Pathophysiology of Shock Part II

8/12/2019 Pathophysiology of Shock Part II

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PATHOPHYSIOLOGY OF SHOCK PART II


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BACKGROUND TO SHOCK

Basics

Defined as inadequate tissue perfusion

Can result from trauma, fluid loss, heartattack, infection, spinal cord injury

Occurs first at cellular level

If allowed, can progress to organ failure,and death


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PHYSIOLOGY OF PERFUSION

Basics

Body cells require a constant supply of

oxygen and nutrients and elimination ofcarbon dioxide and waste products

Needs fulfilled by circulatory system in

conjunction with respiratory and

gastrointestinal systems

Perfusion is dependent on three

components of the circulatory system


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Priority Demand for Oxygen

The heart (circulatory system)

The brain (nervous system) The lungs (respiratory system)

The kidneys


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THREE COMPONENTS

Pump(heart) (rate)

Fluid volume(blood)

Container(blood vessels)

Any derangement of any of these components

can affect perfusion


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THE PUMP

The heart

The pump of the circulatory system

Receives blood from venous system

Pumps it to the lungs to receive oxygen

Pumps it to the peripheral tissues

Stroke volume is the amount of blood pumped

by the heart in one contractionAffected by preload, contractile force, and

afterload


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Cardiac Output

(Stroke Volume) X (Heart Rate)


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PRELOAD

Defined as the amount of blood delivered to

the heart during diastole

Dependent on venous return Variable venous capacitance can increase or

reduce blood return to the heart

Increased preload = increased stroke volume


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CONTRACTILE FORCE

Defined as the force generated by the heart

during each contraction

Frank - Starling mechanism The greater the preload, the more the

ventricles are stretched

The greater the stretch, the greater thecontractile force


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AFTERLOAD

Defined as resistance against which the heartmust pump

When the resistance is overcome, blood canbe ejected

Determined by the degree of arterialperipheral vasoconstriction

Vasoconstriction = increased resistance =increased afterload = decreased strokevolume


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CARDIAC OUTPUT

Defined as the amount of blood pumped by

the heart in one minute or stroke volume x

heart rate = cardiac output Expressed in liters per minute

An increase in stroke volume or heart rate =

increased cardiac output

A decrease in stroke volume or heart rate =

decreased cardiac output


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BLOOD PRESSURE

Defined as cardiac output x peripheral

vascular resistance(afterload) = blood

pressure Increased afterload = increased blood

pressure

Decreased afterload = decreased blood

pressure


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BARORECEPTORS

Sensory fibers located in the aortic andcarotid bodies

Monitor closely for changes in blood pressure If blood pressure, baroreceptors tell the brain

to decrease heart rate, preload, and afterload

If blood pressure falls, baroreceptors signal

the brain to activate the sympathetic nervoussystem to increase heart rate, preload,contractile force, afterload, and cardiac output


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What would you expect to see if the

sympathetic nervous system was

activated?


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THE FLUID

Blood is the fluid of the cardiovascular system

Viscous fluid, thicker, more adhesive, slower

moving than water Because cardiovascular system is closed, an

adequate volume of blood must be present tofill system

Blood transports oxygen, carbon dioxide,nutrients, hormones, metabolic wasteproducts, and heat


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THE CONTAINER

Blood vessels

Serve as container for the cardiovascular system

A continuous, closed, pressurized pipeline thatmoves blood

Includes arteries, arterioles, capillaries, venules,

and veins

Under control of the autonomic nervous system,they regulate blood flow to different areas of the

body by adjusting their size and rerouting blood

flow through microcirculation


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MICROCIRCULATION

Responsive to local tissue needs

Capillary beds can adjust size to supply

undernourished tissue and bypass tissue withno immediate need

Pre-capillary sphincters and post capillary

sphincters open and close to feed or bypass

tissues


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BLOOD FLOW

Occurs because of peripheral resistance and

pressure within the system

Peripheral resistance is dependent on innerdiameter and length of the vessel, and blood

viscosity

Very little resistance in aorta and arteries

Significant changes are seen in arterioles

which can change size fivefold


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SYSTEM PRESSURES

Contraction of the venous side increases

preload and stroke volume

Contraction of the arteriole side increasesafterload and blood pressure


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OXYGEN TRANSPORT

In addition to perfusion, oxygenation of

peripheral tissues is essential

Oxygen diffuses across the alveolar-capillarymembrane

Oxygen binds to the hemoglobin molecule of

the red blood cells

Ideally, 97-100% of hemoglobin saturated with

oxygen

Oxygen diffuses into cells at end organs


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FICK PRINCIPLE

Conditions for effective movement and

utilization of oxygen in the body

Adequate FiO2 ( concentration of O2 ininspired air)

