shock imam
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SHOCK
Dr. Imam Ghozali., SpAn.,MKes
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What is Shock?
Inadequate perfusion of body tissuethat begins at the cellular level and if
left untreated results in death of tissue,organs, organ systems, and ultimatelythe entire organism
IT IS NOT LOW BLOOD PRESSURE!
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Shock is a result of many reasons:
Trauma
Fluid loss
MI Infection
Allergic Reaction
Spinal Cord Injury
Other reasons
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What is adequate perfusion?
Constant and necessary passage ofblood through the bodys tissue
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Perfusion is dependent on afunctioning and intact circulatory
system
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Components of circulatory system
The pump(heart)
The fluid(blood)
The container(blood vessels)
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The Pump
The Heart is the pump of thecardiovascular system
It receives blood from the venoussystem then pumps the blood to thelungs for oxygenation, then to theperipheral tissues
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Stroke Volume
The amount of blood ejected by theheart in one contraction
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Factors affecting stroke volume
Preload
Cardiac Contractile Force
Afterload
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Preload
Amount of blood delivered to the heartduring diastole
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Cardiac Contractile Force
The strength of contraction of the heart
It is affected by circulating hormones
called catecholamines-Epinepherine
-NorEpinepherine
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Frank Starling Mechanism
The greater the stretch of the cardiacmuscle, up to a certain point, the
greater the force of cardiaccontraction(I.E. the rubber band effect)
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Afterload
Resistance against which the ventriclemust contract
Determined by the degree of peripheralvascular resistance
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Cardiac Output
Amount of blood pumped in onecontraction
Stroke volume x Heart rate=Cardiacoutput
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Peripheral Vascular Resistance
Pressure against which the heart mustpump
Blood pressure=cardiac output xperipheral vascular resistance
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Fluid
Blood is thicker and more adhesive thanwater
Consist of plasma and formed elements:
Red cells, White cells, Platelets
Transports oxygen, carbon dioxide,nutrients, hormones, and metabolicwaste
An adequate amount is needed forperfusion
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Container
Blood vessels serve as the container
Under control of the autonomic nervoussystem they can adjust size andselectively reroute blood throughmicrocirculation
Microcirculation is comprised of the
small vessels:Arterioles, Capillaries, and Venules
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Container cont
Capillaries have a sphincter betweenthe arteriole and capillary called the
pre-capillary sphincter Pre-capillary sphincter responds to local
tissue demands such as acidosis,hypoxia, and opens as more blood isneeded
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Major functions of Perfusion
Oxygen transport
Waste Removal
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Inadequate Pump
Inadequate preload
Inadequate cardiac contractile strength
Inadequate heart rate Excessive afterload
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Inadequate Fluid
Hypovolemia (abnormally lowcirculating blood volume)
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Inadequate Container
Dilated container without change influid volume
Leak in container
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Shock at cellular level
The causes of shock vary, however theultimate outcome is impairment of
cellular metabolism
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Impaired use of oxygen
When cells dont receive enough oxygenor cannot use it effectively, they change
from aerobic to anaerobic metabolism
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Glucose breakdown. (A) Stage one, glycolysis, is anaerobic (does
not require oxygen). It yields pyruvic acid, with toxic by-products
such as lactic acid, and very little energy. (B) Stage two is aerobic(requires oxygen). In a process called the Krebs or citric acid
cycle, pyruvic acid is degraded into carbon dioxide and water,
which produces a much higher yield of energy.
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Compensated and Decompensatedshock
Usually the body is able to compensatebut when these mechanisms fail shockdevelops and may progress
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Compensation Mechanisms
Catecholamines may be secreted ( I.E.Epinephrine and norepinephrine)
The Renin-Angitensin system aids inmaintaining blood pressure
Endocrine Response by pituitary gland
results in secretion of anti-diuretichormone (ADH)
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Catecholamine Release
Epinephrine and Norepinephrine releaseaffects the cardiovascular system,causing increase in HR, increase inCardiac contractility strength, arteriolarconstriction which elevates bloodpressure
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Renin-Angiotensin system
Renin is released from the kidneys andacts on specialized plasma proteincalled Angiotensin the produces
AngiotensinI.
