Journal Reading

CIRCULATORY PEMBIMBING :

SHOCK dr. Donni, Sp.An

dr. Satrio, Sp.An
dr. Taufik, Sp.An

KOAS ANESTESI FK UNISSULA RSUD K.R.M.T. WONGSONEGORO SEMARANG

 Circulatory failure that
SHOCK results in inadequate cellular
oxygen utilization

HYPOTENSION HYPERLACTATEMI
HYPOPERFUSION
TACHYCARDIA A
HIPOVOLEMIC OBSTRUCTION

DISTRIBUTIVE
CARDIOGENIC FACTOR

SEPSIS ANAPHILAXIS
DIAGNOSIS
The type and cause of shock may be obvious from the medical history,
physical examination, or clinical investigations.
For example, shock after traumatic injury is likely to be hypovolemic
(due to blood loss), but cardiogenic shock or distributive shock may also
occur, alone or in combination, caused by such conditions as cardiac
tamponade or spinal cord injury.
A full clinical examination should include assessment of skin color and
temperature, jugular venous distention, and peripheral edema. The
diagnosis can be refined with point-of-care echocardiographic
evaluation, which includes assessment for pericardial effusion,
measurement of left and right ventricular size and function, assessment
for respiratory variations in vena cava dimensions, and calculation of the
aortic velocitytime integral, a measure of stroke volume. Whenever
possible, focused echocardiography should be performed as soon as
possible in any patient presenting with shock
 Penanganan Pada Pasien
Syok
Penanganan awal yang adekuat
penting untuk mencegah terjadinya
disfungsi dan kegagalan organ.

Resusitasi dimulai dibarengi dengan

mecari penyebab masalah dan
setelah ditemukan etiologi harus
segera ditangani.

Penanganan syok dapat mengikuti

VIP rule selain mencari penyebab
dari syok.
 Ventilate (Pemberian O2)

VIP rule Infuse (Cairan Resusitasi)

Pump (Pemberian obat vasoaktif)

 Ventilator Support
O2 diberikan segera untuk
meningkatkan pengantaran O2
dan mencegah hipertensi
pulmoner

Pulse oxymetri kurang akurat

untuk menggambarkan keadaan
pasien, monitoring dapat
dilakukan menggunakan BGA
(lebih disarankan)
 Ventilasi Mekanik (VM) diutamakan menggunakan mask.

Intubasi dapat dilakukan jika :

a. Dyspnea berat
b. hipoksemia,
c. persisten atau perburukan acidemia (pH <7,30)

Penggunaan invasif VM dapat bermanfaat untuk mengurangi

kebutuhan O2 otot respiratori dan menurunkan beban
afterload ventrikel kiri dengan meningkatkan tekanan
intrathorak
Infuse

Terapi cairan bertujuan untuk memperbaiki

sirkulasi microvaskuler dan meningkatkan CO
yang penting untuk semua jenis syok.
Pemberian cairan harus harus diawasi karena
dapat menyebabkan edem paru dan
memperburuk keadaan.

Fluid challenges untuk menilai respon pasien

terhadap cairan, sambil membatasi risikonya.
Fluid challenges
Tentukan cairan yang akan digunakan :
cristaloid pilihan pertama karena dapat
ditoleransi dan murah
Tingkat pemberiannya : pemberian cairan
harus cepat untuk memberikan respon pada
pasien. Biasanya 300-500 cc dalam 20-30
mnt
Penilaian Objektif : Tekanan darah, Nadi,
Urin Output
Batas kemanan : untuk menghindari
overload cairan
Keberhasilan Initial Resusitasi
Vasoactive Agent
Vasopressors
If hypotension is severe or if it persists despite fluid
administration, the use of vasopressors is indicated. It is
acceptable practice to administer a vasopressor
temporarily while fluid resuscitation is ongoing, with the
aim of discontinuing it, if possible, after hypovolemia has
been corrected.
Adrenergic agonists are the first-line vasopressors because of
their rapid onset of action, high potency, and short half-life, which
allows easy dose adjustment. Stimulation of each type of
adrenergic receptor has potentially beneficial and harmful effects,
for example:
-adrenergic stimulation can increase blood flow but also
increases the risk of myocardial ischemia as a result of
increased heart rate and contractility. Hence, the use of
isoproterenol, a pure -adrenergic agent, is limited to the
treatment of patients with severe bradycardia.
-adrenergic stimulation will increase vascular tone and
blood pressure but can also decrease cardiac output and
impair tissue blood flow, especially in the hepatosplanchnic
region. For this reason, phenylephrine, an almost pure -
adrenergic agent, is rarely indicated.
Norepinephrine to be the vasopressor of first choice; it has predominantly -
adrenergic properties, but its modest -adrenergic effects help to maintain
cardiac output. Administration generally results in a clinically significant increase
in mean arterial pressure, with little change in heart rate or cardiac output.
The usual dose is 0.1 to 2.0 g per kilogram of body weight per minute.