Appropriate oxygen diffusion from alveoli

into bloodstream

Adequate number of red blood cells

Proper tissue perfusion

Efficient off-loading at the tissue level


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TISSUE PERFUSION

Tissue perfusion dependent on circulatory system andoxygenation by respiratory system

Inadequate tissue perfusion caused by

Inadequate pump

Inadequate preload Inadequate cardiac contractile strength

Excessive afterload

Inadequate heart rate

Inadequate fluid volume Hypovolemia

Inadequate container Excessive dilation without change in fluid volume

Excessive systemic vascular resistance


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PHYSIOLOGICAL RESPONSE TO SHOCK

Normally the body can compensate for some

decreased tissue perfusion through a variety

of mechanisms When composition fails, shock develops and if

uncorrected becomes irreversible


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PHYSIOLOGICAL RESPONSE TO SHOCK

Systemic response

Progressive vasoconstriction

Increased blood flow to major organs Shunted from skin, GI etc

Increased cardiac output

Increased respiratory rate and volumeDecreased urine output

Decreased gastric activity


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SHOCK AT THE CELLULAR LEVEL

Metabolism in normal conditions

Metabolism is aerobic

Cell energy comes from glucose brokendown through glycosis into pyruvic acid

Pyruvic acid further broken down in cycle

into CO2, water, and energy


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METABOLISM/POOR PERFUSION

STATES

Metabolism is anaerobic

Glucose breaks down into pyruvic acid, but

not enough oxygen is present to enter into theKrebs cycle

Pyruvic acid accumulates, degrades into lactic

acid, which also accumulates along with other

metabolic acids

Cells die; tissues die; organs fail; organ

systems fail; death ultimately ensues


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Not enough O2 in the cell for aerobicmetabolism

Shifts to anaerobic metabolism usingglycogen & fat (until stores depleted)

Increased cell permeability

Na+ & H2O enter cell causing cellular swelling

K+ leaks out of cell

Then Ca++ enters cell Build up of lactic acid & Co2 in cell

Cell eventually ruptures


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STAGES OF SHOCK


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COMPENSATED SHOCK

Body defense mechanisms attempt to

preserve major organs

Precapillary sphincters close, blood isshunted

Increased heart rateand strength ofcontractions

Increased respiratory function,

bronchodilation


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COMPENSATED SHOCK

Will continue until problem solved or shockprogresses to next stage

Can be difficult to detect with subtle indicators

Tachycardia

Decreased skin perfusion

Alterations in mental status

Some medications such as propranolol canhide signs and symptoms (B- blockers)


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UNCOMPENSATED SHOCK

Physiological response

Precapillary sphincters open, blood

pressure fallsCardiac output falls

Blood surges into tissue beds, blood flow

stagnates

Red cells stack up in rouleaux


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UNCOMPENSATED SHOCK

Easier to detect than compensated shock

Prolonged capillary refill time

Marked increase in heart rateRapid thready pulse

Agitation, restlessness, confusion

Decreased BP


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IRREVERSIBLE SHOCK

Compensatory mechanisms fail, cell death

begins, vital organs falter

Cannot be differentiated in the field

Patient may be resuscitated but will die later

of (ARDS, renal and liver failure, sepsis)

Organs have been deprived of O2 for too long

and cells have died causing organ failure Brain, lungs, heart, kidneys

Development of DIC (Disseminating

Intravascular Coagulopathy)


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DIC

Presence of injured or lysed cells resultsin the release of phospholipid into theblood triggering the intrinsic pathway

Prolonged states of low CO result ininjury to the vascular endothelium alsotriggers the intrinsic pathway

Systemic coagulation

Diffuse fibrin formation

Clotting factors are exhausted

Activation of coagulation causes activation

of fibrinolytic system


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TYPES OF SHOCK


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HYPOVOLEMIC SHOCK

Shock due to loss of intravascular fluid

volume

Possible causes

Internal or external hemorrhage Traumatic hemorrhage

Long bone or open fractures

Severe dehydration from GI lossesPlasma losses from burns

Diabetic ketoacidosis

Excessive sweating


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HYPOVOLEMIC SHOCK

Also can result from internal third-space loss

Possible causes

Bowel obstruction Peritonitis

Pacreatitis

Liver failure resulting in ascites


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4122Emergency Care andTransportation of the Sick and

Internal Bleeding

Hematemesis: Blood in vomit

Melena: Black, tarry stool

Hemoptysis: Coughing up blood

Pain, tenderness, bruising, or swelling

Broken ribs, bruises over the chest,

distended abdomen


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Emergency Care andTransportation of the Sick and

Characteristics of Bleeding

Arterial

Blood is bright red and spurts.

