1

CHAPTER I
INTRODUCTION

Shock is the clinical syndrome that results from inadequate tissue perfusion.
Irrespective of cause, the hypoperfusion-induced imbalance between the delivery of
and requirements for oxygen and substrate leads to cellular dysfunction. The cellular
injury created by the inadequate delivery of oxygen and substrates also induces the
production and release of damage-associated molecular patterns (DAMPs or "danger
signals") and inflammatory mediators that further compromise perfusion through
functional and structural changes within the microvasculature. This leads to a vicious
cycle in which impaired perfusion is responsible for cellular injury that causes
maldistribution of blood flow, further compromising cellular perfusion; the latter
ultimately causes multiple organ failure (MOF) and, if the process is not interrupted,
leads to death.

The clinical manifestations of shock are also the result, in part, of autonomic
neuroendocrine responses to hypoperfusion as well as the breakdown in organ
function induced by severe cellular dysfunction.1 Shock is a life-threatening condition
that occurs when the body is not getting enough blood flow. Lack of blood flow
means that the cells and organs do not get enough oxygen and nutrients to function
properly. Many organs can be damaged as a result. Shock requires immediate
treatment and can get worse very rapidly.

As many 1 in 5 people who suffer shock will die from it. Shock can be caused by any
condition that reduces blood flow, including, Heart problems (such as heart
attack or heart failure),Low blood volume (as with
heavy bleeding or dehydration,Changes in blood vessels (as with infection or severe
allergic reactions. Certain medicines that significantly reduce heart function or blood
pressure.

Shock is often associated with heavy external or internal bleeding from a serious
injury. Spinal injuries can also cause shock. In this paper we will discuss about
hypovoleic shock and cardiogenic shock. Hypovolemic shock is an emergency
condition in which severe blood or fluid loss makes the heart unable to pump enough
blood to the body. This type of shock can cause many organs to stop working.
Cardiogenic shock is when the heart has been damaged so much that it is unable to
supply enough blood to the organs of the body. A person in shock has extermelly low
blood pressure depends on which shock the person had.

Typically the symtomps, in adults, the systolic arterial pressure is less than 90 mm Hg
or the mean arterial pressure is less than 70 mm Hg, with associated tachycardia.
Second, there are clinical signs of tissue hypoperfusion, which are apparent through
the three windows of the body, cutaneous (skin that is cold and clammy, with
vasoconstriction and cyanosis, findings that are most evident in low-flow states), renal
(urine output of <0.5 ml per kilogram of body weight per hour), and neurologic
2

(altered mental state, which typically includes obtundation, disorientation, and

confusion). Third, hyperlactatemia is typically present, indicating abnormal cellular
oxygen metabolism. The normal blood lactate level is approximately 1 mmol per liter,
but the level is increased (>1.5 mmol per liter) in acute circulatory failure.Both of
them are a serious condition that has to be known immediatelly and treat in a proper
fastest way. (2)
3

CHAPTER II

LITERATUR REVIEW

Pathogenesis and organ response

Microcirculation

Normally when cardiac output falls, systemic vascular resistance rises to maintain a
level of systemic pressure that is adequate for perfusion of the heart and brain at the
expense of other tissues such as muscle, skin, and especially the gastrointestinal (GI)
tract. Systemic vascular resistance is determined primarily by the luminal diameter of
arterioles. The metabolic rates of the heart and brain are high, and their stores of
energy substrate are low. These organs are critically dependent on a continuous supply
of oxygen and nutrients, and neither tolerates severe ischemia for more than brief
periods (minutes). Autoregulation (i.e., the maintenance of blood flow over a wide
range of perfusion pressures), is critical in sustaining cerebral and coronary perfusion
despite significant hypotension. However, when MAP drops to 60 mmHg, blood flow
to these organs falls, and their function deteriorates.

Arteriolar vascular smooth muscle has both - and -adrenergic receptors. The 1
receptors mediate vasoconstriction, while the 2 receptors mediate vasodilation.
Efferent sympathetic fibers release norepinephrine, which acts primarily on 1
receptors as one of the most fundamental compensatory responses to reduced
perfusion pressure. Other constrictor substances that are increased in most forms of
shock include angiotensin II, vasopressin, endothelin 1, and thromboxane A2. Both
norepinephrine and epinephrine are released by the adrenal medulla, and the
concentrations of these catecholamines in the bloodstream rise. Circulating
vasodilators in shock include prostacyclin [prostaglandin (PG) I2], nitric oxide (NO),
and, importantly, products of local metabolism such as adenosine that match flow to
the tissue's metabolic needs. The balance between these various vasoconstrictors and
vasodilators influences acting upon the microcirculation determines local perfusion.

