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7/27/2019 After shock.pptx
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Management of Shock
Pembimbing: dr Rory Denny Saputra
Galih Rahman
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Definition
Failure of delivery oxygen and substrates to meetthe metabolic demands of the tissue beds
SUPPLY < DEMAND
Oxygen delivery < Oxygen ConsumptionDO2 < VO2
Failure to remove metabolic end-products
Result of inadequate blood flow and/or oxygen
delivery
2
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Why should you care?
High mortality - 20-90%
Early on the effects of O2 deprivation on the
cell are REVERSIBLE
Early intervention
reduces mortality
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Oxygen Transport
Oxygen Transport:
Hemoglobin-bound (97%)
Dissolved in plasma (3%)
Monitoring: Hemoglobin-bound (SpO2)
Dissolved in plasma (pO2)
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Oxygen delivery (DO2)
DO2 = CO x CaO2 DO2 : oxygen delivery
CO : Cardiac output
CaO2: arterial oxygen content
CO = HR x SV HR: heart rate
SV: stroke volume
CaO2 = HgB x SaO2 x 1.34 + (0.003 x PaO2) Oxygen content = oxygen carried by HgB + dissolved oxygen
Normal DO2 is 520 to 570 mL/minute/m2
5
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Oxygen Uptake
VO2 = CO X 1.34 X Hb X (SpO2-SvO2)
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Pathophysiology
O2
supply < O2
demand
O2 delivery < O2 consumption
DO2 < VO2
7
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Approach to the Patient in Shock
History Recent illness
Fever
Chest pain
Abdominal pain Comorbidities
Medications
Toxins/Ingestions
Recent hospitalization orsurgery
Baseline mental status
Physical examination Vital Signs
CNS mental status
Skin color, temp, rashes,sores
CV JVD, heart sounds
Resp lung sounds, RR,oxygen sat, ABG
GI abd pain, rigidity,guarding, rebound
Renal urine output
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Empiric Criteria for Shock
4 out of 6 criteria have to be met
Ill appearance or altered mental status Heart rate >100 Respiratory rate > 22 (or PaCO2 < 32 mmHg)
Urine output < 0.5 ml/kg/hr Arterial hypotension > 20 minutes duration Lactate > 4
- Lactate is increased due to:
Decreased O2 --> aerobic metabolism switches over to anaerobic
--> byproduct = lactateDecreased hepatic clearance
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Goals of Treatment
ABCDE
Airway
control work ofBreathing
optimize Circulation
assure adequate oxygen Delivery
achieve End points of resuscitation
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Airway & Breathing
Decision to intubate and initiate ventilatory support
should be made on clinical basis
Determine need for intubation but remember:
intubation can worsen hypotension Sedatives can lower blood pressure
Positive pressure ventilation decreases preload
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Consider Intubation
Generally no need for intubation
3 reasons to intubate in the setting of shock
Inability to oxygenate
Inability to maintain airway
Work of breathing
Treatment: Airway and Breathing
Inability to oxygenate
(Pulmonary edema,
SaO2 88%)
Accessory
Muscle Use
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Recognize signs of early respiratory failure:
Inability to speak Labored breathing
Cyanosis Tachypnea Mental obtundation Paradoxical breathing
Diaphoresis Accessory muscle use
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Optimizing Circulation
Isotonic crystalloids
Titrated to:
CVP 8-12 mm Hg
Urine output 0.5 ml/kg/hr (30 ml/hr)
Improving heart rate
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Maintaining Oxygen Delivery
Decrease oxygen demands Provide analgesia and anxiolytics to relax muscles and
avoid shivering
Maintain arterial oxygen saturation/content
Give supplemental oxygen
Maintain Hemoglobin > 10 g/dL
Serial lactate levels or central venous oxygen
saturations to assess tissue oxygen extraction
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End Points of Resuscitation
Goal of resuscitation is to maximize survival andminimize morbidity
Goal directed approach
Urine output > 0.5 mL/kg/hr
CVP 8-12 mmHg MAP 65 to 90 mmHg
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Shock (Classifications)
Physiological classifications better describe
underlying problem:
Hypovolemic Shock
Cardiogenic Shock
Obstructive Shock
Distributive Shock
Spinal Shock
Septic Shock
Anaphylactic
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Hypovolemic Shock
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Hypovolemic Shock
Non-hemorrhagic Vomiting
Diarrhea
Bowel obstruction, pancreatitis
Burns
Neglect, environmental (dehydration)
Hemorrhagic GI bleed
Trauma
Massive hemoptysis
AA rupture Ectopic pregnancy, post-partum bleeding
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Hypovolemic Shock
Hemorrhagic shock is caused by a loss ofintravascular fluid which is usually wholeblood or plasma
Critical Care and Resuscitation 2000; 2: 55-65
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Hemorrhagic Shock
Compensated Stage
Mechanism: Volume depletion due to bleeding.
