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ASKEP SHOCK SEPSIS,
DISTRIBUTIF & ANAFILAKTIK
Disampaikan pada :
Pelatihan Intensive Care Unit Dewasa
Cilegon 2013
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Distributive Shock
Inadequate perfusion of tissues through
maldistribution of blood flow Intravascular volume is maldistributed
because of alterations in blood vessels
Cardiac pump & blood volume arenormal but blood is not reaching the
tissues
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Vasogenic/Distributive Shock
Etiologies
Septic Shock (Most Common)
Anaphylactic Shock
Neurogenic Shock
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Anaphylactic Shock
A type of distributive shock that results
from widespread systemic allergic reaction
to an antigen This hypersensitive reaction is LIFE
THREATENING
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Pathophysiology Anaphylactic
ShockAntigen exposure
body stimulated to produce IgE antibodiesspecific to antigen
drugs, bites, contrast, blood, foods,vaccines
Reexposure to antigen
IgE binds to mast cells and basophils
Anaphylactic response
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Anaphylactic Response
Vasodilatation
Increased vascular permeability
Bronchoconstriction Increased mucus production
Increased inflammatory mediators
recruitment to sites of antigen interaction
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Clinical Presentation
Anaphylactic ShockAlmost immediate response to inciting
antigen Cutaneous manifestations
urticaria, erythema, pruritis, angioedema Respiratory compromise stridor, wheezing, bronchorrhea, resp.
distress
Circulatory collapse tachycardia, vasodilation, hypotension
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KENALI DINI, TERAPI SCR AGRESIF
AIRWAY SUPPORT
IV EPINEPHRINE (buka jalan nafas)
Antihistamines, diphenhydramine 50mg IV
Corticosteroids
SECEPATNYA JAUHKAN DARI
ANTIGEN JIKA MUNGKIN PENCEGAHAN
PenatalaksanaanAnaphylactic Shock
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Management Anaphylactic
Shock
Pemberian cairan kristaloid scr tepat
Vasopressors mempertahankanperfusi organ
Inotropik positif
penyuluhan pasien
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NEUROGENIC SHOCK
A type of distributive shock that results from
the loss or suppression of sympathetic tone
Causes massive vasodilatation in the venous
vasculature, venous return to heart,cardiac output.
Most common etiology:Spinal cord injury
above T6
Neurogenic is the rarest form of shock!
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Pathophysiology of Neurogenic Shock
Distruption of sympathetic nervous systemLoss of sympathetic tone
Venous and arterial vasodilation
Decreased venous return
Decreased stroke volume
Decreased cardiac output
Decreased cellular oxygen supply
Impaired tissue perfusion
Impaired cellular metabolism
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Assessment, Diagnosis and
Management of Neurogenic Shock
PATIENT ASSESSMENT
Hypotension
Bradycardia
Hypothermia
Warm, dry skin
RAP
PAWP CO
Flaccid paralysis below
level of the spinal lesion
MEDICAL
MANAGEMENT
Goals of Therapy are totreat or remove the
cause & prevent
cardiovascular
instability, & promoteoptimal tissue
perfusion
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PENATALAKSANAAN SHOCK
NEUROGENIk
Jika Hipovolemia terapi cairan dng hati-hati.Th cairan jika TD
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Lanjutan.
Observasi adanya Bradycardia-majordysrhythmia
Observasi DVT ( trombus vena dalam )penumpukan
cairan vena di ekstremitas beresiko tinggi tjd>>P.E.
(emboli paru )
K/P gunakan Use peralatan pencegahan [TEDS,
ROM,Sequential stockings, anticoagulation]
NURSING DIAGNOSIS
Fluid Volume Deficit r/t relative loss Decreased CO r/t sympathetic blockade
Anxiety r/t biologic, psychologic or social integrity
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Lanjutan .
Kolaborasi : Alpha agonist tomeningkatkan ketonusan jika perfusi
masih tetap tidak adequate
dopamine at alpha doses (> 10
mcg/kg per min)
ephedrine (12.5-25 mg IV every 3-4
hour)
Terapi bradikardi dng:
atropine 0.5-1 mg dosis maximum
3 mg Mungkin membutuhkan pace maker
transcutaneous or transvenous
temporer
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SEPSIS
Systemic Inflammatory Response
(SIRS) to INFECTION manifested
by two or > of following:
Temp > 38 or < 36 centigrade
HR > 90
RR > 20 or PaCO2 < 32
WBC > 12,000/cu mm or > 10%Bands (immature wbc)
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SEPTIC SHOCK
SEPSIS WITH:
Hypotension (SBP < 90 or > 40reduction
from baseline) &
Tissue perfusion abnormalities invasion of
the body by microorganisms & failure of
bodys defense mechanism.
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Risk Factors Associated with Septic
Shock Age Malnutrition
General debilitation Use of invasive catheters
Traumatic wounds
Drug Therapy
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Pathophysiology of Septic shock
Initiated by gram-negative (most common) orgram positive bacteria,fungi, or viruses
Cell walls of organisms contain Endotoxins
Endotoxins release inflammatory mediators(systemic inflammatory response) causes...
Vasodilation & increase capillary permeability
leads toShock due to alteration in peripheral circulation
& massive dilation
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Pathophysiology of Septic Shock
IMMUNE / INFLAMMATORY RESPONSE
Microorganisms enter body
Mediator Release
Activation of Complement, kallikrein / kinin/ coagulation
& fibrinolytic factors platelets, neutrophils ¯ophages>>damage to endothelial cells.
ORGAN DYSFUNCTION
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Clinical Presentation Septic
Shock
Two phases:
Warm shock - early phase
hyperdynamic response,VASODILATION
Cold shock - late phase
hypodynamic response
DECOMPENSATED STATE
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Clinical Manifestations
EARLY---HYPERDYNAMIC
STATE---COMPENSATION
Massive vasodilation
Pink, warm, flushedskin
Increased Heart Rate
Full bounding pulse Tachypnea
Decreased SVR*
Increased CO & CI
SVO2 will be
abnormally high
Crackles
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Clinical Manifestations
L ATE--HYPODYNAMIC
STATE--
DECOMPENSATION
Vasoconstriction
Skin is pale & cool
Significant
tachycardia
Decreased BP
Change in LOC
Increase SVR
Decreased CO Decreased UOP
Metabolic &
respiratoryacidosis with
hypoxemia
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PENATALAKSANAAN KOLABORATIF
PeNCEGAHAN !!
ASEPTIK TEHNIK
Cari & matikansumber infeksi
Resusitasi Cairan
Vasoconstrictors
Obat-obat Inotropik
Maksimalkan O2
delivery Support
Nutritional Support
Comfort & Emotional
support
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Sequelae Septic Shock
EFEK dari Endotoxin-endotoksin bakteri dapatterus berlanjut walaupunbakteri telah mati !!
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RangkumanTerapi Shock
Identifikasi pasien dng resiko tinggiterkena shock
Kontrol atau kurangi PENYEBAB
LAKUKAN & KOLABORASI TINDAKAN-TINDAKAN u/ peningkatan perfusi
jaringan
KOREKSI Ketidak seimbangan asam basa TERAPI disarithmia jantung
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