LECTURE 11

SHOCK IN ADULT

IGAG Utara Hartawan

OBJECTIVE
1. To understand the definition, type and pathophysiology of shock
2. Implement a general strategy in the patient's approach to shock through symptoms,
physical examination and special technique examination.
3. Able to perform assessment, differential diagnosis, provide early treatment and refer
patients with shock
4. Knowing the patient's prognosis with shock.

INTRODUCTION
Shock is a clinical expression of circulatory failure that results in inadequate cellular oxygen
utilization. Shock is a common condition that often occurs in critical conditions, which occurs in more
than one-third of patients treated in intensive care. The diagnosis of shock can be established
based on clinical, haemodynamic and biochemical criteria, which can generally appear in 3 forms.
The first is arterial hypotension, but the magnitude of hypotension can vary widely, especially in
patients with chronic hypertension. Typically, in adults, the systolic arterial pressure is less than 90
mmHg or an average arterial pressure less than 70 mmHg, with tachycardia. Secondly, there is a
clinical sign of tissue hypoperfusion, seen through the three "Windows" of the body: skin (cold and
moist skin, with vasoconstriction and cyanosis), kidney (urine output <0.5 ml per kilogram body
weight per hour), and neurologic (changed mental state, which usually includes obtundation,
disorientation, and confusion). Third, accompanied by conditions of hyperlactatemia, which indicate
abnormal cellular oxygen metabolism (> 1.5 mmol per liter). Shocks are classified as: hypovolemic,
cardiogenic, obstructive and distributive.

PATHOPHYSIOLOGY
Shock may originate from four conditions of pathophysiological mechanisms: hypovolemia
(from internal or external fluid loss), cardiogenic factors (eg, acute myocardial infarction, end- stage
cardiomyopathy, advanced heart valve disease, myocarditis, or cardiac arrhythmias), obstructive
(eg embolism Lung, cardiac tamponade, or tension pneumothorax), and distributive factors (such
as severe sepsis or anaphylaxis with the release of inflammatory mediators). The first three
mechanisms are characterized by low cardiac output and, therefore, inadequate oxygen transport.
In distributive shocks, the major deficits are located on the peripheral, accompanied by decreased
systemic vascular resistance and oxygen extraction disorders. Usually, in such cases cardiac output
increases, although it may be low due to associated myocardial depression. Patients with acute
circulatory failure often have this combination. For example, patients with distributive shock from
severe pancreatitis, anaphylaxis, or sepsis also experience hypovolemia and cardiogenic shock in
the form of myocardial depression.
The three main factors that determine the delivery of oxygen to the tissues are cardiac output,
defined as the stroke volume of heart rate; oxygen saturation bound to Hgb / O2 X100 capacity and
the amount of dissolved oxygen in the blood, defined as O2 content (ml/dl blood) = ( Hgb x 1.39
X% sat O2 + (0.003 x PaO2).
 Any or all of these factors may be disrupted resulting in a decrease in the release of oxygen
to tissue levels in the vital organs. The result of a disturbance in these vital organs is called shock.
Shock begins with a simple state, to the very severe state of the imbalance between the supply
and the need for oxygen.
Hypovolaemia leads to increased activity of baroreceptor of the aortic arch and carotid. There
is also an increase in baroreceptor activity in the right atrium. The activity of the sympathetic nervous
system increases and results in stimulation of the heart and peripheral vasoconstriction. The
pituitary gland releases ACTH and ADH, resulting in increased cortisol levels in the blood and
sodium and water retention. Increased adreno-cortical activity was soon followed by epinephrine
and norepinephrine release. Increased plasma renin-angiotensin- aldosterone results in greater
water and sodium retention and peripheral vasoconstriction occurs more severely. As the
hypovolemia weighs up, the compensation mechanism becomes lost and the organ functional
disorder becomes more severe.
In addition, the vasoactive hormone is released during shock syndrome, such as
prostaglandin, histamine, bradykinin, serotonin, β-endorphin, MDF (myocardial depressant factor)
and cachectin. All of these substances will affect the perfusion of internal organs and may increase
the permeability of blood vessels and myocardium and platelet function.

SYMPTOMPS
Hypotension and vasoconstriction appear in hemorrhagic shock, hypovolemic shock and
cardiogenic shock due to decreased perfusion and abnormalities of vital organs. Where there is a
change of the regional vascular resistance thereby reducing the perfusion pressure, thus perfusion
to the vital organs can be maintained. In general, the skin becomes cold, moist and wrinkled.
Superficial veins will collapse. Brain circulation is also disrupted as well as skin and other organs,
which can lead to classic symptoms of confusion and disorientation. Cerebral perfusion pressure is
the difference between mean arterial pressure and intracranial pressure or right atrial pressure,
which is higher (CPP = MAP - ICP). Brain auto regulation is still good at mean arterial pressure
between 50 mmHg and 150 mmHg with a rightward shift in chronic hypertension. In hypotension
that accompanies shock occurs mental status changes ranging from agitation, anxiety
accompanied by feelings of hovering, then going into a coma. This occurs due to the decrease of
cerebral perfusion below the critical value. Of course the patient's response will be clear and
appropriate after resuscitation action to improve the hemodynamic state in shock.
The state of shock will affect the heart. Coronary perfusion pressure (pressure difference
between diastolic pressure and left ventricular diastolic end pressure) will decrease due to
hypotension and shock. Tachycardia or bradycardia reflex will also decrease diastolic filling of the
coronary arteries. A decrease in mean arterial pressure is an important sign due to decreased
systolic blood pressure; Peripheral vascular pressure increases and cardiac output decreases.
In septic shock where cardiac output increases and systemic vascular resistance decreases,
heat, seizures and blood cell count are often elevated in this state. The pulse becomes fast and not
palpable. Increased left ventricular diastolic end pressure may result in pulmonary edema and
respiratory failure that may occur along with hypoxemia. If diastolic pressure decreases, coupled
with increased LVEDP (left ventricle end-diastolic pressure) indicates coronary hypo perfusion and
myocardial ischemia. Diastolic blood pressure is directly
related to arterial vasoconstriction, whereas pulse (systolic-diastolic) is associated with large stroke
volume and number of aortic branches and aortic stiffness. Systolic blood pressure reflects all
combinations of these factors. In cardiogenic shock that may be due to chronic heart failure (CHF),
shortness, tachypnea, pulmonary edema with a decrease in PaO2 and the sound gallop or the third
heart sounds (S3 gallop).

Table 14. Early symptoms on shock

Organ System Clinical signs / symptoms Cause

CNS Decrease of consciousness Decrease in CPP

CVS Tachycardia The Adrenergic Stimulus

Dysrhythmias Ischemic Coronary

Hypotension Decreased contractility, MDF

ischaemia, or RVF, also
decreased SVR or preload

Murmurs Valvular dysfunction

JVP increase / decrease Decrease in volume / preload

or RV failure

Respiration Takipneu Pulmonary edema, respiratory

muscle failure, sepsis, acidosis,
hypoxemia

Renal Oliguria Decreased perfusion,

constriction of afferent
arterioles

Skin Cold, pale, sweat Vasoconstriction, sympathetic

stimulation

Other Lactic acidosis Anaerobic metabolism

Fever Infection of hepatic

dysfunction
CNS = central nervous system; CVS = cardiovascular system; CPP = cerebral perfusion pressure; MDF =
myocardial depressant factor; RVF = right ventricular failure; SVR = systemic vascular resistance.

