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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
p p
p
|. 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
p p
p
j 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
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.
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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 · afterload«
m · blood pressure.
m · Peripheral
vasodilation«
peripheral vascular
resistance«
afterload«
blood pressure.
m · fluid volume«
· preload«
· contractility (Starling¶s
Law)«
preload«
contractility (Starling¶s
Law)«
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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.
ontcoensate
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.
ontcoensate
m Neurogenic
m Anaphylactic
m Septic
V
m
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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
Vomiting
Diarrhea (This is a typical condition in
cholera)
m Burns
|
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
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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
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Int ntions ational
Monitor vital sign (respiration rate, blood Tachypnea, tachycardia and elevated blood
pressure and SPO2) pressure are sign of compromised
respiratory status.
Monitor patient skin and breathing pattern. To detect for early sign of airway
Encourage patient to rest in bed. compromise and for early intervention.
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.