Body detects decrease in cardiac output.
Sympathetic nervous system is stimulated releasing epinephrine and
norepinehrine to stimulate alpha and beta receptors.
Alpha = Vasoconstriction Beta = bronchodilation and cardiac stimulation.
21
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Hemorrhagic (Classic) Shock: Compensated
Signs and Symptoms
MentalStatus
Alert orslight
anxiety
Skin
Becomescool, pale.
Sweating
begins atupper lip
and
spreads to
other
areas
BloodPressure
Normal
Pulse
Normal torapid
Respiration
Normal torapid
Other
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Hemorrhagic (Classic) Shock: Progressive
Progressive Stage:
Mechanism: Kidneys release anti-diuretic hormone which
increases vasoconstriction by closing the capillary sphincters,
greatly reducing peripheral circulation.
Increased hypo-perfusion causes increase in metabolic acid
build up
23
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Hemorrhagic (Classic) Shock: Progressive
Signs and Symptoms
Mental
Status
Lethargic,
sleepy,
combative
Skin
Cool ,
clammy,
Pale.
Mottling:Cyanosis
around
nose and
mouth at
first,spreads to
extremities
.
Blood
Pressure
Begins to
fall.
Capillary
refill
delayed
Pulse
Rapid and
weak
Respiration
Rapid and
shallow
Other
Decreased
urination.
24
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Hemorrhagic (Classic) Shock: Irreversible
Mechanism:
Compensatory mechanisms fail.
Pre-capillary sphincters open releasing metabolic acids,
micro-emboli and other wastes into circulation.
Cell damage, organ failure and death occur.
25
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Hemorrhagic (Classic) Shock: Irreversible
Signs and Symptoms
Mental
statusSkin Blood
pressure
Pulse Respiration Other
Decreased
LOC, tounrespon-
siveness.
Grey,
mottled,cyanotic,
waxen.
Sweating
stops.
Decreases
Becomesundetect-
able
Slows then
disappears.
Agonal
Respiration
Irritable
Heart,Brady-
Cardia,
Leads to
Asystole
.
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Grades of Hypovolemic Shock
Sign &
symptom
Class I Class II Class III Class IV
Blood loss (mL) Up to 750 750-1500 1500-2000 >2000
%Blood volume Up to 15 15-30 30-40 >40
Pulse rate 100 >120 >140
Blood pressure N N Capillary refill N
RR N 20-30 30-40 >35
Urinary output
(ml/hr)
>30 20-30 5-15 Negligible
Mental status Mild anxiety Anxiety Confused Lethargic
Fluid
replacement
1 2 Lcrystalloid, +maintenance
2 L crystalloid,re-evaluate
2 L crystalloid, re-evaluate,replace blood loss 1:3crystalloid, 1:1 colloid or bloodproducts. Urine output >0.5
mL/kg/hr
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Grades of dehydration
Mild < 5% Moderate 5-10% Severe >10%
Pulse rate N
Blood pressure N N Respiratory rate N N Rapid
Capillary return 5 seconds
Urine Output N Negligible/absent
Mucous membran Moist Dry Parched
CNS/mental status N/restless Drowsy Lethargic/comatose
5% dehydration = loss of 5 ml of fluid per 100 g body weight or 50 ml per kg
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Ringanatau
Sedang
Beratatau
Syok
Dibagi rata
dlm 24 jam
PERUBAHAN :
-Gx Klinis
-Hematokrit
-Plasma elektrolit
-CVP
Tahap I (rehidrasi cepat) :
20-40 cc/KgBB/1-2 jam
Tahap II :
sisa defisit 6 jam sisanya 16-17 jam
Klasifikasi
Pemberian
Cairan
Defisit
+ Maintenance
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Response to Initial Fluid Resuscitation
Rapid Response Transient Response No Response
Vital Sign Return to Normal Transient
improvement,
recurrent of BP
and HR
Remain abnormal
Estimated blood
loss
Minimal (10%-20%) Moderate and
ongoing (20%-40%)
Severe (>40%)
Need for more
crystalloid
Low High High
Need for blood Low Moderate to high Immediate
Blood preparation Type and cross
match
Type-specific Emergency blood
release
Need for operative
intervention
Possibly Likely Highly likely
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Monitor terhadap pemberian cairan, meliputi :
Perbaikan perfusi (akral hangat, nadi lebih besar,
kesadaran membaik dsb) Pantau produksi urin, produksi urin normal :
Dewasa : 30-50 cc/jam atau 0.5 cc/KgBBAnak : 1 cc /KgBBBayi : 2 cc /KgBB
Monitoring syok
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Monitor Respon terhadap pemberian cairan :
Bila respon terhadap cairan tidak baik, selalupertimbangkan kemungkinan syok non-hemoragik
Bila respon buruk kemungkinan perdarahanberlanjut, cari sumber perdarahan
Cari sumber perdarahan lain :
Jika ada therapi stop perdarahan Jika tidak ada berarti non hemoragik, therapi
sesuai penyebab
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Cardiogenic Shock
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Cardiogenic Shock
The heart cannot pump
enough blood to meet
the metabolic demands
of the body.
