After shock.pptx

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

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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

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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

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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.

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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

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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.

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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.

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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=1


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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=1


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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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Documents

After shock.pptx