PROBLEM

2B
Group 17
Thursday, Oct
th
10 ,2013

Group 17 Membership
TUTOR

Dr. Haming

Silvia Isditya

405080088 scriber

Ludolfus Bertolomeus Temu

405080175

Stephanie

405090231

Amran Cleo Petra Sinaga

405090267

Queencia Editha Morin

405090269

Hotris Anandita Vitalli

405100002 secretary

Theresia Veronika

405100017

Yowendru

405100111

Karina Eda Clearesta

405100120 leader

Vivi Anggelia

405100154

Theresia Jasmine

405100157

Billy Anthonio Khuana

405100279

Tax
tA 50 year old man was admitted to emergency department

due to loss of consciousness since 1 hour before admission.

Since 3 days before admission, he got a high fever with
productive purulent sputum an difficulty of breathing. He
had taken OTC (over the counter) medicines but his
condition did not improve. He also developed diarrhea for
>10X/day and vomiting. Since 6 hour before admission, he
suddenly felt pain on his left chest, radiating to the neck
and left arm, palpitation, and sweating all over his body he
had history of uncontrolled hypertension and DM. On
physical examination: somnolent, BP 80/50 mmHg, pulse
120X/mnt, weak, breathing 28X/mnt, temperature 39C. He
was found to have rales on both lungs and gallop on heart
sound. ED doctor performed chest X-ray and found bilateral
lung infiltrates with cardiomegaly and on the patients ECG
was found extensive myocardinal infarction. The lab results
was insignificant except for the leukocyte count of
15.000/ml and increased of troponin-T. He was given
resuscitation in the ED and immediately transferred to
intensive care unit. After 2 hour in the ICU, he suddenly
stopped breathing and no pulse was found. The ICU team
performed CPR for 30 mnt and finally his breathing and
pulse returned spontaneously to normal.
What can we learn from this case?

LO (Learning Objective)
1. MM. Shock

MM.
MM.
MM.
MM.

Shock
Shock
Shock
Shock

cardiogenic
hypovolemic
obstructive
distributive

Shock neurogenic
Shock anaphylactic
Shock septic

Shock
shock failure of the
circulatory system to
oxygenate and nourish
the body adequately
Identifies shock by linking
the clinical impression,
synthesized from
The patients history of
present illness
Age
underlying health status
general appearance
quantitative data vital
signs, blood chemistry,
urine output, and direct
measurements of
oxygenation

shock first affects

the mitochondria
When mitochondria
have inadequate
oxygen, cell
catabolizes fuels to
lactate,
accumulates and
diffuse into the
blood.

Syok
Hipovolemik

Syok
Kardiogenik
SYOK
Syok
Obstruktif

Kehilangan darah/syok
hemoragik
Kehilangan
plasma
Kehilangan cairan dan
elektrolit
Disritmi
a
Kegagalan pompa
jantung
Disfungsi katup
akut
Ruptur septum
ventrikel
Tension
pneumotorax
Peny.perikardium
Peny.pembuluh darah
paru
Tumor
jantung
Trombus mural atrium
kiri
Penyakit katup
obstruktif
Syok
septik
Syok anafilatik

Syok
Distributif

Syok neurogenik
Obat2 vasodilator
Insufisiensi adrenal akut

Clinical features

Rapid recognition of shock requires immediate history

and physical examination
In general:
appear ill, pale, often sweating, usually tachypneic, and
often with a weak and rapid pulse
Urine output provides an excellent indicator of organ
perfusion and is readily available with insertion of a Foley
catheter
normal (>1.0 mL/kg/hr), reduced (0.51.0 mL/kg/hr), or
severely reduced (<0.5 mL/kg/hr)
A lactate concentration greater than 4.0 mM or a base
deficit more negative than 4 mEq/L predicts circulatory
insufficiency severe multiple organ failure

lab and radiographic

A chest radiograph
Electrocardiogram
finger-stick glucose measurement
complete blood count (CBC)
Urinalysis
serum electrolytes
kidney and liver function tests
Serum lactate should be performed as
early as possible in patients with suspected
shock

Syok Hipovolemik
Terganggunya
sistem sirkulasi
akibat volume
darah dalam
pembuluh darah
yang berkurang.

