Shock Imam

8/10/2019 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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Respiratory System

- Breathing difficulty

- Sneezing, Coughing- Wheezing, Stridor

- Laryngeal edema

- Laryngospasm


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Cardiovascular System

- Vasodilation

- Increased heart rate- Decreased blood pressure


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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

Shock Imam

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