The renal auto regulation system is also maintained, but with decreased perfusion due to
hypotension, decreased glomerular filtration, which is clinically known as oliguria (<25-30 ml/ hr/ 70
kg). In this situation there will be redistribution of cortical renal blood flow to the medulla and urine
becomes more concentrated. Sodium urine decreased <10 mEq/ L. The presence of oliguria is one
sign of shock, and urine repair is an important key in successful resuscitation in shock patients.
Sometimes a lot of urine production occurs in renal failure and is confusing at the start of the
diagnosis, especially in kidneys with normal or increased urine production.
 Integumentary systems are also affected by decreased perfusion and vasoconstriction
reflected from cold skin, changing from pale to grayish to cyanosis. The activity of the sympathetic
nervous system results in increased production of sweat (a cholinergic sympathetic response).
Metabolic acidosis almost always accompanies shock with the accumulation of lactic acid into
hypoxemia. Anaerobic metabolism as a complication due to decreased liver function that can
produce lactic acid.
Thus, shock indicates a perfusion disorder characterized by decreased cardiac output or
distribution disturbance. It may also be the inability of the tissue to utilize a substrate, thereby
resembling a state of hypo perfusion. Blood flow to various organs is seen from the relationship
between perfusion pressure and blood vessel resistance in these organs. In shock, this relationship
is influenced by many factors.

PRIORITY AND TARGET THERAPY

In general, there are four phases in shock treatment. Target therapy and monitoring need to
be adapted to each phase. In the first phase (salvage), the goal of therapy is to achieve minimum
blood pressure and adequate cardiac output for minimal survival. Close monitoring is required; in
many cases, invasive monitoring can also be used in arterial and central venous catheters.
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. In the
second phase (optimization), the goal is to increase the availability of cellular oxygen, as well as
interventions that target hemodynamic status. Adequate hemodynamic resuscitation reduces
inflammation, impaired mitochondrial function, and caspase activation. Measurement of SvO2 and
lactate can help guide therapy. Cardiac monitoring should be considered. In the third phase
(stabilization), the goal is to prevent permanent organ dysfunction, even after hemodynamic stability
has been achieved. The supply of oxygen to the tissues is no longer a major problem, and the organ
of support becomes more relevant. Finally, in the fourth phase (de-escalation), the goal is to wean
patients from vasoactive agents and achieve spontaneous polyuria conditions or provoke fluid
elimination through the use of diuretics or ultrafiltration to achieve a negative fluid balance. However,
specific treatment of course depends on the type of shock and pathophysiology causes the shock.

Shock Hipovolemik/ Hemoragik

In hypovolemic shock indicates the occurrence of bleeding. It is important to know the

percentage of blood volume lost as a basis in providing appropriate therapy. In general, physical
examination alone is not enough, but by following the scheme this can be helped. As an assumption
that the perceived normal blood volume is 7.5 ml / kgbb, the hypovolemic shock is divided into four
groups based on the estimated number of bleeds:
I. 10-15% blood loss from Estimate Blood Volume (EBV) causes mild tachycardia and shock
has not occurred.
II. Blood loss of 15-25% of EBV (1000-1250ml / 70kg) arises moderate shock, with tachycardia,
systolic pressure and pulse pressure drop, slightly increased diastolic pressure, slow
capillary refill. Urine production is still within normal limits.
III. Blood loss 25-35% EBV (1250-1750 ml / 70kg) causes severe shock, with prominent
symptoms: the skin is cold, wrinkled, and pale. Blood pressure decreased between 30-
 40% (systolic pressure and pulse pressure) and an increase in diastolic pressure of about
15-20%. Vasoconstriction stands out and oliguria develops. Prominent CNS disorder is
confusion, which is severe until stupor occurs. Tachypnea results from secondary metabolic
acidosis to hypoxemia, tissue hypo perfusion and anaerobic metabolism. The pulse rate is
greater than or equal to 120x / min.
IV. Blood loss of 35-45% of EBV (1750-2250 ml / 70 kg) causes very severe shock, usually a
preterminal condition. Unmeasured blood pressure, peripheral pulses are not palpable and
carotid pulse is also may not palpable.
Hemorrhagic shock is accompanied by hemodilution and widespread plasma volume
expansion at any given time and therefore, the hematocrit does not change for 3 to 4 hours in acute
bleeding.

SHOCK CARDIOGENIC
Cardiogenic shock (CGS) is a shock characterized by many factors that interfere with the
normal functioning of the heart, or (in particular) adverse factors to preload, afterload, contractility,
heart rate or heart rhythm. For example right or left ventricular myocardial infarction, and in
situations where cardiac pump failure, or ventricular filling or impaired cardiac discharge.
The above changes occur in hypovolemic / hemorrhagic shock and also in cardiogenic shock.
In cardiogenic shock caused by myocardial infarction, there is a decrease in mean arterial
pressure, cardiac output, stroke work index, left ventricular diastolic end pressure and volume and
venous oxygen content. Heart rate, central venous pressure and increased arterial and venous
oxygen content, and peripheral vascular resistance also increase as a result of compensation. The
basic problem is the failure of the heart to pump blood to peripheral tissue, whatever the cause.
Therapy in all types of shock, aimed at the underlying cause while conducting circulatory
resuscitation efforts. What is more important is to save myocardial ischemia and limit the size of
infarction through improvement of hemodynamic abnormalities and dysrhythmias. Myocardial
revascularization, balloon angioplasty and thrombolytic therapy are all part of the treatment plan.

SEPTIC SHOCK

Incident and Etiology

One of the most common forms of distributive shock is septic shock. The complication of this
shock is about 40% of cases by bacteremia gram negative, with a mortality rate of around 40-90%.
Septic shock may be caused by bacteria, both gram-negative and gram-positive (gram
- endotoxin and gram + endotoxin); For example, staphylococci, S. pneumonia, N.meningitidis,
H.gonorrhea or Clostridia, sepsis; Fungi, rickettsia or viruses. Lipopolysaccharides from endotoxin
released from gram-negative cell wall bacteria may be a major part of this syndrome. Septic shock
is caused by sequester or misdistribution of normal or high cardiac output in different parts of the
body. Tumor necrosis factor (cachectin) is known to be a very important mediator of clinical and
humoral manifestations in shock caused by endotoxins (A- and -O lipid chains) or by all gram-
negative bacteria. Vasoactive mediators such as histamine, complement activation, quinine
activation (especially precancerrein), prostaglandins and possibly other substances that give rise to
vasodilation without compensation to maintain cardiac output. Leucocyte aggregation may cause
capillary blockage with inadequate blood flow results in
capillaries. Micro vascular thrombosis is determined by the amount of platelets and clotting factors
and manifestations of stimuli of fibrinolysis systems such as DIC and resulting bleeding. DIC is
caused by sepsis associated with a decrease of factor XII, but endotoxin is triggered by intrinsic
and extrinsic blood clotting systems.
One theory says that hemorrhagic shock can develop into septic shock as a result of
increased permeability of mucous membranes that facilitate enteric bacteria entering the
bloodstream. In this model, severe cellular damage increases the permeability of cell membranes
and extracellular fluid displacement into cells associated with impaired cell barrier function and
disrupts the entry of gram negative or gram-positive bacteria into the bloodstream. This cellular
damage can be overcome if resuscitation is successful, secondary phase bacteremia can be
delayed. Survival may be improved if pre shock therapy is anticipated with broad-spectrum
antibiotics. Both gram-positive and gram-negative bacteria appear to cause both cardiovascular
abnormalities.