Kehilangan cairan
ekstraseluler

Muntah
Dehidrasi
Diare
Terapi Diuretik
Diabetes Insipidus
Insufisiensi Adrenal

Penyebab Syok Hipovolemik

Perdarahan
Hematom
Subkapsular Hati
Aneurisma Aorta
Pecah
Perdarahan
Gastrointestinal
Perlukaan Berganda

Kehilangan Plasma

Luka Bakar Luas

Pankreatitis
Deskuamasi Kulit
Sindrom Dumping

Gejala Klinis Syok

Hipovolemik
Ringan (<20%
volume darah)

Sedang (20-40%
volume darah)

Berat (>40%
volume darah)

Ekstremitas dingin

Sama, ditambah
takikardi

Sama, ditambah:
Hemodinamik tdk
stabil

Waktu pengisian
kapiler meningkat

Takipnea

Takikardia

Diaporesis

Oliguria

Hipotensi

Vena kolaps

Hipotensi Ortostatik

Perubahan kesadaran

Cemas

Diagnosis
Ditemukan tanda berupa
ketidakstabilan hemodinamik dan
ditemukan adanya sumber
perdarahan.
Kehilangan plasma ditandai
hemokonsentrasi
Kehilangan cairan bebas ditandai
hipernatremia

Tatalaksana
Menempatkan pasien dengan posisi
kaki lebih tinggi
Menjaga jalur napas
Resusitasi cairan (iv)
Kateter CVP (central venous
pressure) atau jalur intraarterial

Syok Kardiogenik
Definisi : Gangguan yang disebabkan
oleh penurunan curah jantung
sistemik pada keadaan volume
intravaskular yang cukup, dan dapat
mengakibatkan hipoksia jaringan.
Penyebab terbanyak infark miokard
akut (elevasi segmen ST)

Etiologi
Komplikasi mekanik akibat infark
miokard akut:
ruptur septal ventrikel,
disfungsi otot papillaris,
ruptur miokard keseluruhan,
gagal ventrikel kiri

Takiaritmia,bradiaritmia rekuren
Aritmia supraventrikular, ventrikular
Penyakit Jantung Iskemia

Pathophysiology
Left Ventricle

The emergency management of patients with cardiogenic shock,

acute pulmonary edema, or both is outlined.
*Furosemide: <0.5 mg/kg for new-onset acute pulmonary edema without
hypervolemia; 1 mg/kg for acute on chronic volume overload, renal
insufficiency.
For management of bradycardia and tachycardia, see Chaps. 232 and
233.
*Indicates modification from published guidelines. ACE, angiotensinconverting enzyme; BP, blood pressure; MI, myocardial infarction.

Prediktor
Klasifikasi Killip berdasarkan gambaran
klinis :

Tanda gagal jantung kongestif

Suara s3 gallop, ronki
Edema paru
Syok kardiogenik

Klasifikasi Forrester berdasarkan keadaan

hemodinamik :
Angka PCWP (Pulmonary Capillary Wedge
Pressure) & CI (Cardiac Index)
Semakin tinggi nilain PCWP & semakin rendah
CI mortalitas meningkat

The emergency management of patients with cardiogenic shock,

acute pulmonary edema, or both is outlined.
*Furosemide: <0.5 mg/kg for new-onset acute pulmonary edema without
hypervolemia; 1 mg/kg for acute on chronic volume overload, renal
insufficiency.
For management of bradycardia and tachycardia, see Chaps. 232 and
233.
*Indicates modification from published guidelines. ACE, angiotensinconverting enzyme; BP, blood pressure; MI, myocardial infarction.

Shock septik
Definisi
Merupakan suatu kegagalan sirkulasi perifer
dengan perfusi jaringan yang tidak adekuat
akibat septikemia (terdapatnya multiplikasi
bakteri dalam darah).
Syok septik mengenai :
Jantung
Sistem vaskular
Hampir semua organ

Septic/Inflammatory Shock
Signs:

Early warm w/ vasodilation, often adequate urine

output, febrile, tachypneic.
Late-- vasoconstriction, hypotension, oliguria,
altered mental status.

