SHOCK

- Shock is defined as acute circulatory failure leading to inadequate end organ tissue perfusion
with oxygen and nutrients.
Shock progresses from an initial insult to ccompensated ( reversible), decompensated (
progressive) then finally refractory ( irreversible) shock.
(i) Compensated shock : physilogical mechanism initially compensate to combat the
circulatory failure. These include hyperventilation as a result of acidosis, sympathetic
mediated tachycardia, and vasoconstriction and the diversion of blood from the
gastrointestinal and renal tracts to the brain, heart and lungs.
(ii) Decompensated shock : inadequate tissue perfusion results in increasing anaerobic
glucolysis and metabolic acidosis, cellular injury with the fluid and protein leakage
and deteriorating cardiac output from vascular dilatation and myocardial depression
(iii) Irreversible shock : this enses when vital organs fail and cell death occurs. severe
and progressive shock states cause multi organ failure or end in cardiac arrest with
pulseless electrical activity. Once shock deteriorates to othis degree, it is difficult or
imposisble to reverse.
- aim to identiy abnormal tissue perfusion early, ideally before the systolic blood pressure
drops, treat aggressively and avoid the irreversible phase. Investigation and treatment are
concurrent
(i) a normal blood pressure doesnt exclude the diagnosis of shock
(ii) the absolute value of the SBP associated with poor perfusion varies greatly, but an
SP < 90 mmHg s usually insufficient to maintain adequate vital organ perfusion.
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- Co dipengaruhi oleh preload, afterload, and contractility. MAP : diatolic + 1/3(sistol-diastol).

SVR directly impair MAP but also CO. The physiologic mecanis of oxygen delivery to the
peripheral tissue (d02) is describe as the equaton. Recognize that blood pressure is not
represented in this equation. Patient in shock may initially have normal blood pressures (
cryptic shock), yet have other objecive signs of shock. It is from these basc equation that the
concept of preload influencing stroke volume, which itself influences CO and DO2 has
beccome fundamental in shock management.
- Co is dependent on the interplay of cardiac inotropy 9 speed and shortening capacity of
myocardium), chronotropy ( heart contraction rate), lusitropy ( ability to relax and fill heart
chambers). Determinants of inotropy include from symphatetic activation parasympahtetic
inhibiton, circulating cathecolamine and short lived responses t an increase in afterload or
heart rate. Increase in inotropic state help to maintain stroke volume at high hearts rates.
Under certain conditions, such as shock states, higher levels pf epinephre will be produced
and reinforce adregenic tone. Epinephrne are significantly elevated during induced
hemorrhagic shock, but these leels subsequently reduce to almost normal levels after
adequate blood pressure is restored. Chronotroopy and lusitropy are both influenced by
sympathetic input. Norephinephrine interact with cardiac b1 receptor, resulting in increase
camp, leads to preoces of intracellular signaling with an increased chronotrophy and
sequestration of calcium, leading to myocardial relaxation.
- Ketika ga bisa kompensasi untuk imbalacne antara tissue supply and demand, anaerobic
metablism occurs and results in the formation of lactic acid. Most cases of lactic acidosis are
result of inadequate oxygen delivery, but lactic acidosis occasionally can develop from an
excessively high oxygen demand ( status epilepticus). Bisa juga occurs karena imparied tissue
oxygen utilization ( septic shock or postresuscitation phase of cardiac arest). Elevated lactate
 is a marker of impaired ocysgen delivery or utilization and correlates with short term
prognosis of critically ill patients in ED.
- Compensatory mechanism of shock :
(1) Arteriolar vasoconstriction, resulting in redistirbution of blood flow from the skin,
skeletal muscle, kidneys and splanchnic viscera
(2) An increase in heart rate and contractility that increases CO
(3) Constriction of venous capacitance vessels, which augments venous return
(4) Release of the vasoactive hormones epinephirne, norepinehphrine, dopamine and
cortisol to increase arteriolar and venous tone,
(5) Release of antidiuretic hormone and activation of RAAAS to enhace water and sodium
conservation to maintain intravascular volume.

The compensatory mechanism attempt to maintain D)2, to the most critical organs ( heart
and brain) but blood flow to other organs such as kidnyes and GI tract may be compromised.
The cellular response to decresed D02 ( adenosine triphosphate depletion) leads to ion
pump dysfunction, influx of sodium, efflux of potasium and reduction in membrane resting
potential lama lama buat cell deaths. These pathologic events give rise to a cascade of
metabolic features including hyperkalemia, hyponatremia, aotemia, hyper or hypoglucemia
and lactic acidosis.