Clinical Manifestations
The cardiovascular system is affected by septic shock, at both the myocardial and peripheral
levels. Misdistribution of blood flow followed by myocardial depression, with normal or increased
bulk followed by decreased systemic vascular resistance (SVR). Heart rate increased, meanwhile
mean arterial pressure, stroke volume, stroke work, oxygen consumption and arterial venous
oxygen content all decreased. As already explained, cardiac output may have been normal or
increased. Patients with this condition require large amounts of fluids due to peripheral
vasodilation. The decrease of Left Ventricular Ejection Fraction (LVEF) and Right Ventricular
Ejection Fraction (RVEF) especially biventricular dilatation occurs 2-4 days after onset of
hypotension. Patients who can be rescued from a septic shock their hemodynamic value will return
to their original state of 7-10 days from the onset of septic shock. It has been argued that what can
be saved in septic shock is more likely than cannot be saved with decreased LVEF and left
ventricular dilatation, where left ventricular dilatation gives the impression of a compensatory effort
through the Frank-Starling mechanism. The irreversible to normal heartbeat, cardiac output or
systemic vascular resistance (SVR), whereas improvement can occur within 24 hours. Mortality can
generally be seen from hypotension that is irreversible due to depression of systemic vascular
resistance (SVR) and cardiac depression so that normal values cannot be maintained within normal
limits or above normal until the patient dies. So at first hyper dynamic state with high and normal
cardiac output with low cardiac filling pressure and decreased systemic vascular resistance. The
oxygen saturation of the mixed-vein may be normal or low. In high cardiac output, where abnormal
systolic function (decreased stroke volume and decreased ejection of left ventricular fraction) and
ventricular compliance. The relationship between pulmonary capillary pressure (PCWP) and left
ventricular diastolic end (LVEDV) volume is not normal. At the next stage, there is a decrease in
dynamic state and the picture resembles a cardiogenic shock. Regarding respiration, where
respiratory frequency increases, hyperpnoea, tachypnea and respiratory alkalosis. The antigen-
antibody complex activates the complement system. Septicemia is often followed by ARDS as a
complication. Patients with manifest dyspnea, hypoxemia, bilateral diffuse pulmonary infiltrate,
reduction of lung compliance and have usually unchanged pulmonary capillary pressure from the
baseline (especially if lung function before shock is normal).
Therapy
The primary goal of treating patients with septic shock is eradication / removal of causal
factors, such as infection, the harmful effects of bacterial toxins or endogenous toxins from the host
and attempts to improve the cardiovascular system and other systems.
Many ongoing research experiments to study drugs to counteract the effects of toxins on
septic shock. For the practical use of anesthesia, most of these are clinically unimportant and are
mentioned only for the completeness of the data. Currently, monoclonal antibodies as part of
gram-negative bacteria, naloxone, prostaglandin inhibitors, lipid X, tumor necrosis factor antibodies
(TNF), genetically engineered protease inhibitors and other recombinants or synthetic protease
inhibitors. Cardiovascular support for septic shock patients consists of fluids and vasopressors
required.
Fluid is required for optimization of preload and cardiac output above normal values so that
MAP returns to the baseline if possible or at least initially 60 mmHg. Pulmonary capillary pressure
(PCWP) is optimally 12-15 mmHg and should be monitored by invasive techniques with pulmonary
artery catheter. The selected fluid type did not seem to provide much benefit with respect to the
expected results, although experimental experiments in experimental animals with septic shock
resulted in a significant improvement in cardiac output, Lung Water Extravascular Extension (PVR)
and Venous Admixture (VR) vascular cavity when given Dextran 70 compared to Ringer's Lactate.
Fluid resuscitation has shown effective results for increasing oxygen delivery (DO2) and oxygen
consumption (VO2) in septic shock.
The arrangement of ventricular function following Frank-Starling law and the category of
patients corresponding to the functional can assist in decision-making of inotropic drugs, diuretics
and vasopressors for patient resuscitation. Optimal oxygen transport through correction of anemia
and also followed by improvement in serum albumin levels of at least 2 g / 100 ml is important as
adjunctive therapy. If only with volume correction alone the hypotension is not corrected, while
maintaining the pulmonary capillary pressure (PCWP) greater than or equal to 15mmHG, the
vasopressor may be added cautiously, starting with low dopamine doses (1-3μg / kg / min) and
norepinephrine If large doses of dopamine are ineffective to increase mean arterial pressure (MAP)
or side effects (tachycardia, dysrhythmias). If norepinephrine is also ineffective, it should be
substituted with epinephrine or dobutamine or when low cardiac output is required to use beta-
mimetic adrenergic agonism.

OBSTRUCTIVE SHOCK

Obstructive shock is a form of shock associated with physical obstruction of the great vessels
or the heart itself. Pulmonary embolism and cardiac tamponade are considered forms of obstructive
shock. Obstructive shock has much in common with cardiogenic shock, and the two are frequently
grouped together. It was described as involving obstruction to flow in the cardiovascular circuit and
characterized by impairment of diastolic filling or excessive afterload. The consequent obstruction
of blood flow into or out of the heart causes a decrease in cardiac output, and hence inadequate
oxygen delivery, which is manifest by the classic signs and symptoms of the shock state.
Obstructive shock is rare in pediatrics, though the most common causes generally include tension
pneumothorax, cardiac tamponade, and pulmonary embolism. Also included in this category
physiologically, and more specific to pediatrics, are congenital heart lesions characterized by left
ventricular outflow tract obstruction, including critical aortic
stenosis, coarctation of the aorta, interrupted aortic arch, and hypoplastic left heart syndrome.
Herein, we will briefly review the major causes of obstructive shock found in children.