Transport to cells depends on microcirculatory flow; capillary permeability; the

diffusion of oxygen, carbon dioxide, nutrients, and products of metabolism through
the interstitium; and the exchange of these products across cell membranes.
Impairment of the microcirculation that is central to the pathophysiologic responses in
the late stages of all forms of shock, results in the derangement of cellular metabolism
that is ultimately responsible for organ failure.

The endogenous response to mild or moderate hypovolemia is an attempt at restitution

of intravascular volume through alterations in hydrostatic pressure and osmolarity.
Constriction of arterioles leads to reductions in both the capillary hydrostatic pressure
and the number of capillary beds perfused, thereby limiting the capillary surface area
across which filtration occurs. When filtration is reduced while intravascular oncotic
pressure remains constant or rises, there is net reabsorption of fluid into the vascular
bed, in accord with Starling's law of capillary interstitial liquid exchange. Metabolic
changes (including hyperglycemia and elevations in the products of glycolysis,
4

lipolysis, and proteolysis) raise extracellular osmolarity, leading to an osmotic

gradient that increases interstitial and intravascular volume at the expense of
intracellular volume.

Table I

Cellular Responses

Interstitial transport of nutrients is impaired in shock, leading to a decline in

intracellular high-energy phosphate stores. Mitochondrial dysfunction and uncoupling
of oxidative phosphorylation are the most likely causes for decreased amounts of
adenosine triphosphate (ATP). As a consequence, there is an accumulation of
hydrogen ions, lactate, and other products of anaerobic metabolism. As shock
progresses, these vasodilator metabolites override vasomotor tone, causing further
hypotension and hypoperfusion. Dysfunction of cell membranes is thought to
represent a common end-stage pathophysiologic pathway in the various forms of
shock. Normal cellular transmembrane potential falls, and there is an associated
increase in intracellular sodium and water, leading to cell swelling that interferes
further with microvascular perfusion. In a preterminal event, homeostasis of calcium
via membrane channels is lost with flooding of calcium intracellularly and a
concomitant extracellular hypocalcemia. There is also evidence for a widespread but
5

selective apoptotic (programmed cell-death) loss of cells, contributing to organ and

immune failure.

Neuroendocrine Response

Hypovolemia, hypotension, and hypoxia are sensed by baroreceptors and

chemoreceptors that contribute to an autonomic response that attempts to restore
blood volume, maintain central perfusion, and mobilize metabolic substrates.
Hypotension disinhibits the vasomotor center, resulting in increased adrenergic output
and reduced vagal activity. Release of norepinephrine from adrenergic neurons
induces significant peripheral and splanchnic vasoconstriction, a major contributor to
the maintenance of central organ perfusion, while reduced vagal activity increases the
heart rate and cardiac output. Loss of vagal activity is also recognized to upregulate
the innate immunity inflammatory response. The effects of circulating epinephrine
released by the adrenal medulla in shock are largely metabolic, causing increased
glycogenolysis and gluconeogenesis and reduced pancreatic insulin release. However,
epinephrine also inhibits production and release of inflammatory mediators through
stimulation of -adrenergic receptors on innate immune cells.

Severe pain or other stresses cause the hypothalamic release of adrenocorticotropic

hormone (ACTH). This stimulates cortisol secretion that contributes to decreased
peripheral uptake of glucose and amino acids, enhances lipolysis, and increases
gluconeogenesis. Increased pancreatic secretion of glucagon during stress accelerates
hepatic gluconeogenesis and further elevates blood glucose concentration. These
hormonal actions act synergistically to increase blood glucose for both selective tissue
metabolism and the maintenance of blood volume. Many critically ill patients have
recently been shown to exhibit low plasma cortisol levels and an impaired response to
ACTH stimulation, which is linked to a decrease in survival. The importance of the
cortisol response to stress is illustrated by the profound circulatory collapse that
occurs in patients with adrenal cortical insufficiency (Chap. 342).