Venous

Blood is dark red and does not spurt.

Capillary

Blood oozes out and is controlled easily.


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External Bleeding

Hemorrhage = bleeding

Body cannot tolerate greater than 20%

blood loss. The average adult male has about 6 L

of blood.

Blood loss of 1 L can be dangerous inadults; in pediatrics, loss of 100-200 mlis serious.


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Hypovolemic shock is a volume

problem

What signs and symptoms wouldyou expect to see?

How would you treat this patient?


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Controlling External BleedingDirect Pressure and Elevation

Direct pressure is the most commonand effective way to control bleeding.

Elevation controls bleeding.

Wrap a pressure dressing around the

wound once bleeding is controlled.

If bleeding continues, apply additionaldressings on top.


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C t lli E t l Bl di


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Controlling External BleedingPressure Points

If bleeding continues, apply pressure on

pressure point.

Pressure at proximalpulse point greatly

slows down circulation to extremity.

The brachial artery and femoral arteryare the two most common pressure

points used.

C t lli E t l Bl di


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Controlling External BleedingPressure Points

C t lli E t l Bl di


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Controlling External BleedingApplying a Tourniquet

Fold a triangular bandage into 4 cravat.

Wrap the bandage.

Use a stick as a handle to twist and

secure.

Write TKand time and place on

patient.

ONLY USED AS A LAST RESORT


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Controlling a Nosebleed

Follow BSI techniques.

Help the patient sit and lean forward.

Apply direct pressure by pinching the

patients nostrils. Place a piece of gauze bandage under

the patients upper lip and press.

Apply ice over the nose. Provide transport.


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Volume replacement with isotonic

solution

NS/LR

PRBCs

Definitive treatment is the OR!


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CARDIOGENIC SHOCK

Inability to pump enough blood to supply all

body parts

Primary cause is severe left ventricular failure(AMI, CHF)

Accompanying hypotension decreases coronary

artery perfusion, worsening the situation

Other compensatory mechanisms-increasedperipheral resistance, increased myocardial O2

demand -worsen situation


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CARDIOGENIC SHOCK

Other causes

Chronic progressive heart disease

Rupture of papillary heart muscles orintraventricular septum

End-stage valvular disease

Patients may be normovolemic or

hypovolemic

Usually have pulmonary edema


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584Emergency Care and

Transportation of the Sick and

Pump failure (cardiogenic shock)

Inadequate function of the heart

The heart muscle can no longer generateenough pressure to circulate blood to all

organs.

Causes a backup of blood into the lungsResults in pulmonary edema

M di l I f i


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Myocardial Infarction

Myocardial dysfunction

Hypotension

Systemic

acidosisDecreased coronary

Blood flow

Myocardial

hypoxia

Dysrhythmias


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A major difference between cardiogenic

and other types of shock is the presence

of pulmonary edema which will beaccompanied dyspnea.


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Cardiogenic shock is a pump failure

problem

What signs and symptoms wouldyou expect to see?

How would you treat these

patients?


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Oxygen IV (TKO)

EKG monitor

Consider diuretic Lasix 40-80mg

Consider Dopamineto elevated BP (CO)

2-20mcg/min

Consider Dobutamineto increase contractile

force with little effect on the HR

2-20mcg/min


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NEUROGENIC SHOCK

Shock resulting from inadequate

peripheral resistance due to widespread

vasodilation

Common causes

Spinal cord injury

Central nervous system injuries

No sympathetic response


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Neurogenic shock is a pipe problem

What signs and symptoms would

you expect to see?How would you treat these

patients?


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Solu medrol

anti inflammatory

30mg/kg over 15 min 5.4mg/kg/hr next 23 hours


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Septic Shock

Shock resulting from systemic

vasodilation

Systemic increased vascularpermeability

Usually a result of gram (-) bacteria

infection Development of bacteremia


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7Emergency Care and


septic shock

Vessel and content failure ()

Caused by severe bacterial infections,

toxins, or infected tissues

Toxins damage vessel walls, causing them

to leakand become unable to contract well.

Leads to dilationof vessels and loss of

plasma, causing shock


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How do you want to treat

these patients?