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Cardiogenic Shock : Causes
Decreased Contractility (Myocardial Infarction, myocarditis,cardiomypothy, Post resuscitation syndrome following cardiac arrest)
Mechanical Dysfunction (Papillary muscle rupture post-MI, Severe Aortic
Stenosis, rupture of ventricular aneurysms etc)
Arrhythmia (Heart block, ventricular tachycardia, SVT, atrial fibrillationetc.)
Cardiotoxicity (B blocker and Calcium Channel Blocker Overdose)
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Pathophysiology of Cardiogenic Shock
Often after ischemia, loss of LV function
Lose 40% of LV clinical shock ensues
CO reduction = lactic acidosis, hypoxia
Stroke volume is reduced
Tachycardia develops as compensation
Ischemia and infarction worsens
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http://www.tctmd.com/expert-presentations/table-2.html?product_id=8769&title=Cardiogenic%20Shock%20&%20Hemodynamic%20Support&sort_key=27&large_image_p=17/27/2019 After shock.pptx
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http://www.tctmd.com/expert-presentations/table-2.html?product_id=8769&title=Cardiogenic%20Shock%20&%20Hemodynamic%20Support&sort_key=27&large_image_p=17/27/2019 After shock.pptx
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Obstructive Shock
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Syok Obstruktif Disebabkan oleh obstruksi mekanis thd cardiac output
dgn penurunan perfusi sistemik
Penyebab:
a. Cardiac tamponade
b. Tension pneumothorax
c. Emboli paru masif
d. Emboli udara
Tanda: distensi vena jugularis, muffled heart sound(tamponade), suara nafas unilateral (pneumothorax)
Tx: memaksimalkan preload dan mengatasi obstruksi
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Distributive Shock
Types Sepsis
Anaphylactic
Neurogenic
S k di ib if
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Syok distributif
Disebabkan oleh vasodilatasi sistemik krnpenyebab yg muncul (infeksi, anafilaksis)hipoperfusi sistemik
Syok distributif ditingkatkan oleh responinflamasi
Terjadi hipoksia seluler karena gangguanfungsi mitokondria.
Penyebab lain: anaphylaxis, severe trauma,severe liver dysfunction, and neurogenicshock.
h l h k
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Anaphylactic Shock
Shock resulting from
widespread hypersensitivity.
Form of distributive shock.
Killer Bee
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Anaphylactic Shock
Anaphylaxis a severe systemic hypersensitivityreaction characterized by multisystem involvement
IgE mediated
Anaphylactoid reaction clinicallyindistinguishable from anaphylaxis, do not require
a sensitizing exposure
Not IgE mediated
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Anaphylactic Shock
Drugs: Penicillin and related
antibiotics
Aspirin
Trimethoprim-
sulfamethoxazole (Bactrim,Septra)
Vancomycin
NSAIDs
Other: Hymenoptera stings
Insect parts and molds
X-Ray contrast media (ionic)
Foods and Additives: Shellfish
Soy beans
Nuts
Wheat
Milk Eggs
Monosodium glutamate
Nitrates and nitrites
Tartrazine dyes (food colors)
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Anaphylactic Shock
What are some symptoms of anaphylaxis?