Tension Pneumothorax
A pneumothorax is defined as the accumulation of air in the pleural space, a cavity that is
normally filled with a small amount of pleural fluid. It can be spontaneous (more common in
adolescent males) or secondary to underlying lung pathology, such as trauma (both penetrating
and blunt trauma), asthma, cystic fibrosis, and pneumonia. Also included in this subcategory are
iatrogenic causes such as barotrauma during positive pressure ventilation or during placement of
central venous catheters in the chest vessels.
The incidence of secondary pneumothorax in pediatric patients is not well described,
however, in critically ill children requiring mechanical ventilation it is reported to be 4-15%. Notably,
the incidence of secondary pneumothorax in mechanically ventilated pediatric patients has declined
markedly since the introduction of protective lung strategies. Pneumothoraces can be well tolerated
in some patients, though signs and symptoms of obstructive shock can develop if the
pneumothorax is under tension. In this scenario, the air in the pleural space continues to collect
under a one-way or ball valve effect, such that air enters during inhalation, but cannot exit during
exhalation. Eventually, enough air accumulates such that the intrathoracic pressure of the affected
hemi-thorax equilibrates with atmospheric pressure, leading to complete lung collapse or
atelectasis. Air under tension also causes a shifting of the mediastinum, compression and total
collapse of the lung and great vessels, thereby compromising both cardiovascular and respiratory
function. Studies in animal models have shown that the early clinical features of a tension
pneumothorax include hypoxemia, tachycardia, and respiratory distress due to compression and
collapse of lung segments. As mechanical compromise of venous structures develops, there is a
drastic and profound reduction in venous return to the heart as well, clinically manifested by
symptoms of shock and poor perfusion. Thus, overt hypotension may be a late sign. Complete
occlusive mechanical compression is suggested by equalization of the Mean Intrathoracic Pressure
(MIP) and Central Venous Pressure (CVP), which is a very late event and results in cardiovascular
collapse. Treatment of a tension pneumothorax requires emergent needle decompression, usually
performed by placing a sterile needle in the second intercostal space along the midclavicular line.
Definitive treatment requires thoracostomy tube placement.

Cardiac Tamponade
The pericardial sac around the heart is relatively noncompliant, and the accumulation of even
small amounts of fluid can be sufficient to produce cardiac tamponade physiology. While
acute pericardial fluid changes are usually symptomatic, the chronic accumulation of fluid may occur
with little to no hemodynamic derangements, as the pericardium slowly stretches to accommodate
the excess volume over time. Pericardial effusions can develop as a result of any type of
pericardial inflammation (i.e., pericarditis), causing a range of physiologic perturbations along the
spectrum of minor flu-like symptoms (i.e., manifestations of the pericarditis itself) to a life-
threatening state characterized by cardiac tamponade and obstructive shock. Historically, the
most common cause of pericardial effusions was infectious pericarditis, though a recent
review suggests that idiopathic
and neoplastic causes are much more frequent due to the success of childhood vaccinations.
Other common causes include postpericardiotomy syndrome (following cardiac surgery for
congenital heart disease) and trauma, most often causing hemopericardium. Effusions may also
develop as a result of a central line that erodes through the thin wall of the right atrium, a
phenomenon that appears primarily limited to neonates and young infants. The pathophysiology of
cardiac tamponade is welldescribed. Briefly, increased intrapericardial pressure limits venous return
to the heart and causes right ventricular compression. There is a progressive decline in right
ventricular end-diastolic volume as diastolic filling lessens, worsening cardiac output. In severe
tamponade, venous return during inspiration into the compressed right ventricle bows the
interventricular septum into the left ventricle, further diminishing systemic cardiac output. As
pericardial pressure increases and surpasses ventricular end-diastolic pressure, the ventricular
volumes grow smaller and smaller and cardiac output worsens. Tamponade is a clinical diagnosis
and classically, patients with critical cardiac tamponade present with Beck’s triad of symptoms
including hypotension, quiet (“muffled”) heart sounds, and raised jugular venous pressure. Patients
may present with dyspnea, compensatory tachycardia, and poor perfusion. On auscultation, a
friction rub and distant heart sounds may be present. Pulsus paradoxus, defined as a decline in
systolic blood pressure greater than or equal to 10 mm Hg during inspiration, results from the
inspiratory reduction in pleural pressure that produces a fall in left ventricular output and arterial
systolic pressure. An electrocardiogram may show electrical alternans due to the heart swinging
within the large effusion. Formal evaluation with an urgent echocardiogram should be performed in
those patients with symptoms suspicious for cardiac tamponade. However, emergent management
should not wait for echocardiography and is frequently based upon the recognition of tamponade
physiology in the appropriate clinical context. Pericardiocentesis is the lifesaving procedure of
choice for children with cardiac tamponade and can safely be done with bedside echocardiographic
guidance. Medical stabilization with fluid resuscitation and inotropic support is temporary at best
and somewhat controversial as fluid resuscitation may worsen tamponade physiology, especially in
children who are either normovolemic or hypervolemic. In the latter scenario, fluid administration
will increase intracardiac pressures further, hence increasing intrapericardial pressures and
worsening tamponade.

Pulmonary Embolism
Pulmonary embolism (PE) is uncommonly diagnosed in children, making its true incidence
difficult to determine. However, the incidence of PE does appear to be on the rise, though this may
be due to a heightened index of clinical suspicion and better recognition by pediatric providers.
Alternatively, it may be due to the fact that more children are surviving from previously fatal
conditions that place them at an increased risk for developing PE, such as congenital heart disease
and malignancy. In addition, more children are requiring central venous catheterization for
vascular access, a major risk factor for venous thromboembolism (VTE), which can lead to a PE.
PE is frequently fatal and difficult to diagnose. In a recent literature review comparing pediatric PE
with adult PE, pediatric cases were more often diagnosed at autopsy and were associated with a
higher mortality rate than adults. The clinical presentation often is confusing, perhaps compounded
by the fact that very few pediatricians have much experience with this disorder. Results of
screening tests, such as oxygen saturation, electrocardiography, and chest radiography, may be
normal. Thus, a high index of clinical
suspicion is necessary. Evaluation should be performed with spiral computed tomography (CT)
venography, which is now widely considered the study of choice due to its >90% sensitivity and
specificity in adults. Ventilation/ Perfusion (V/Q) scans are also available but are more difficult to
obtain and to interpret in pediatrics. As a cause of cardiogenic shock, a massive PE has a profound
impact upon gas exchange and hemodynamics. Obstruction to flow through the pulmonary artery
results in increased dead space ventilation where affected lung segments are ventilated but
not perfused, observed clinically as a substantial decrease in the end-tidal CO2 (ETCO2) that no
longer reflects arterial PCO2. A widened alveolar- arterialgradient (A-a) is present as well. The
mechanism for hypoxemia likely involves several mechanisms. In some pediatric patients,
an intracardiac right-to-left shunt through a patent foramen ovale may be present and as
right atrial pressure increases and eventually exceeds the left atrial pressure, deoxygenated blood
can shunt directly into the systemic circulation. In addition, V/Q mismatching is compounded by the
accompanying fall in cardiac output that results from massive PE, leading to mixed venous
desaturation. PE increases the right ventricular (RV) afterload, resulting in an increase in the RV
end-diastolic volume (EDV). The increase in RVEDV adversely affects left ventricular
hemodynamics through ventricular interdependence. Specifically, the interventricular septum bows
into the left ventricle (LV) and impairs diastolic filling, resulting in decreased LV preload and
subsequently diminished cardiac output and hypotension. These physiologic phenomenon are
manifested by respiratory distress, hypoxia, and decreased cardiac output with signs of shock.
Treatment of an acute pulmonary embolus in children should begin with initiation of a heparin
infusion with or without fibrinolytic agents such as tPA, depending on the child and the
extent of the clot. In the resolution period, the child will then warrant at least 3-6 months of
anticoagulation with low molecular weight heparin (LMWH) or warfarin.