AngiotensinI is converted toAngiotensinII by enzymes in the lungscalled Angiotensin Converting Enzyme(ACE)
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Renin-Angiotensin System (cont)
AngiotensinII is a potent vasoconstrictor
Angiotensin II stimulates production of
aldostrone, which causes the kidneys toreabsorb sodium
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Anti-Diuretic Hormone
Causes the kidneys to reabsorb watercreating an additive to the aldostrone
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Compensated Shock
Early stages of shock where the bodyscompensatory mechanisms are able tomaintain normal perfusion
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Types of shock
Cardiogenic shock (Inadequate Pump)
Hypovolemic shock (Inadequate Fluid)
Neurogenic shock (Inadequate Container)
Anaphylactic shock Septic shock
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Cardiogenic Shock
The heart loses the ability to supply allbody parts with blood
Usually the result of left ventricular failuresecondary to acute MI or CHF
Many patients will have normal blood
pressures
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S/S of Cardiogenic Shock
Major difference between other types of
shock is presence of Pulmonary Edema Difficulty breathing
Wheezes, Crackles, Rales are heard as fluid
levels increase
Productive cough with white or pink-tingedfoamy sputum
Cyanosis
Altered mentation
Oliguria ( decreased urination)
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TX for Cardiogenic ShockAssure open airway
Adminster oxygenAssist ventilations as needed
Keep patient warm
Place patient in position of comfort Establish Iv with minimal fluid
administration
Monitor Vitals May need to administer Dopamine or
Dobutamine
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Hypovolemic Shock
Internal or external hemorrhage
Trauma
Long bone or open FXs
Dehydration Plasma loss due to burns
Excessive sweating
Diabetic Ketoacidosis with resultant osmoticdiuresis
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S/S of Hypovolemic Shock
Pale, cool, clammy skin
Blood pressure may be normal then fall
Pulse may be normal then become rapid,finally slowing and disappearing
Urination decreases
Cardiac dysrhythmias may occur
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Tx for Hypovolemic Shock
Airway control
Administer high flow oxygen
Control severe bleeding
Keep patient warm Elevate lower extremities
Establish IV and administer bolus of
crystalloid solution for fluid replacement
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Neurogenic Shock
Results from injury to brain or spinal cordcausing interruption of nerve impulses toarteries
Arteries lose tone and dilate causinghypovolemia
Sympathetic nerve impulses to the adrenalglands are lost, which prevents the releaseof catecholamines and their compensatoryeffects
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Neurogenic Shock (cont)
High cervical injuries cause interruption ofimpulse to peripheral nervous systemcausing
Neurogenic shock is most commonly due tosevere injury to spinal cord or totaltransection of cord (spinal shock)
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S/S of Neurogenic Shock
Warm, Dry, Red Skin
Low Blood Pressure Slow Pulse
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TX for Neurogenic Shock
Airway control
Maintain body temperature
Immobilization if indicated
Consider other causes of shock
IV and medications that increase peripheralvascular resistance (I.E. Norepinephrine,Dopamine)
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S/S of Anaphylactic Shock
Skin
- Flushing
- Itching
- Hives-Swelling
-Cyanosis
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S/S of Anaphylactic Shock
Respiratory System
- Breathing difficulty
- Sneezing, Coughing- Wheezing, Stridor
- Laryngeal edema
- Laryngospasm
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S/S of Anaphylactic Shock
Cardiovascular System
- Vasodilation
- Increased heart rate- Decreased blood pressure
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S/S of Anaphylactic Shock
Gastrointestinal System
- Nausea, vomiting
- Abdominal cramping- Diarrhea
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TX for Anaphylactic Shock
Airway protection which may includeEndotracheal Intubation
Establish IV with crystalloid solution
Pharmacological interventions: Epinephrine,Antihistamines(Benadryl),Corticosteroids(dexamethasone),
Vasopressors(dopamine, Epinephrine), andinhaled beta agonist(albuterol)
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Septic Shock
An infection enters bloodstream and iscarried throughout body
Toxins released overcomecompensatory mechanisms
Can cause dysfunction of one organsystem or cause multiple organdysfunction
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S/S of Septic Shock
Increased to low blood pressure
High fever, no fever, hypothermic
Skin flushed, Pale, Cyanotic Difficulty breathing and altered lung
sounds
Altered LOC
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TX of Septic Shock
Airway control
Administer oxygen
IV of crystalloid solution Dopamine for blood pressure support
Monitor other vitals
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Progression To MODS
Infection
Sepsis
Septic shock MODS
Death(if not corrected early)
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Primary MODS
Organ damage due to specific cause suchas ischemia or inadequate tissueperfusion from shock, trauma, or majorsurgery
Stress and inflammatory responses maybe mild or undetected
During the response, neutrophils,macrophages, and mast cells are thoughtto be primed by cytokines
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Secondary MODS
The next time there is injury, ischemia, orinfection the primed cells are activated,producing and exaggerated inflammatoryresponse
The inflammatory response enters a self-perpetuating cycle causing damage andvasodilation
And exaggerated neuroendocrine responseis triggered causing futher damage
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24 hours post resuscitation
Low grade fever
Tachycardia
DyspneaAltered mental status
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Within 24 to 72 hours
Pulmonary failurebegins
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Within 7 to 10 days
Hepatic failure begins
Intestinal failure begins
Renal failure begins
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After 21 days
Hematologic failure begins
Myocardial failure begins
Altered Mental status resulting fromEncephalopathy
Death