First- Pruritus, flushing, urticaria appear
Next- Throat fullness, anxiety, chest tightness,shortness of breath and lightheadedness
Finally- Altered mental status, respiratorydistress and circulatory collapse
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SISTEM REAKSI GEJALA TANDA
Saluran napas Rinitis Bendungan nasal & gatal Edema mukosa
Sembab laring Dispne Stridor laring
Sembab pita suara
Bronkospasme Batuk Batuk
Mengi (Wheezing) Mengi
Sensasi opresi Ronkhi
Retrosternal Gawat napas
Takipne
Sistem Kardiovaskular Hipotensi Sinkop Hipotensi
Takikardia
Aritmia Perubahan EKG :
ST nonspesifik
Perubahan gelombang T,
Ritme nodal,
Fibrilasi atrial, tak ada nadi
Henti jantung
(cardiac arrest)
Perubahan EKG :
Asistol ventrikular
Fibrilasi ventrikular
Kompleks Gejala Anafilaksis
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SISTEM REAKSI GEJALA TANDA
Kulit Urtikaria Pruritus Lesi Urtikaria tipis
Hives
Angioedema Nonpruritik Edema sering asimetris
Pembengkakan
ekstremitas, perioral,
periorbital
Sistem gastro intestinal Nausea, muntah, nyeri
perut, diare
Mata Konjungtivitish Gatal okular, lakrimasi Inflamasi konjungtival
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Terapi Reaksi Anafilaktik dan Anafilaktoid
Jamin jalan napas bebas
RINGAN
SEDANG
BERAT
Lokasikan tempat yang kena racun
Pasang ikatan proksimal bila tempat tsbsuatu ekstremitas
Adrenalin 0,3 0,5 ml lar 1 : 1000 lokal
ke dalam tempat tsb
Tambahkan oksigen
Adrenalin 0,3 0,5 ml lar 1 : 1000 subkutan (ringan) atau intravena
(berat)
Aminofilin 5 6 mg / kg iv dosis pertama, kemudian :
0,4 0,9 mg/kg jam iv (untuk bronkospasme yang menetap)
Pertahankan kadar serum pada 10-20 mcg/kg
Cairan (gunakan derajat hemokonsentrasi sebagai penutntun)
Pemantauan hemodinamik (tekanan arterial dan pengisian jantung, curah jantung)
Cairan
Pengobatan inotropik positif menurut variabel hemodinamik
Zat vasoaktif
Bantuan hidup dasar dan lanjut sesuai metoda dan pengobatan konvensional
Henti Jantung Paru (standar ACLS )
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Tabel 4
Obat obat yang bermanfaat dalam terapi anafilaksis
Obat Kerja farmakolog padaanafilaksis
Kerja selular Dosis (dewasa) Indikasi
Adrenalin
alfaagonis
Vasokonstriksi di kulit,
mukosa dan
splankhnikus
Meninggikan
cAMP
0,3 ml 1:1000 IM Terapi segera dan
awal pada
semua
bentuk
anafilaksis
Betagonis Dilatasi bronkus dan kontriksi
arteriole otot
Isoproterenol
betaagonis
HCL
Dilatasi bronkus & stimulasi
jantung inotropik
Meninggikan
cAMP
1,0 mg dalam 1000 ml
5% dekstrosa
dalam air lewat
tetesan IV +
Dapat dipakai
pada
hipotensi
normovolemi
k (perlu
pantauan
jantung
Noradrenalin
alfaagonis
Dilatasi bronkus & stimulasi
jantung inotropik
Menurunkan
cAMP
4,0 ml lar 0,2% dalam
1000 ml 5%
dekstrosa dalam
air lewat tetesan
IV
Hipotensi berat
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Metaraminol
alfaagonis bitartrat
Meninggikan ta-hanan
vaskular periferi
100 mg da-lam 1000 ml
5% dekstrosa dalam airle-wat tetesan IV +
Hipotensi
Efedrin alfaagonis
sulfat
Sama dengan adrenalin 25 mg per oral tiap 6 jam Reaksi yang ber-
kepanjangan yang
memerlukan pemakaian
kontinyu betaagonis
Aminofilin Dilatasi bronkus Meninggikan
cAMP
250 mg IV selama 10
menit
Bronkospasme yang tak
dapat diatasi dengan
adrenalin
Difenhidramin HCl Inhibitor kompetitif histamin
pada sel sasaran
50 mg tiap 6 jam IV atau
per oral
Semua bentuk
anafilaksis kecuali bron-
kospasme yg menetap
Hidrokortison Tidak diketahui 100 mg tiap 6 jam IV Bronkospasme yang
menetapHipotensi lama
Tabel 5 : Garis Besar Terapi Anafilaksis
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Reaksi Terapi segera Terapi supportif
Ringan Berat
Konyungtivitis
Rinitis
Urtikaria
Pruritus
Eritema
Adrenalin HCl
0,3 ml 1:1000
SC, IM
Difenhidramin HCl 50
mg per oral
Difenhidramin HCl tiap 6
jam
Sembab laring Adrenalin HCl
0,3 ml 1:1000 IM
Difenhidramin HCl
50 mg IV
Difenhidramin HCl
50 mg tiap 6 jam
Efedrin sulfat 25 mg tiap 6
jam
Oksigen
Pantau gas darah
Trakeostomi
Difenhidramin HCl, 50 mg tiap 6 jam
Efedrin Sulfat 25 mg tiap 6 jam Hidrokortison
Bronkospase Adrenalin HCl
0,3 ml 1:1000 IM
Difenhidramin HCl
50 mg IV
Adrenalin HCl
0,3 ml 1:1000 IM
Aminofilin 250 mg IV
selama 10 menit
Oksigen
Pantau gas darah
Aminofilin 500 mg IV tiap 6 jam
Cairan IV
Hidrokortison
Awasi terhadap gagal napas
Hipotensi Adrenalin HCl
0,3 ml 1:1000 IM
Difenhidramin HCl
50 mg IV
Metaraminol bitartrat 100
mg dalam 1000 ml 5%
dekstrosa dalam air
Oksigen
Metaraminol bitartrat atau
noradrenalin IV
Pantau EKG
Pantau volume darah
Cairan IV
Isoproterenol HCL dalam hipotensi
normovolemik dengan curah jantung rendah
Aritmia Terapi manifestasi primer dengan O2,
vasopresor.