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Check BS

Fluid bolus

Antibiotics

Dopamine Inotrope

5-20 mcg/kg

Epinephrine 2-10 mcg/min

Norepinephrine

0.5- 20 mcg/min


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Anaphylactic Shock

Widespread hypersensitivity reaction to aspecific antigen resulting in vasodilation,

peripheral pooling, relative hypovolemia

leading to decreased perfusion and impaired

cellular metabolism

Provokes an extensive immune &

inflammatory response

Vasodilation Increased permeability

Peripheral pooling

Tissue edema


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Sudden onset and death can occur in

minutes

Anxiety

Difficulty breathing

GI cramps

Edema

Urticaria

Pruritis


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Allergic Reactions

Vasodilation = produces drop in BP

Bronchoconstriction = dyspnea

Anaphylaxis Signs & Symptoms


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Anaphylaxis Signs & Symptoms

Hives (urticaria) are raised, blanched, irregularly

shaped lesions with surrounding redness.


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How would you treat this patient?


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Epinephrine

SYMPATHOMIMETIC

Moderate

Epinephrine 1:1,000 SQ

0.3-0.5 mg

Severe Epinephrine 1:10,000

IV

0.3-0.5 mg (ml)


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Solu medrol (methylprenisone)

Anti inflammatory, steroid

125-240 mg IV


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Benadryl (diphenhydramine)

Antihistamine

Blocks histamine receptors

antiemetic 25-50 mg

SIVP

Psychogenic shock


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10Emergency Care and


Psychogenic shock

Caused by sudden reaction of the nervous

system that produces a temporary,

generalized vascular dilation

Commonly referred to as fainting or

syncope

Causes range from fear or bad news tounpleasant sights.


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EVALUATION OF SHOCK VICTIM


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INITIAL APPROACH

Be alert during initial approach to patient,

information gleaned from the view at the door

Mental statusRespiratory effort

Skin color


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PRIMARY ASSESSMENT

Airway and breathing

Check for airway patency; correct problems

Assess breathing rate, quality, correct anyproblems


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PRIMARY ASSESSMENT

Circulation

Correct any obvious external breathing

Location of palpable pulse as indicator ofcirculatory status

Radial pulse - BP at least 80 mm Hg

Femoral pulse - BP at least 70 mm Hg

Carotid pulse - BP at least 60 mm Hg


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PRIMARY ASSESSMENT

Assess skin color, temperature, and moisture

Pale = decreased diffusion

Cyanotic = inadequate oxygenationMottled = late sign of shock

Cool = indicates vasoconstriction

Assess capillary refill time ( less than 2seconds normal)


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PRIMARY ASSESSMENT

Disability

Level of consciousness is very early sign of

impending circulatory collapse

Manifestations of reduction in cerebral flow include

Agitation

Disorientation

Confusion Inappropriateness of response

Unresponsiveness


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PRIMARY ASSESSMENT

While altered mental status may result from

drug/alcohol intake, probably safest to

assume cause is decreased cerebral

perfusion


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SECONDARY ASSESSMENT

Rapid transport for life-threatening conditions

Ideally, expose the head, neck, chest , and

abdomen Reassess vital signs

Patient history


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GENERAL SHOCK MANAGEMENT


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ASSURE PATENT AIRWAY

Maintain cervical spine support

Maintain airflow through the use of airway

adjuncts or intubation, preferred in

unresponsive shock patients

Provide suctioning as necessary

MAINTAIN ADEQUATE RESPIRATORY


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Q

FUNCTION

Assist ventilations with BVM or other

appropriate adjunct

Perform other interventions as needed to

correct shock-related conditions leading to

respiratory compromise

Bronchodilators


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OXYGENATE THE PATIENT

Provide high flow oxygen as soon as possible

BVM

NonrebreatherNasal Cannula if mask not tolerated

Demand valve if necessary


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CONTROL MAJOR BLEEDING

Direct pressure

Pressure points

Tourniquet (last resort) PASG for intra-abdominal and lower extremity

bleeding


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TREAT HYPOTENSION

Positioning of patient

Supine with legs elevated 10-12 inches

Upright if cardiogenic shock with pulmonaryedema

Check respirations and assist as needed


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PNEUMATIC ANTI-SHOCK GARMENT

Three chambered unit wrapped around the

lower body and inflated to provide

circumferential pneumatic pressure to

underlying structures


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PASG BENEFITS

Increase in blood pressure

Increased blood flow to the brain, heart, and

lungs

Bleeding control

Stabilization of fractures of lower limb and

pelvis


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PASG INDICATIONS

Control of bleeding

Stabilization of fractures in hypotensive

patients with lower extremity injury

Raising of blood pressure

Controlling External Bleeding


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g gPneumatic Antishock Garment (PASG)