Epinephrine, which is a stronger agent, has predominantly -adrenergic effects

at low doses, with -adrenergic effects becoming more clinically significant at
higher doses. However, epinephrine administration can be associated with an
increased rate of arrhythmia and a decrease in splanchnic blood flow and can
increase blood lactate levels, probably by increasing cellular metabolism.
Prospective, randomized studies have not shown any beneficial effects of
epinephrine over norepinephrine in septic shock. We reserve epinephrine as a
second-line agent for severe cases.
 The use of other strong vasopressor agents as continuous infusions (e.g.,
angiotensin or metaraminol) has largely been abandoned. Nonselective
inhibition of nitric oxide has not been shown to be beneficial in patients with
cardiogenic shock and is detrimental in patients with septic shock.
Vasopressin deficiency can develop in patients with very hyperkinetic forms
of distributive shock, and the administration of low-dose vasopressin may
result in substantial increases in arterial pressure. In the Vasopressin and
Septic Shock Trial (VASST), investigators found that the addition of low-dose
vasopressin to norepinephrine in the treatment of patients with septic shock
was safe and may have been associated with a survival benefit for patients
with forms of shock that were not severe and for those who also received
glucocorticoids. Vasopressin should not be used at doses higher than 0.04 U
per minute and should be administered only in patients with a high level of
cardiac output.
Terlipressin, an analogue of vasopressin, has a duration of action of several
hours, as compared with minutes for vasopressin. For this reason, we do not
believe it offers an advantage over vasopressin in the ICU. Vasopressin
derivatives with more selective V1-receptor activity are currently being
studied.
Inotropic Agents
We consider dobutamine to be the inotropic agent of choice for increasing cardiac output, regardless
of whether norepinephrine is also being given. With predominantly -adrenergic properties,
dobutamine is less likely to induce tachycardia than isoproterenol. An initial dose of just a few
micrograms per kilogram per minute may substantially increase cardiac output. Intravenous doses in
excess of 20 g per kilogram per minute usually provide little additional benefit. Dobutamine has
limited effects on arterial pressure, although pressure may increase slightly in patients with myocardial
dysfunction as the primary abnormality or may decrease slightly in patients with underlying
hypovolemia. Instead of routine administration of a fixed dose of dobutamine to increase oxygen
delivery to supranormal, predetermined levels, the dose should be adjusted on an individual basis to
achieve adequate tissue perfusion. Dobutamine may improve capillary perfusion in patients with septic
shock, independent of its systemic effects

Phosphodiesterase type III inhibitors, such as milrinone and enoximone, combine inotropic and
vasodilating properties. By decreasing the metabolism of cyclic AMP, these agents may reinforce the
effects of dobutamine. They may also be useful when -adrenergic receptors are downregulated or in
patients recently treated with beta-blockers. However, phosphodiesterase type III inhibitors may have
unacceptable adverse effects in patients with hypotension, and the long half-lives of these agents (4 to
6 hours) prevent minute-to-minute adjustment. Hence, intermittent, short-term infusions of small doses
of phosphodiesterase III inhibitors may be preferable to a continuous infusion in shock states.
 Levosimendan, a more expensive agent, acts primarily
by binding to cardiac troponin C and increasing the
calcium sensitivity of myocytes, but it also acts as a
vasodilator by opening ATP-sensitive potassium
channels in vascular smooth muscle. However, this
agent has a half-life of several days, which limits the
practicality of its use in acute shock states.
Vasodilators
By reducing ventricular afterload, vasodilating agents
may increase cardiac output without increasing
myocardial demand for oxygen. The major limitation of
these drugs is the risk of decreasing arterial pressure
to a level that compromises tissue perfusion.
Nevertheless, in some patients, prudent use of nitrates
and possibly other vasodilators may improve
microvascular perfusion and cellular function.
Mechanical Support
Mechanical support with intraaortic balloon counterpulsation
(IABC)

reduce left ventricular afterload and increase coronary

blood flow.