Terapi aritmia dengan obat antiaritmik
Tabel 5 : Garis Besar Terapi Anafilaksis
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Neurogenic Shock
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Neurogenic Shock
Interruption in the CNSconnections with the
periphery (spinal cord
injury).
Form of distributive shock.
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Neurogenic Shock
Occurs after acute spinal cord injury
Sympathetic outflow is disrupted leaving unopposedvagal tone
Results in hypotension and bradycardia
Spinal shock- temporary loss of spinal reflex activitybelow a total or near total spinal cord injury (not thesame as neurogenic shock, the terms are not
interchangeable)
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Neurogenic Shock
Loss of sympathetic tone results in warm and
dry skin
Shock usually lasts from 1 to 3 weeks
Any injury above T1 can disrupt the entire
sympathetic system
Higher injuries = worse paralysis
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Neurogenic Shock
Loss of sympathetic tone results in warm and
dry skin
Shock usually lasts from 1 to 3 weeks
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Neurogenic Shock- Treatment
A,B,Cs Remember c-spine precautions
Fluid resuscitation Keep MAP at 85-90 mm Hg for first 7 days
Thought to minimize secondary cord injury If crystalloid is insufficient use vasopressors
Search for other causes of hypotension
For bradycardia
Atropine Pacemaker
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Neurogenic Shock- Treatment
Methylprednisolone
Used only for blunt spinal cord injury
High dose therapy for 23 hours
Must be started within 8 hours
Controversial- Risk for infection, GI bleed
Septic Shock
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Septic Shock
Component of
systemic inflammatory
response syndrome
(SIRS).
Form of distributive
shock.
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Septic Shock
67
Temp >38 or < 36 Tachycardia (>90x/mnt)
Tachypnea (RR > 20)
WBC or , bands
SIRS
SIRS
Infection(presumed orknown)
Sepsis
Sepsis Hypotension
End organdysfunction
SevereSepsis
Sepsis
Hypotension after 40 ml/kg
Pressor requirement
Further evidence of lowperfusion (lactate, oliguria,AMS)
SepticShock
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Treatment of Sepsis
Antibiotics- Survival correlates with how quickly thecorrect drug was given
Cover gram positive and gram negative bacteria Zosyn 3.375 grams IV and ceftriaxone 1 gram IV or
Imipenem 1 gram IV Add additional coverage as indicated
Pseudomonas- Gentamicin or Cefepime
MRSA- Vancomycin
Intra-abdominal or head/neck anaerobic infections- Clindamycin
or Metronidazole Asplenic- Ceftriaxone for N. meningitidis, H. infuenzae
Neutropenic Cefepime or Imipenem
Treatment Algorithm
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Treatment Algorithm
Rivers E et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock N Engl J Med. 2001:345:1368-1377.
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To Summarize
Type ofShock Insult PhysiologicEffect Compensation
Cardiogenic Heart fails to pump
blood out
CO BaroRc
SVR
Obstructive Heart pumps well, but
the outflow is obstructed
CO BaroRc
SVR
Hemorrhagic Heart pumps well, but
not enough blood
volume to pump
CO BaroRc
SVR
Distributive Heart pumps well, but
there is peripheral
vasodilation
SVR CO
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The End
Pediatric septic shock
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Pediatric septic shock
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