MONITORING SHOCK
Hemodynamic Monitoring
Patients with shock are a critical condition and require invasive hemodynamic monitoring
especially in cases where vasoactive drugs are used for resuscitation or are used to support the
cardiovascular system. Generally, it is classified into routine and exceptional or non-routine
monitoring. Regular monitoring are used in patients with critical condition who receive / get state of
the art care in the intensive care room. Extraordinary or non-routine monitoring are used in patients
who need to be monitored continuously in the ICU, for example in the extravascular lung water.
Meanwhile, blood pressure changes must be correctly measured in shock because blood flow
is determined by the relationship between cardiac output and systemic vascular resistance, but in
shock, blood pressure should be measured by continuous monitoring with beat to beat arterial
pressure. To be able to see the rapid changes can be installed sphygmomanometer or Doppler
placed on the artery line. In addition, monitoring of all patients includes: heart rate and rhythm,
breath frequency, body temperature, right and left heart pressure, ECG and hematocrit. In the
installation of arterial catheters that settle arterial blood samples can be taken in a peiodic manner
to determine the state of electrolytes and the properties of blood clotting and arterial lactate levels.
The catheter insertion into the pulmonary artery may be excellent for assessing pulmonary artery
pressure, pulmonary artery occlusion pressure, cardiac output and other parameters including
vascular resistance. Pulmonary artery catheters have the ability to assess
venous blood saturation, particularly in patients with cardiogenic shock. Central venous pressure
monitoring is sometimes used to determine or determine the amount of blood lost, given that a
500-800ml blood loss for 70kg weight will lower central venous pressure by about 7cmH2O.
Patients with shock who also get general anesthesia, decreased arterial blood pressure may
be faster than patients who are not publicly anesthetized because the compensation of tone
sympathetic nervous system is removed by anesthesia and in this patient, invasive blood pressure
monitoring by continuously beat to beat, will be very helpful. Korotkoff sounds decreased or
inaudible in severe shock which received general anesthesia and subsequently assisted with an
invasive monitor.
Assessment of electrolytes and hematocrit from arterial blood samples can provide important
information during resuscitation and shock management. Assessment of blood volume and
circulatory function can be better assessed in patients who have serial laboratory results. Blood loss
of about 3-4 times in acute bleeding can lead to significant changes in hematocrit. The decrease in
capillary hydrostatic pressure with bleeding is characterized by increased intravenous interstitial
fluid absorption. As a result, intravascular fluids multiply and hematocrit decreases as a result of
fewer percentage of red blood cells in intravascular fluid. It should still be assessed during shock
therapy and monitoring of fixed hemodynamic variables, and there is no evidence to suggest that
simple correction by assessment of common parameters can result in greater outcomes or lower
morbidity.
Of the hemodynamic variables, two things that need attention in the assessment of shock
sufferers are: oxygen delivery and oxygen consumption. Oxygen delivery (DO2) is the result of
arterial oxygen content and cardiac index. DO2 = CaO2 x CI x 10, where CaO2 = 1.39 x Hgb x%
saturation + (PaO2 x 0.003) and CI = cardiac output / body surface area. The normal value for DO2
is 520-720ml/ min/ m2. Oxygen consumption (VO2) is the result of arterial oxygen content minus
venous oxygen content and cardiac index times 10 (VO2 = CaO2 - CVO2 x CI x 10). The normal
value for VO2 is 100-180ml / min / m2. VO2 describes the sum of all oxidative metabolic outcomes
and thus is a measure of total body metabolism.
Of the hemodynamic variables that need attention include the counting of shunt fraction Q2
/ Qt and A-aDO2 or the oxygen difference between alveolar and arterial. The direct flow of the
pulmonary artery catheter is a therapeutic change in shock sufferers with modification of Starling's
law. In general, it is used given that the mean pulmonary artery pressure of about 5- 10mmHg is
greater than the pulmonary capillary wedge pressure (PCWP), and the pulmonary arterial diastolic
pressure is approximately 0-3mmHg greater than PCWP. PCWP is almost identical with left atrial
pressure or diastolic final pressure except in cases with mitral stenosis, where the left ventricular
end diastolic pressure (LVEDP) can not be determined or estimated from pulmonary capillary
wedge pressure (PCWP). Cardiac output may also be demonstrated by using thermodilatory
techniques if there is no intracardiac shunt (left to right or right to left).

Central Vein Pressure

Interpreting Central Venous Pressure (CVP) separately on the shock has a small value of
significance. Central venous pressure response to fluids is questionable, although important as a
guide in therapy. If the central venous pressure changes little or does not change with the increase
in pulse pressure after fluid administration, subsequent fluid administration may be indicated. If
CVP increases after fluid bolus or doubt, subsequent fluid administration may be
discontinued and to achieve the desired blood pressure, need to be pharmacologically or
otherwise.

Pulmonary Arterial Diastolic Pressure (PAdP)

PAdP is usually worth about 1-2mmHg greater than pulmonary capillary pressure (PCWP) in
the absence of pulmonary hypertension. If PAdP is reduced PCWP greater than 5mmHg, it means
pulmonary hypertension. PAdP changes are used to assess the benefits of the effects of fluid
therapy on shock.

Lactate levels
Monitoring arterial lactate levels is important in shock and associated with prognosis. In shock,
lactate levels increase and the lactate-pyruvate ratio also increases. Arterial blood lactate levels
are greater than 2.5mM / L, statistically the likelihood of survival decreases dramatically and at
4.5mM / L, the chance of survival is only about 50%. When more than 7.0mM / L the chance to
survive less than 10%.
Patients who can be rescued from shock seem to have low lactate levels compared with those
that do not and also appear to decrease lactic acid at least 10% per hour immediately after therapy,
while patients who can not be saved by therapy, lactate levels do not decrease. The level of lactate
is expressed in milligrams of milliliters or milliliters of perliter. Apparently, lactate levels may be
measured from arterial blood or from a central vein of the pulmonary artery with the same degree
of accuracy. One study showed that there was no correlation between arterial blood lactate levels
and oxygen delivery changes in septic shock or non septic shock. However, continuous monitoring
of lactate levels is very useful to know the severity of shock.
 SHOCK IN ADULT

A-22 year old male presents following a motorcycle crash. He complains of the inability to move
or feel his legs. His blood pressure is 80/50 mm Hg, heart rate is 100, respiratory rate is 20.
GCS is 15. Temp 37 Oxygen is 99%on 2L nasal prongs. Chest X-ray, pelvic X-ray, FAST are
normal. Extremities are normal.
1. What the diagnose
Jawaban :
Kata kunci :
- Motorcycle crash : kecelakaan motor (penyebab shock)
- Tidak mampu merasakan dan menggerakkan kaki : paraplegia
- BP 80/50 mmHg : hipotensi
- HR 100x/min : normal
- RR 20x/min : normal
- GCS 15 : sadar, no penurunan kesadaran
- Temp 37 : normal
- O2 99% 2L nasal prongs
- Chest x ray, pelvic x ray, fast normal, ekstremitas normal
Dx : syok spinal
Manifestasi Klinis Syok Spinal