a recent randomized, controlled trial showed no beneficial

effect of IABC in patients with cardiogenic shock, and its
routine use in cardiogenic shock is not currently
recommended.
Goals of Hemodynamic Support
Restoring a mean systemic
arterial pressure of 65 to 70
mm Hg is a good initial goal,
Arterial but the level should be adjusted
Pressure to restore tissue perfusion
 Basis of
mental
status

restore
tissue
perfusion
Urine Skin
output appearance
Goals of Hemodynamic Support
Cardiac Output and Oxygen Delivery
Since circulatory shock represents an imbalance between oxygen supply and oxygen
requirements,maintaining adequate oxygen delivery to the tissues is essential, but all the
strategies to achieve this goal have limitations.

Measurements of mixed venous oxygen saturation (SvO2) may

be helpful in assessing the adequacy of the balance between
oxygen demand and supply; SvO2 measurements are also very
useful in the interpretation of cardiac output.
Goals of Hemodynamic Support

Blood Lactate Level

The primary mechanism of
hyperlactatemia is tissue
hypoxia with development of
anaerobic metabolism,but in
An increase in the blood In all cases, alterations in
distributive shock, the
lactate level reflects clearance can be due to
pathophysiology is more
abnormal cellular function. impaired liver function.
complex and may also
involve increased glycolysis
and inhibition of pyruvate
dehydrogenase.
 In patients with shock and a
blood lactate level of more
than 3 mmol per liter, Jansen
et al. found that targeting a
decrease of at least 20% in
the blood lactate level over a
2-hour period seemed to be
associated with reduced in-
hospital mortality.
Goals of Hemodynamic Support
Microcirculatory Variables
Near-infrared spectroscopy is a technique that uses near-infrared light to
determine tissue oxygen saturation from the fractions of oxyhemoglobin
and deoxyhemoglobin. Analysis of the changes in tissue oxygen
saturation during a brief episode of forearm ischemia can be used to
quantify microvascular dysfunction
Analysis of the changes in tissue oxygen saturation during a brief
episode of forearm ischemia can be used to quantify microvascular
dysfunction32; such alterations are associated with worse outcomes.33
Various therapeutic interventions have been shown to have an effect on
these microcirculatory variables, but whether therapy that is guided by
monitoring or targeting the microcirculation can improve outcomes
requires further study and cannot be recommended at this time.
Therapeutic Priorities and Goals
Therapeutic Priorities and Goals
First (salvage) phase, the goal of therapy is to achieve a
minimum blood pressure and cardiac output compatible with
immediate survival. Lifesaving procedures (e.g., surgery for
trauma, pericardial drainage, revascularization for acute
myocardial infarction, and antibiotics for sepsis) are needed to
treat the underlying cause.
Monitoring : TTV & Urin Output
Second (optimization) phase, the goal is to increase cellular
oxygen availability, and there is a narrow window of opportunity
for interventions targeting hemodynamic status. Adequate
hemodynamic resuscitation reduces inflammation mitochondrial
dysfunction, and caspase activation
Monitoring : SpO2 & BGA
Respon terhadap terapi cairan
Therapeutic countd
Third (stabilization) phase, the goal is to prevent
organ dysfunction, even after hemodynamic stability
has been achieved. Oxygen supply to the tissues is no
longer the key problem, and organ support becomes
more relevant.
Fourth (de-escalation) phase, the goal is to wean the
patient from vasoactive agents and promote
spontaneous polyuria or provoke fluid elimination
through the use of diuretics or ultrafiltration to achieve
a negative fluid balance.
Conclusions
Circulatory shock is associated with high morbidity and
mortality. Prompt identification is essential so that
aggressive management can be started. Appropriate
treatment is based on a good understanding of the
underlying pathophysiological mechanisms. Treatment
should include correction of the cause of shock and
hemodynamic stabilization, primarily through fluid infusion
and administration of vasoactive agents. The patients
response can be monitored by means of careful clinical
evaluation and blood lactate measurements; microvascular
evaluation may be feasible in the future