Monitor/findings: Earlyhyperglycemia, respiratory

alkylosis, hemoconcentration,
WBC typically normal or low.
Late Leukocytosis, lactic acidosis
Very Late Disseminated Intravascular
Coagulation & Multi-Organ
System Failure.
Tx : ABCs, IVF, Blood cx, ABX, Drainage (ie abscess)
pressors.

Etiologi

Kuman gram negatif

Predileksi : sal. kemih, sal. napas, sal. cerna
Kulit dan luka juga merupakan sumber infeksi.
Insidens meningkat antara lain :
Pemberian antibiotik yang berlebihan
Meningkatnya penggunaan obat sitotoksik dan
imunosupresif
Meningkatnya frek. penggunaan alat invasif
Meningkatnya infeksi yang disebabkan
organisme yang resisten terhadap antibiotik

Patofisiologi

Tanda dan Gejala

1. Tekanan Darah

Tekanan arteri rata-rata (Mean Arterial Pressure,

MAP) 60 mmHg atau
Tekanan arteri sistolik 90 mmHg.

2. Tanda- tanda gangguan perfusi organ/jaringan

yang terkena, yaitu :

Kulit : dingin dan sianosis

Ginjal : produksi urin menurun dan mungkin
mengarah ke gagal ginjal.
Hati : mungkin menyebabkan hiperbilirubinemia.
Otak : kekacauan/kebingungan dan bila menetap
dapat menyebabkan koma.
Paru : menimbulkan gejala sindrom gawat napas
dewasa.
Bila mengenai multi organ dapat menimbulkan
asidosis metabolik oleh asam laktat yang
tertumpuk dalam darah. Peningkatan kadar laktat
merupakan tanda buruk.

Tanda dan Gejala

3. Tanda/gejala infeksis sistemik serius yaitu :
Tanda klinis sepsis berat :
Demam, menggigil, lesu, mual dan
muntah.
Pemeriksaan laboratorium :
Leukositosis dengan pergeseran ke kiri
Kadang trombositopenia atau neutropenia

Penatalaksanaan
1. Pemberian antibiotik spektrum luas tanpa
menunggu hasil pemeriksaan biakan dan uji
resistensi kuman.
2. Terapi cairan untuk memperbaiki konsumsi
oksigen menggunakan cairan kristaloid
(NaCl, Ringer laktat) atau koloid.
3. Dopamin
4. Kortikosteroid
5. Imunoglobulin

Penatalaksanaan
6. Memperbaiki asidosis metabolik dengan natrium
bikarbonat sampai pH normal dan memperbaiki
gangguan elektrolit dengan pemberian elektrolit.
7. Memperbaiki hipoksia dengan pemberian oksigen
menetap.
8. Memperbaiki hiperglikemia atau hipoglikemia.
9. Memperbaiki azotemia dan oliguria
10.Bila terjadi pembekuan intravaskular menetap
(KID) mengobati penyakit dasarnya saja.

Selama pengobatan, dilakukan pemantauan

hemodinamik yaitu :
Pemasangan monitor EKG.
Pemasangan kateter arteri/vena mengukur
keseimbangan cairan.
Pemasangan kateter urin mengukur urin.
Pemasangan manset mengukur tekanan
darah.
Px analisis gas darah, elektrolit, asam laktat,
uji pembekuan darah menilai fs. metabolik.
Px serial fs. ginjal dan hati.
Pemasangan infus cairan, O2, dan bila
diperlukan oksigen agresif dapat dipasang
PEEP.

Treatment of Sepsis
Antibiotics- Survival correlates with how
quickly the correct 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 infectionsClindamycin or Metronidazole
Asplenic- Ceftriaxone for N. meningitidis, H. infuenzae
Neutropenic Cefepime or Imipenem

Neurogenic Shock
High cervical spinal cord injury, inadvertent
cephalad migration of spinal anesthesia, or
devastating head injury Interruption of
sympathetic vasomotor input
Arteriolar dilation, venodilation pooling in the
venous system, decreases venous return and
CO.
The extremities are often warm