Stabilizes fractures of the pelvis and

femurs

Controls blood loss associated withpelvis and femur fractures

Controls massive bleeding of the lower

extremities

Controls shock due to internal bleeding


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ABSOLUTE CONTRINIDICATIONS

Acute pulmonary edema secondary to heart

failure

Controlling External Bleeding


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Controlling External BleedingPASG Contraindications

Pregnancy (do not inflate abdomen)

COPD & CHF patients (fluid in the lungs)

Penetrating chest injuries Groin injuries

Major head injuries

Abdominal eviscerations

Impaled objects


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PASG COMPLICATIONS

Lower extremity compartment syndrome

Metabolic acidosis after prolonged use

Decreased renal function Decreased respiratory function


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INTRAVENOUS THERAPY

Reasons for procedure

Administration of drugs

Fluid replacementObtaining blood samples


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INTRAVENOUS THERAPY

Necessary supplies

Protective gloves and eyewear

IV solution Crystalloid most common in field

Administration tubing

Macrodrip (10gtts/ml) shock, fluid replacement

Microdrip (60gtts/ml) cardiac, peds, medicalemergencies

Extension set


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CANNULAS

Angiocath (catheter over a hollow needle)

preferred in field

14 -16 gauge for rapid fluid replacement

18, 20, - 22 gauge for IV lifeline


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OTHER EQUIPMENT

Venous constricting band

Tape or Venigaurd device

Antibiotic swab Antibiotic ointment

Gauze dressing (2x2, 4x4)

10 TO 35 cc syringe

Padded armboard


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VENOUS ACCESS

Peripheral veins preferred

Dorsal veins of hand

ForearmAntecubital fossa


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VENOUS ACCESS

Begin IV distally, move upwards if problems

occur

In cardiac arrest, use the antecubital fossa

External jugular as an alternative

Scalp veins in infants

Intraosseus infusion


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INTRAVENOUS CANNULATION

Troubleshooting points to keep in mind

Did you remove the tourniquet?

Is there swelling at the site?

Are the tubing valves open?

Is the cannula against a valve or wall of the vein?

Is the IV bag high enough?

Is the drip chamber completely filled with solution?

CO CA O S O A


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COMPLICATIONS OF IV THERAPY

Pain

Due to needle puncture or extravasation

Use smaller gauge catheter



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Hematoma or infiltration

Remove catheter and establish another IV

site

Local infection

Clean area properly before venipuncture



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Pyrogenic reaction

Characterized by fever, chills, backache,

headache, nausea/vomiting

Immediately terminate the IV if suspected

Catheter shear

Never draw the catheter back over the

needle



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Inadvertent arterial puncture

Recognized by spurting bright red blood

Withdraw catheter and apply directpressure to site for 5 minutes



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Circulatory overload

Closely monitor the IV flow rate

Look for signs of pulmonary congestion andedema

Reduce or terminate IV flow if signs appear



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Thrombophlebitis

Inflamation of a vein common in long term

IV therapy

Redness, swelling, tenderness, pain at site

Terminate IV and apply warm compress to

site



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Air embolism

Usually during central vein cannulation

Can occur when air has not been clearedout of IV tubing

FLOW RATES


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FLOW RATES

To keep open (TKO) rate for medication

administration

Rapid rate for hypovolemia, trauma where

fluids are being used to replace circulatory

volume

2-3 liters maximum that should be

administered in field Flow rate can be increased in cases of severe

blood loss by wrapping BP cuff around bag

and inflating

MAINTAINING BODY TEMP


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MAINTAINING BODY TEMP.

Keep as close to normal as possible

Protect patient from elements

Remove wet clothing Cover patient, but dont get them too warm,

causing vasodilation

MODS


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MODS

Multiple organ dysfunction syndrome

Consequence of inability of the body tomaintain end organ perfusion

Progressive failure of two or more organsystems after a severe injury or illness

Septic shock most common cause

Mortality 60-90%

Usually within 24 hrs of resuscitation

Neuroendocrine SystemActivation


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Activation

Cortisol

Epinephrine

Norepinephrine Endorphins


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Sympathetic NS stimulation

Vascular endothelium becomes

permeable Fluid & cells leak into interstitial space

Hypotension, hypoperfusion

Microvascular coagulationDue to initial insult and release of mediators


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Typically first organs to manifest signs of

dysfunction are lungs and kidneys

dypnea Hepatic failure occurs later

Clinical Presentation


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Clinical Presentation

History

Low grade fever

Tachycardia Dyspnea

Altered mental status

Hypermetabolic state

Pathophysiology of Shock Part II

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