- In the early phases of shock, these physioogic changes may produce a clinical syndrome
called th systemic inflammatroy response syndrome or SIRS. As the sirs progresses, shock
ensues, followed by the multiorgan dysfunction syndrome, which is manifested y renal
failure, respi failure, myocardial depression, liver failure, DIC.
- Hypovolemic shock occurs due to inappropiately low intravascular volume leading to
decreased preload, decrease stroke volume and decreased co. Hypovolemic shock can be
due to decreased intravascular fluid or decreased volume. Biasanya karena hemoorhage,
severe hemorrhage can result in decreased myocardial red blood cells, can result in
decreased myocardial oxygen delivery, further decreasing co, with primary compenstory
responses of autonomic nervous system mediated increases in svr.
- Distributive shock : characterized by profound systemicc vasodilation and is commonly
associated with relative intravascular volume depletion. Managemetn often involves
addressing both distributive and hypovolemic pathophysiology. Primary compensatory
responses to decreased systemic vasular rsistance in distributive shock include increased CO,
tachycardia, and hyperdinamic left ventricular systolic contraction. In addition, decreased
systemic vascula resistance and increasedvenous capacitane results in decreased preload,
compromising co depsite increases in heart rate and contractility. Up to 40% patients with
distributive shock due to sepsis may develop a transient cardiomyopathy. Cardiomyopahty
of sepsis is characterized by decreased left ventriular inotrophy and decreased cardiac
output. While septic shock is the most common cause of distributive shock, other proesses
can cause distributive pathophysiology including anaphylaxis, adrenal insufficiency,
transfusion reactions and liver failure. Although neurogenic sock is pathophysiologically
cahracterized as distributive shock, clinical management of neyrogenic shock is disticnt from
other forms of distributive shock. Sepsis can present with characteristics of distributive,
hypovolemic, and even cardiogenic shock. \
 - Cardiogenic shock is due to the falure of the left ventricle to generate adequate arterial flow
to deliver oxygenated blood to peripheral tissues. Cardiogenic shock may be due to
disruptions in stroke volume and or heart rate. Failure of the left ventricle to generate
adequate oxygen delivery may be due to processes such as right vventricle failure or valvular
disease. pathophysiologic process that negtively affect stroke volume include abbertions
inpreload, affter load and myocardial contractility. Abnormal heart rates can also causes
cardiogenic shock. Bradyarrhytmias can reult inlow co, and tachyarrhythmias can reult in
decrease preload due to decreased diastolic filling time ( resulting in critically compromised
stroke volume and decreased CO). The primary systemic compensatory response to
decreased cardiac output is an autonomic nervous system mediated increase in systemic
vascular resistance. The increase in systemic vascular resistance causes the common finding
of cold and clammy extremities in patiennts with cardiogenic shock.
- Obstructive shock results form either critical decrease in preload or an increase in left
ventricle outflow obstruction. Extracardial processes that increase intrathoracic pressure can
result in obstructive shock by decreasing cardiaca compliacne and interrupting venous
return by compressing the inferior or superior vena cava. Tetnsion pneutmothorax,
herniation of abdominal contents into the thorax and positive pressure ventilation are
processes that result in decreased cardiac compliance and obstruction of the vena cava,
decreased preload and decreased cardiac output.

SEPSIS DAN SEPTIC SHOCK

- Sepsis adalah disfungsi organ yang mengancam jiwa akibat disregulasi respon mtubuh
terhadap infeksi. Sedangkan syok septik adalah bagian dari sepsis dimana terjadi
abnormalitas sirkulasi dan metabolisme selular yang dapat meningkatkan mortalitas.
- Adapun kriteria klinis pasien sepsis apat diketahui dengan menggunakan skor Sequential (
sepsis related) Organ Failure Assessment ( SOFA). Apabila pasien yang mengalami infeksi
didapatkan skor SOFA >= 2 maka sepsis dapat ditegakkan.
- Ketika mendapatkan pasien infeksi perlu dilakukan skrining kemungkinan terjadinya sepsis
dengan quick SOFA ( qSOFA). 2 dari 3 kriteria berarti harus dilanutkan dengan skoring SOFA.
- sIRS is a pro inflammatory state, usually but not necessarily caused by infection. SIRS criteria
are no longer required for the diagnosis of sepsis. As approximately 10-12% of patients with
sepsis in intensive care unit may nit have >= 2 SIRS criteria, using the SIRS criteria alone will
not identify all patients with sepsis. However, the presence of systemic inflammatory
response may still have an important role in identifying patients with infection.
Syok septik

- Pasien dengan syok septik dapat diidentifikasi dengan adanya klinis sepsis dengan hipotensi
menetap yang membutuhkan vasopresor untuk mempertahankan MAP >= 65 mmHg dan
kadar laktat serum > 2 mmol/L (18mg/dL) meskipun volume resusitasi meemadai.

Tatalaksana :

- Sepsis dan syok septik termasuk dalam kategori kedaruratan medis yang memerlukan
resusitasi yang adekuat.
- Target dalam 6 jam
a. MAP >= 65 mmHg
b. Urine output of 0,5 mL/kg/hour
c. CVP 8-12 mmHg
d. Superior vena cava saturation of 70% or mixed venous oxygen sturation of 65%.
- The use of empirical high flow oxygen is no longer recommendid in the Sepsis Si bundle, and
oxygen should be used to keep oxygen at >94%, unless there is a history or clinical suspicion
of COPD, and type 2 respi failure, in which case alower target oxygen should be used.
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- Gunakan beberapa parameter atau kombinasi parameter untuk memutuskan apakah pasien
medis perlu ditambahkan cairan atau menambahkan terapi vasopressor dan atau inotropik :
a. Tekanan darah/ nadi
b. Produksi urine
c. Capillary filling time
d. Frekuensi napas
e. Mottling score
f. suhu
g. CVP, SCV02, CO2 gap
h. USG kardiothoraks
i. Laktat
j. Pengukuran dinamik seperti menilai PLR, stroke volume variation
- Pertimbangkan penggunaan dopamin sebagai vasopressor alternatif apabila terdapat sinus
braikardi atau patients with low risk of tachyarryhtmias.
- Pertimbangkan pemberian phenyephrine bila terjadi takiaritmia yang berbahaya akibat
pemberian ne or epinephrine, cardiac output is known to be high and blood pressure
persistently low or as salvage therpy when combined inotrope or vasopressore drugs and
low dose vasopressin have failed to achieve MAP.
- A trial of dobutamine ( inotropic) infusion up to 20 micrograms/kgmin be administered or
added too vasopressor ( if in use) in the presence of
a. Miocardial dysfunction as suggested by elevated cardiac filling pressure and low cardiac
output
b. Ongoing sign of hypoperfusion, despite achieving adequate intravascular vlume and
adequate MAP.
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