PATOFISIOLOGI
Syok neurogenik cedera pd medula spinalis
g3 aliran keluar otonom simpatis
Sinyal tsb berasal dr kornu grisea lateralis medula
spinalis antara T1 & L2
Konsekuensi penurunan tonus adrenergik
ketidakmampuan meningkatkan kerja inotropik
jantung scr tepat & konstriksi buruk vaskularisasi
perifer sbg respons thd stimulasi eksitasional
Tonus vagal yg tdk mengalami perlawanan
hipotensi & bradikardia
Vasodilatasi perifer kulit hangat & kemerahan

 Hipotermia tdk adanya

vasokonstriksi pengatur otonomik pd
redistribusi darah ke inti tubuh
Lbh tinggi tingakat cedera medula
spinalis, lbh berat syok
neurogenik lbh byk massa tbh yg
tpotong dr regulasi simpatisnya
Syok neorogenik tdk tjd jk cedera di
bwh T6

DIAGNOSIS
Pemeriksaan fisik hipotensi,
bradikardia, kulit hangat, kering,
tanda awal yg menyebabkan cedera
medula

PENATALAKSANAAN
Hipotensi cairan IV kristaloid
Obat presor (dopamin, dobutamin),
pemantauan invasif respons thd
cairan IV suboptimal
Bradikardia atropin, tp pacing kasus
refrakter
Kortikosteroid cedera medula spinalis
traumatik
Evaluasi neurogenik & bedah saraf
semua kasus

Treatment
Involves a simultaneous approach to the
relative hypovolemia and to the loss of
vasomotor tone.
Excessive volumes of fluid : restore normal
hemodynamics
norepinephrine or a pure -adrenergic
agent (phenylephrine) augment
vascular resistance and maintain an
adequate mean arterial pressure.

Adjunctive Therapies

The sympathomimetic amines dobutamine, dopamine, and

norepinephrine are widely used in the treatment of all forms of shock.

DOBUTAMINE : inotropic with simultaneous afterload reduction

minimizing cardiac-oxygen consumption increases as CO increases.

DOPAMINE : inotropic and chronotropic supports vascular resistance

NOREPINEPHRINE : inotropic without chronotropy vasoconstriction and

increases myocardial oxygen consumption
while placing marginally perfused tissues such as extremities and splanchnic
organs ischemia or necrosis

Arginine-vasopressin (antidiuretic hormone) increase afterload

better protect vital organ blood flow and prevent pathologic vasodilation.

Rewarming
Hypothermia, temperatures <35C (<95F), is a
frequent adverse consequence of massive volume
resuscitation
The infusion of large volumes of refrigerated
blood products and room temperature crystalloid
solutions rapidly drop core temperatures if fluid
is not run through warming devices.
Hypothermia :
Depress cardiac contractility impair cardiac output
and oxygen delivery/utilization.
Impairs the coagulation pathway coagulopathy.

 Rapid rewarming : decreases the

requirement for blood products and
produces an improvement in cardiac
function.
Endovascular countercurrent warmers
through femoral vein cannulation.
Can rewarm from 30 to 35C (86 to
95F) in 3060 minutes.

Humans Immune system

innate system (the first line of defense) :
effector components : mast cells, macrophages, dendritic
cells, natural killer cells, granulocytes, anti- microbial
peptides, complements, and cytokines.
Mast cells (and basophils) and their contents the
central effector cells and mediators in allergy and
anaphylaxis

adaptive system :
must allow time for the antigen-specific cells (B and T cells)
to amplify through a process known as clonal expansion to
mount an effective immune response.
effector components : B and T lymphocytes and cytokines.
characterized by having an immune memory and enormous
diversity.
Rosens Emergency

Anaphylactoid reaction
a syndrome clinically similar to anaphylaxis that is not mediated by
IgE.
direct degranulation of mast cells (and basophils) and may follow a
single, first-time exposure to certain inciting agents.

Anaphylaxis ; Greek (ana, against; phylax, guard or protect),

meaning against protection.
refers to a life-threatening allergic syndrome (i.e., IgE mediated)
characterized by multiorgan involvement and rapid onset.
IgE- and non-IgE-mediated reactions. (immunologic)
prominent pruritic urticaria, orolaryngeal edema, bronchospasm,
hypotension, and central nervous system and gastrointestinal (GI)
symptoms.
deaths usually result from acute respiratory failure / cardiovascular
collapse.