 Paralisis flaksid di bawah tingkat cedera

 Tak adanya sensasi kutan. dan proprioseptif
 Hipotensi dan bradikardI
 Tak adanya aktivitas refleks di bawah tingkat cedera; ini dapat menyebabkan retensi urine, paralisis usus
dan ileus
 Kehilangan kontrol suhu;
vasodilatasi dan ketidakmampuan untuk menggigil membuat ini sulit bagi pasien untuk mengubah panas
dalam lingkungan dingin, dan ketidakmampuan untuk berkeringat mencegah pendinginan normal pada
lingkungan panas
 Penampakan ulang refleks yang telah ditekan setelah cedera adalah tanda bahwa syok spinal membaik

2. Describe the emergency problem of the patient

Jawaban :
KOMPLIKASI
- Neurogenik shock.
- Hipoksia.
- Gangguan paru-paru
- Instabilitas spinal
- Orthostatic Hipotensi
- Ileus Paralitik
- Infeksi saluran kemih
- Kontraktur
- Dekubitus
- Inkontinensia blader
- Konstipasi
3. How the management
Jawaban :
Prinsip-prinsip utama penatalaksanaan traumaspinal:
 1. Immobilisasi
Tindakan immobilisasi harus sudah dimulai dari tempatkejadian/kecelakaan sampai ke unit gawat darurat.. Yang pertama
ialahimmobilisasi dan stabilkan leher dalam posisi normal; denganmenggunakan ’cervical collar’. Cegah agar leher tidak terputar
(rotation).Baringkan penderita dalam posisi terlentang (supine) pada tempat/alasyang keras. Pasien diangkat/dibawa dengan cara
”4 men lift” ataumenggunakan ’Robinson’s orthopaedic stretcher’.

1. Stabilisasi Medis
Terutama sekali pada penderita tetraparesis/etraplegia:

1. Periksa vital signs

2. Pasang ’nasogastric tube’

3. Pasang kateter urind.

4. Segera normalkan ’vital signs’.

Pertahankan tekanan darah yang normal dan perfusi jaringan yang baik. Berikan oksigen, monitor produksi urin, bila perlu
monitor AGD(analisa gas darah), dan periksa apa ada neurogenic shock. Pemberianmegadose Methyl Prednisolone Sodium
Succinate dalam kurun waktu 6 jam setaleh kecelakaan dapat memperbaiki konntusio medula spinalis.

1. Mempertahankan posisi normal vertebra (”Spinal Alignment”)

Bila terdapat fraktur servikal dilakukan traksi dengan Cruthfield tongatau Gardner-Wells tong dengan beban 2.5 kg perdiskus. Bila
terjadidislokasi traksi diberikan dengan beban yang lebih ringan, beban ditambahsetiap 15 menit sampai terjadi reduksi.

1. Dekompresi dan Stabilisasi Spinal

Bila terjadi ’realignment’ artinya terjadi dekompresi. Bila’realignment’ dengan cara tertutup ini gagal maka dilakukan
’openreduction’ dan stabilisasi dengan ’approach’anterior atau posterior.

1. Rehabilitasi.
Rehabilitasi fisik harus dikerjakan sedini mungkin. Termasuk dalam program ini adalah ’bladder training’, ’bowel training’, latihan
otot pernafasan, pencapaian optimal fungsi – fungsi neurologik dan programkursi roda bagi penderita paraparesis/paraplegia.

1. J. Pengkajian Keperawatan

1. Primary Survey

1. Airway
Adanya sumbatan jalan nafas/obstruksi/adanya penumpukan sekret akibat kelemahan reflek batuk.
 1. Breathing
Suara nafas, RR, pernafasan, irama dan jenis pernafsan.

1. Circulation
Tekanan darah normal/meningkat/menurun, akral, sianosis, capillary refil.

1. Disability
Kesadaran, GCS, pupil (diameter dan ukuran — isokor), reflek cahaya, AVPU (Alert, Verbal, Pain, Unresponsive).

1. Exposure
Suhu dan ada atau tidaknya jejas

PENATALAKSANAAN CEDERA MEDULA SPINALIS (FASE AKUT)

1) Terapi dilakukan untuk mempertahankan fungsi neurologis yang masih ada, memaksimlkan
pemulihan neurologis, tindakan atas cidera lain, yang menyertai, mencegah, serta mengobati
komplikasi dan kerusakan neural lebih lanjut. Reabduksi atas subluksasi (dislokasi sebagian pada
sendi di salah satu tulang-ed). Untuk mendekompresi koral spiral dan tindakan imobilisasi tulang
belakang untuk melidungi koral spiral.
2) Operasi lebih awal sebagai indikasi dekompresi neural, fiksasi internal, atau debrideben luka
terbuka.
3) Fikasi internal elekif dilakukan pada klien dengan ketidakstabilan tulang belakang, cidera ligaemn
tanpa tanpa fraktur, deformitas tulang belakang progresif, cidera yang tak dapat direbduksi, dan
fraktur non-union.
4) Terapi steroid, nomidipin, atau dopamine untuk perbaiki aliran darah koral spiral. Dosis tertinggi metil
prednisolon/bolus adalah 3mg/kgBB diikuti 5,4 mg/kgBB/jam untuk 23 jam berikutnya. Bila diberikan
dalam 8 jam sejak cedera akan memperbaiki pemulihan neurologis. Gangliosida mungkin juga akan
memperbaiki pemulihan setelah cedera koral spiral.
5) Penilaian keadaan neurologis setiap jam, termasuk pengamatan fungsi sensorik, motorik, dan
penting untuk melacak deficit yang progresif atau asenden.
6) Mempertahankan perfusi jaringan yang adekuat, fungsi ventilasi, dan melacak keadaan
dekompensasi.
7) Pengelolaan cedera stabil tanpa deficit neurologis seperti angulasi atau baji dari bahan luas tulang
belakang, fraktr psoses transverses, spinosus, dan lainnya, tindakannya simptomatis (istirahat baring
hingga nyeri berkurang), imobilisasi dengan fisioterapi untuk pemulihan kekuatan otot secara
bertahap.
8) Cedera tak stabil disertai deficit neurologis. Bila terjadi pergeseran, fraktur memerlukan reabduksi
dan posisi yang sudah baik harus dipertahankan.
a) Metode reabduksi antara lain :
 Transaksi memakai sepit (tang) metal yang dipasang pada tengkorak. Beban 20kg tergantung dari tingkat ruas tulang
belakang, ulai sekitar 2,5 kg pada fraktur C1.
 Manipulasi dengan anestesi umum
 Reabduksi terbuka melalui operasi
b) Metode imobilisasi antara lain :
  Ranjang khusus, rangka, atau selubung plester.
 Transaksi tengkorak perlu beban sedang untuk memperahankan cedera yang sudah direabduksi.
 Plester paris dan splin eksternal lain.
 Operasi.
9) Cedera stabil disertai deficit neurologis. Bila fraktur stabil, kerusakan neurologis disebabkan oleh:
a. Pergeseran yang cukup besar yang terjadi saat cedera menyebabkan trauma langsung terhadap koral spiral atau
kerusakan vascular.
b. Tulang belakang yang sebetulnya sudah rusak akibat penyakit sebelumnya seperti spondiliosis servikal.
c. Fragmen tulang atau diskus terdorong ke kanal spiral.
10) Pengelolaan kelompok ini tergantung derajat kerusakan neurologis yang tampak pada saat pertama kali diperiksa:
1. Transeksi neurologis lengkap terbaik dirawat konservatif
2. Cedera di daerah servikal, leher di mobilisasi dengan kolar atau sepit (kapiler) dan di beri metal
prednisolon.
3. Pmeriksaan penunjang MRI.
4. Cedera neurologis tak lengkap konservatif.
5. Bila terdapat atau didasari kerusakan adanya spondiliosis servikal, ttraksi tengkorak, dan metal
prednisolon.
6. Bedah bila spondiliosis sudah ada sebelumnya.
7. Bila tak ada perbaikan atau ada perbaikan tetapi keadaan memburuk maka lakukan mielografi.
8. Cedera tulang tak stabil.
9. Bila lesinya total, dilakukan reabduksi yang diikuti imobilisasi. Melindungi imobiisasi seperti
penambahan perawatan paraplegia.
10. Bila deficit neurologis tak lengkap, dilakukan reabduksi, diikuti imobilisasi untuk sesuai jenis
cederanya.
11. Bila diperlukan operasi dekompresi kanal spiral dilakukan pada saat yang sama.
12. Cedera yang menyertai dan komplikasi:
 cedera mayor berupa cedera kepala atau otak, toraks, berhubungan dengan ominal, dan vascular.
 cedera berat yang dapat menyebabkan kematian, aspirasi, dan syok. (Fransisca B. Batticaca 2008).

