic.
m Late-- vasoconstriction, hypotension,
oliguria,altered mental status.
m þdentification of source of infection
m Broad Spectrum Antibiotics
m þV fluids
m Vasopressors
m Steroids ??
m Bicarbonate if pH < 7.1
erogenics ock
uechanism: Loss of autonomic innervation of
the cardiovascular system (arterioles, venules,
small veins, including the heart)
Cause by decreased sympathetic control of
blood vessel tone due to defect in vasomotor
center in the brain stem.
Characterized by loss of vascular tone &
reflexes.
erogenics ock

Vasomotor center can be interrupted by:

|.Brain injury/ppinal cord injury
2.Regional anesthesia
3.Drugs - (opiods, benzodiazepines)
4.Neurological disorders
5.hypoxia or lack of glucose
pinals ock

m Spinal shock and neurogenic shock are not

same disorder.
m Spinal shock occurs in person with spinal
cord injury at T5 and above.
m Patient with spinal shock will experience
absence of all voluntary and reflex
neurological activity below the level of injury.
linicalresentation

m Temperature- increase or decrease

(due to hypothalamic dyfunction)
m pkin- Decrease skin perfusion- skin
dry or warm (massive dilation)
m Hypotension and bradycardia.
Cardiogenic shock ( heart does not pump enough
blood) is caused by:
uyocardial infarction Y



weak cardiac
As a
muscle contraction result of Ischemia
Arrhythmia ( such as ventricular fibrillation, which
will stop the heart pump and that will decrease BP
m Note: pupraventricular (Atria) fibrillation will
not cause shock because 75% of the blood
transfer from the atrium to the ventricles by
passive transport.

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m Myocardial þnjury or Obstruction to Flow
Arrythymias
valvular lesions
AMþ
Severe CHF
VSD
Hypertrophic Cardiomyopathy
m Presentation will be according to underlying
disease process.
m Chest wall trauma
‡ þnability to ventilate adequately
m Tension pneumothorax
‡ Compression of lung tissue and kinking of
vena cava
m Cardiac tamponade
Pressure against the ventricles that reduces
cardiac output
m Pulmonary embolus
Obstruction of the pulmonary artery, þnefficient
loading of RBC at the lungs
m Pulmonary Edema
m JVD
m hypotensive
m weak pulses
m oliguria

Treatment strategies
m Correct underlying disorder if possible and then
direct efforts at increasing the blood pressure
to increase oxygen delivery to the tissues.
m Bradycardia: atropine
m Tachycardia: vagal maneuver, oxygen and
fluid
m Myocardial trauma: oxygen, fluid bolus if no
signs of pulmonary edema
m Mþ/CHF: oxygen; other medications if BP
allows for their administration
m Attempt to correct problem and increase
cardiac output by diuresing and providing
inotropic support. þABP is utilized if medical
therapy is ineffective. Catheterization if
ongoing ischemia
m Cardiogenic shock is the exception to the rule
that NS is always given for hypotension NS
will exacerbate cardiac shock.
m Keep O2 sats >92%, intubate if neccesary
rsinganageent

m Manage the emergency

m Determine the underlying cause
m Definitive management or support

anaget e ergency
m Assess ABC
m Monitor vital sign and extremities for early shock
sign for example, capillary refill, skin temperature
and skin color.
m Control airway and breathing
m Maximize oxygen delivery
m Place lines, tubes, and monitors
m Get and run þVF on a pressure bag
m Get and run blood (if appropriate)
m Administer medication as order.
m Stop bleeding, diarrhea and vomiting.
m Normal Saline should be administered
anytime a patient is hypotensive.
m þf possible give blood as it replaces colloid.
m Vasopressors
m þnotropic agents for cardiogenic shock
m Anti inflammatory agent.
§efinitive
anageent

m Hypovolemic ± Fluid resuscitate (blood or

crystalloid) and control ongoing loss
m Cardiogenic - Restore blood pressure
(chemical and mechanical) and prevent
ongoing cardiac death
m Distributive ± Fluid resuscitate, pressors for
maintenance, immediate abx/surgical
control for infection, steroids for
adrenocortical insufficiency
§eterinet ease
m Often obvious based on history
m Trauma most often hypovolemic
(hemorrhagic)
m Postoperative most often hypovolemic
(hemorrhagic or third spacing)
m Debilitated hospitalized pts most often septic
m Must evaluate all pts for risk factors for Mþ
and consider cardiogenic
m Consider distributive (spinal) shock in trauma
1. þneffective airway clearance
2. Fluid volume deficit r/t volume loss
3. Activity intolerance r/t disease process
4. Hyperthermia r/t inflammatory process
5. Pain r/t disease process.
6. Knowledge deficit r/t disease process

 |
 neffectiveairwayclearance
Int  ntions
Monitor vital sign (respiration rate, blood
pressure and SPO2)
Monitor patient skin and breathing pattern.
Encourage patient to rest in bed.
›ational
Tachypnea, tachycardia and elevated blood
pressure are sign of compromised
respiratory status.
To detect for early sign of airway
compromise and for early intervention.

Administer Oxygen and do suction if having To maintain tissue perfusion.

secretion block the airway.

Assist patient needed such as, toileting, feeding To save energy and reduce fatigue.
and so on.
Administer medication as ordered by doctor, for To correct the causes or problem.
example bronchodilator.
To prevent fatigue and reduce oxygen
Teach and assist to use technique of control demands.
breathing pattern.
a) Pursed ± lips breathing. To help :
b) Abdominal breathing. a) Keep airway open by maintains
positive pressure.
b) þmprove lung expansion.