Rosens Emergency

Classification
3 main classifications of anaphylaxis :
Anaphylactic shock systemic
vasodilation that causes low BP.
Biphasic anaphylaxis recurrence of
symptoms within 172 hours (typically 8 hours)
with no further exposure to the allergen.
Pseudoanaphylaxis or anaphylactoid
reactions does not involve an allergic
reaction but is due to direct mast cell
degranulation.

wikipedia

Rosens Emergency

Risk factor

atopy is a risk factor for anaphylaxis in an all-cause

anaphylactic series.
mucosal route (food)
parenterally (e.g., penicillin)

summer and early fall (the outdoor season),

higher socioeconomic status
women >30 years, and in adults
dose, frequency, duration, and route of administration of a
drug (>> parenteral and topical).
anaphylactic reaction may not occur in a susceptible patient as
long as a drug is administered at regular intervals.
the more distant the last exposure, the lower the risks of
anaphylaxis upon reexposure, presumably because of some
forgetfulness of the immune memory.

Rosens Emergency

4 types of hypersensitivity
reactions

Type I (immediate hypersensitivity) is IgE (and IgG4) mediated

accounts for most allergic and anaphylactic reactions observed in humans.

Type II (cytotoxic) denotes antibody-mediated cytotoxic reaction.

In this scheme, complement-fixing IgG (or IgM) engages cell-bound antigen,
activating the classic complement pathway

fixation of membrane attack complexes and cell lysis

anaphylatoxins C3a and C5a cause mast cell mediators of anaphylaxis
to be released.

Type III (immune complex) is IgG or IgM complex mediated.

antigen-antibody immune complexes from the circulation perivascular
interstitial space activating the complement system.
Blood transfusions, blood component therapy overlap of type II and type III
reactivity; classified as complement-mediated or immune complex-mediated
anaphylaxis.

Type IV (delayed hypersensitivity) is T cell mediated

anaphylaxis

Rosens Emergency

Pathophysiology

Rosens Emergency

Mediators of anaphylaxis
Preformed mediators (degranulation of mast cells and basophils) :
Histamine is an essential mediator in immediate hypersensitivity
and inflammation.
Histamine is produced and stored in preformed granules (pg) in mast
cells and basophils, 1 or 2 pg/cell.
3 classes of histamine receptorsH1, H2, and H3 :
H1 receptor stimulation bronchial, intestinal, and uterine smooth
muscle contraction; increased vascular permeability; nasal mucus
production; coronary artery spasm; and increased eosinophil and neutrophil
chemokinesis and chemotaxis.
H2 receptor stimulation increases the rate and force of ventricular and
atrial contraction, gastric acid secretion, airway mucus production, and
vascular permeability while also causing bronchodilation and inhibition of
basophil histamine release.
H3 receptors found in neurons (in the central nervous system) and
peripheral tissues control the synthesis and release of histamine.

Rosens Emergency

Mediators of anaphylaxis
Cytokines and lipid metabolites (activation of mast cells and
basophils) :
PGD2
hypotension, inhibition of platelet aggregation, and bronchospasm;
30x > potent than histamine in causing bronchoconstriction.

The leukotrienesLTB4, LTC4, LTD4, and LTE4also referred to

as cysteinyl leukotrienes or slow- reacting substances of anaphylaxis
cholinergic-independent bronchospasm, increased vascular
permeability, and increased mucous gland production.
slow onset, > duration of action, 10 to 1000x > potent than histamine
in causing bronchoconstriction when administered by aerosol.

Platelet-activating factor (PAF) is an unstored phospholipid

aggregation of human platelets, decreased myocardial contractile
force, coronary vasoconstriction, pulmonary edema, and a prolonged
increase in total pulmonary resistance with a decrease in dynamic
compliance.

Rosens Emergency

Rosens Emergency

References
http://circ.ahajournals.org/content/11
7/5/686.full
IPD/ harrisons
Rosens emergency

Conclusion & Sugestion

Kesimpulan problem 2a

Kami telah
mempelajari

MM. Shock cardiogenic

MM. Shock
hypovolemic
MM. Shock obstructive
MM. Shock distributive

Shock neurogenic
Shock anaphylactic
Shock septic

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