A-56 years male admitted to the ICU for 1 week initially treated patients with symptoms of
urinary tract infections. Patient suddenly loss of consciousness followed by shortness
followed decreased urine output. On Physical examination are BP 90/50 pulse 120 RR 30 temp
40
1. Diagnose for ths patient
Jawaban :
Kata kunci :
- Usia : 56 th – tua
- ICU 1 minggu
- Urinary tract infection
- Suddenly loss of consciousness
- Decreased urine ouput
- BP : 90/50 = hipotensi, perlu tahu gimana profil hemodinamiknya apakah akral dingin? Kl iya
hipoperfusi
- HR : 120x/min = takikardi (normal = 60-100x/min)
- RR : 30x/min = takipnea (normal = 12-20x/min)
- Temp : 40 = suhu tubuh tinggi : hyperthermia
Diagnosis = syok sepsis
2. Decribe the management
 Jawaban :

 Tata laksana syok sepik meliputi banyak factor yang harus dipenuhi:
o Perbaikan Hemodinamik --> Banyak pasien syok septik yang mengalami penurunan
volume intravaskuler, sebagai respon pertama harus diberikan cairan jika terjadi penurunan tekanan
darah. Cairan koloid dan kristaloid diberikan. Jika disertai anemia berat perlu transfusi darah dan
CVP dipelihara antara 10-12 mmHg. Untuk mencapai cairan yang adekuat pemberian pertama 1 L-
1,5 L dalam waktu 1-2 jam. Tujuan resusitasi pasien dengan sepsis berat atau yang mengalami
hipoperfusi dalam 6 jam pertama adalah CVP 8-12 mmHg, MAP >65 mmHg, urine >0.5 ml/kg/jam dan
saturasi oksigen >70%. Bila dalam 6 jam resusitasi, saturasi oksigen tidak mencapai 70% dengan
resusitasi cairan dengan CVP 8-12 mmHg, maka dilakukan transfusi PRC untuk mencapai hematokrit
>30% dan/atau pemberian dobutamin (dosis 5-10 μg/kg/menit sampai maksimal 20
μg/kg/menit). Dopamin diberikan bila sudah tercapai target terapi cairan, yaitu MAP 60mmHg
atau tekanan sistolik 90-110 mmHg. Dosis awal adalah 2-5 μmg/Kg BB/menit. Bila dosis ini gagal
meningkatkan MAP sesuai target, maka dosis dapat di tingkatkan sampai 20 μg/ KgBB/menit. Bila
masih gagal, dosis dopamine dikembalikan pada 2-5 μmg/Kg BB/menit, tetapi di kombinasi
dengan levarterenol (norepinefrin). Bila kombinasi kedua vasokonstriktor masih gagal, berarti
prognosisnya buruk sekali. Dapat juga diganti dengan vasokonstriktor lain (fenilefrin atau
epinefrin).
o Pemakaian Antibiotik --> Setelah diagnosa sepsis ditegakkan, antibiotik harus
segera diberikan, dimana sebelumnya harus dilakukan kultur darah, cairan tubuh, dan eksudat.
Pemberian antibiotik tak perlu menunggu hasil kultur. Untuk pemilihan antibiotik diperhatikan
dari mana kuman masuk dan dimana lokasi infeksi, dan diberikan terapi kombinasi untuk gram
positif dan gram negatif. Terapi antibiotik intravena sebaiknya dimulai dalam jam pertama sejak
diketahui sepsis berat, setelah kultur diambil. Terapi inisial berupa satu atau lebih obat yang
memiliki aktivitas melawan patogen bakteri atau jamur dan dapat penetrasi ke tempat yang
diduga sumber sepsis. Oleh karena pada sepsis umumnya disebabkan oleh gram negatif,
penggunaan antibiotik yang dapat mencegah pelepasan endotoksin seperti karbapenem memiliki
keuntungan, terutama pada keadaan dimana terjadi proses inflamasi yang hebat akibat
pelepasan endotoksin, misalnya pada sepsis berat dan gagal multi organ. Pemberian antibiotik
kombinasi juga dapat dilakukan dengan indikasi :
 Sebagai terapi pertama sebelum hasil kultur diketahui
 Pasien yang dapat imunosupresan, khususnya dengan netropeni
 dibutuhkan efek sinergi obat untuk kuman yang sangat patogen (pseudomonas
aeruginosa, enterococcus).'
o Pemberian antimikrobial dinilai kembali setelah 48-72 jam berdasarkan data
mikrobiologi dan klinis. Sekali patogen penyebab teridentifikasi, tidak ada bukti bahwa terapi
kombiasi lebih baik daripada monoterapi

 Terapi suportif
o Oksigenasi --> Pada keadaan hipoksemia berat dan gagal napas bila disertai dengan
penurunan kesadaran atau kerja ventilasi yang berat, ventilasi mekanik segera dilakukan.
o Terapi cairan
 Hipovolemia harus segera diatasi dengan cairan kristaloid (NaCl 0.9% atau
ringer laktat) maupun koloid
 Pada keadaan albumin rendah (<2 g/dL) disertai tekanan hidrostatik
melebihi tekanan onkotik plasma, koreksi albumin perlu diberikan
 Transfusi PRC diperlukan pada keadaan perdarahan aktif atau bila kadar Hb
rendah pada kondisi tertentu, seperti pada iskemia miokard dan renjatan septik. Kadar Hb yang
akan dicapai pada sepsis masih kontroversi antara 8-10 g/dL.
o Vasopresor dan Inotropik --> Sebaiknya diberikan setelah keadaan hipovolemik
teratasi dengan pemberian cairan adekuat, akan tetapi pasien masih hipotensi. Vasopresor
diberikan mulai dosis rendah dan dinaikkan (titrasi) untuk mencapai MAP 60 mmHg atau tekanan
darah sistolik 90mmHg. Dapat dipakai dopamin >8μg/kg.menit,norepinefrin 0.03-
1.5μg/kg.menit, phenylepherine 0.5-8μg/kg/menit atau epinefrin 0.1-0.5μg/kg/menit. Inotropik
dapat digunakan: dobutamine 2-28 μg/kg/menit, dopamine 3-8 μg/kg/menit, epinefrin 0.1-0.5
μg/kg/menit atau fosfodiesterase inhibitor (amrinone dan milrinone)
o Bikarbonat --> Secara empirik bikarbonat diberikan bila pH <7.2 atau serum
bikarbonat <9 mEq/L dengan disertai upaya untuk memperbaiki keadaan hemodinamik
o Disfungsi renal --> Akibat gangguan perfusi organ. Bila pasien
hipovolemik/hipotensi, segera diperbaiki dengan pemberian cairan adekuat, vasopresor dan
inotropik bila diperlukan. Dopamin dosis renal (1-3 μg/kg/menit) seringkali diberikan untuk
mengatasi gangguan fungsi ginjal pada sepsis, namun secara evidence based belum terbukti.
Sebagai terapi pengganti gagal ginjal akut dapat dilakukan hemodialisis maupun hemofiltrasi
kontinu.
o Nutrisi --> Pada metabolisme glukosa terjadi peningkatan produksi (glikolisis,
glukoneogenesis), ambilan dan oksidasinya pada sel, peningkatan produksi dan penumpukan
laktat dan kecenderungan hiperglikemia akibat resistensi insulin. Selain itu terjadi lipolisis,
hipertrigliseridemia dan proses katabolisme protein. Pada sepsis, kecukupan nutrisi: kalori (asam
amino), asam lemak, vitamin dan mineral perlu diberikan sedini mungkin.
o Kontrol gula darah --> Terdapat penelitian pada pasien ICU, menunjukkan terdapat
penurunan mortalitas sebesar 10.6-20.2% pada kelompok pasien yang diberikan insulin untuk
mencapai kadar gula darah antara 80-110 mg/dL dibandingkan pada kelompok dimana insulin
baru diberikan bila kadar gula darah >115 mg/dL. Namun apakah pengontrolan gula darah
tersebut dapat diaplikasikan dalam praktek ICU, masih perlu dievaluasi, karena ada risiko
hipoglikemia.
o Gangguan koagulasi --> Proses inflamasi pada sepsis menyebabkan terjadinya
gangguan koagulasi dan DIC (konsumsi faktor pembekuan dan pembentukan mikrotrombus di
sirkulasi). Pada sepsis berat dan renjatan, terjadi penurunan aktivitas antikoagulan dan supresi
proses fibrinolisis sehingga mikrotrombus menumpuk di sirkulasi mengakibatkan kegagalan organ.
Terapi antikoagulan, berupa heparin, antitrombin dan substitusi faktor pembekuan bila
diperlukan dapat diberikan, tetapi tidak terbukti menurunkan mortalitas.
o Kortikosteroid --> Hanya diberikan dengan indikasi insufisiensi adrenal.
Hidrokortison dengan dosis 50 mg bolus IV 4x/hari selama 7 hari pada pasien dengan renjatan
septik menunjukkan penurunan mortalitas dibandingkan kontrol. Keadaan tanpa syok,
kortikosteroid sebaiknya tidak diberikan dalam terapi sepsis.
 A 67 year man unconcious felt down from 5 meters of tree, there are stab wound in posteror
of head. The backbone are fuly pain and can’t move legs. On Physical examination are BP
80/50 pulse 88RR 20 temp 37. Paraparese found in lower extremitas
1. what is the diagnose
jawaban :
kata kunci :
- 67 tahun
- tidak sadar
- jatuh 5 meter dari pohon
- stab wound di posterior kepala
- backbone nyeri
- tidak mampu menggerakkan kaki
- BP 80/50 mmHg
- HR 88x/min
- RR 20x/min
- Temp 37
- Paraparese di lower extremitas
Dx :
2. what the supporting examination do you need?
3. describe the management this patient

A 24 year woman arrives in ER with dyspneau and skin rash on her chest and abdominal, the
woman unconsious and her lip was thiked and numbness, history of allergic was denied. On
Physical examination are BP 100/90 Pulse 100x/menit RR 37x/mnt temp 37, wheezing +/+ on right
and left pulmo, rhonki -/- angioodema was found.

1. Diagnose the patient

2. The different diagnose are
3. can describe the algorithm of management
4. Describe the Hypersensitivity Reaction

A 22-year-old man sustains a shotgun wound to the left shoulder. His blood pressure is initially
80/40. After two liters of Ringer's lactate solution his blood pressure increases to 122/84. His
pulse rate is now 100 beats per minute and his respiratory rate is 28 breaths per minute.
His breath sounds are decreased in the left hemithorax,
1. Diagnose and the differential diagnosis
Jawaban :
Kata kunci :
- Shotgun wound
- BP I 80/40 mmHg – BP II 122/84 (setelah diberi cairan ringer laktat)
- HR 100x/min :normal
- RR 28x/min : takipnea (normal : 12-20x/min)
- Breath sound decreased pada left hemithorax
b. Dx : syok obstruktif
Syok obstruktif (gangguan kontraksi jantung akibat di luar jantung): (a) Tamponade jantung; (b)
Pneumotorak; dan (c) Emboli paru.
Syok Obstruktif.
 Syok obstruktif adalah syok yang diakibatkan oleh gangguan pengisian pada ventrikel kanan maupun
kiri yang dalam keadaan berat bisa menyebabkan penurunan Cardiaac Output. Hal ini biasa terjadi
pada obstruksi vena cava, emboli pulmonal, pneumotoraks, gangguan pada pericardium (misalnya :
tamponade jantung) ataupun berupa atrial myxoma.

Pernapasan cepat & dangkal

2. Nadi capat dan lemah
3. Akral pucat, dingin & lembab
4. Sianosis : bibir, kuku, lidah & cuping hidung
5. Pandangan hampa & pupil melebar

2. Describe the management

Jawaban :
ketika datang pasien dengan klinis syok hal pertama yang
harus dilakukan adalah evaluasi ABC dan memberikan
tatalaksana umum pasien syok. Sembari melakukan berbagai
pemeriksaan fisik dan penunjang, selanjutnya diidentifikasi
diagnosis penyebab syok. Setelah berhasil mengidentifikasi
apakah pasien mengalami syok hipovolemik atau syok
 kardiogenik (atau syok yang lain) selanjutnya diberikan
tatalaksana spesifik syok.
Syok Obstruktif
- Lakukan penanganan syok secara umum.
- Penanganan sesuai dengan penyebab :
Tamponade :Pericardiosintesis
Emboli paru : Trombokinase