Renin release is increased in response to adrenergic discharge and reduced perfusion

of the juxtaglomerular apparatus in the kidney. Renin induces the formation of
angiotensin I that is then converted to angiotensin II, an extremely potent
vasoconstrictor and stimulator of aldosterone release by the adrenal cortex and of
vasopressin by the posterior pituitary. Aldosterone contributes to the maintenance of
intravascular volume by enhancing renal tubular reabsorption of sodium, resulting in
the excretion of a low-volume, concentrated, sodium-free urine. Vasopressin has a
direct action on vascular smooth muscle, contributing to vasoconstriction, and acts on
the distal renal tubules to enhance water reabsorption.

Cardiovasular Response

Three variablesventricular filling (preload), the resistance to ventricular ejection

(afterload), and myocardial contractilityare paramount in controlling stroke volume
(Chap. 224). Cardiac output, the major determinant of tissue perfusion, is the product
of stroke volume and heart rate. Hypovolemia leads to decreased ventricular preload
that in turn reduces the stroke volume. An increase in heart rate is a useful but limited
compensatory mechanism to maintain cardiac output. A shock-induced reduction in
6

myocardial compliance is frequent, reducing ventricular end-diastolic volume and

hence stroke volume at any given ventricular filling pressure. Restoration of
intravascular volume may return stroke volume to normal but only at elevated filling
pressures. Increased filling pressures stimulate release of brain natriuretic peptide
(BNP) to secrete sodium and volume to relieve the pressure on the heart. Levels of
BNP correlate with outcome following severe stress. In addition, sepsis, ischemia,
myocardial infarction (MI), severe tissue trauma, hypothermia, general anesthesia,
prolonged hypotension, and acidemia may all also impair myocardial contractility and
reduce the stroke volume at any given ventricular end-diastolic volume. The
resistance to ventricular ejection is significantly influenced by the systemic vascular
resistance, which is elevated in most forms of shock. However, resistance is depressed
in the early hyperdynamic stage of septic shock or neurogenic shock, thereby initially
allowing the cardiac output to be maintained or elevated.

The venous system contains nearly two-thirds of the total circulating blood volume,
most in the small veins, and serves as a dynamic reservoir for autoinfusion of blood.
Active venoconstriction as a consequence of -adrenergic activity is an important
compensatory mechanism for the maintenance of venous return and therefore of
ventricular filling during shock. On the other hand, venous dilation, as occurs in
neurogenic shock, reduces ventricular filling and hence stroke volume and potentially
cardiac output.

Pulmonary Response

The response of the pulmonary vascular bed to shock parallels that of the systemic
vascular bed, and the relative increase in pulmonary vascular resistance, particularly
in septic shock, may exceed that of the systemic vascular resistance, leading to right
heart failure. Shock-induced tachypnea reduces tidal volume and increases both dead
space and minute ventilation. Relative hypoxia and the subsequent tachypnea induce a
respiratory alkalosis. Recumbency and involuntary restriction of ventilation secondary
to pain reduce functional residual capacity and may lead to atelectasis. Shock and, in
particular, resuscitation-induced oxidant radical generation, is recognized as a major
cause of acute lung injury and subsequent acute respiratory distress syndrome
(ARDS). These disorders are characterized by noncardiogenic pulmonary edema
secondary to diffuse pulmonary capillary endothelial and alveolar epithelial injury,
hypoxemia, and bilateral diffuse pulmonary infiltrates. Hypoxemia results from
perfusion of underventilated and nonventilated alveoli. Loss of surfactant and lung
volume in combination with increased interstitial and alveolar edema reduces lung
compliance. The work of breathing and the oxygen requirements of respiratory
muscles increase.

Renal Response

Acute kidney injury, a serious complication of shock and hypoperfusion, occurs less
frequently than heretofore because of early aggressive volume repletion. Acute
tubular necrosis is now more frequently seen as a result of the interactions of shock,
sepsis, the administration of nephrotoxic agents (such as aminoglycosides and
7

angiographic contrast media), and rhabdomyolysis; the latter may be particularly

severe in skeletal muscle trauma. The physiologic response of the kidney to
hypoperfusion is to conserve salt and water. In addition to decreased renal blood flow,
increased afferent arteriolar resistance accounts for diminished glomerular filtration
rate (GFR) that together with increased aldosterone and vasopressin is responsible for
reduced urine formation. Toxic injury causes necrosis of tubular epithelium and
tubular obstruction by cellular debris with back leak of filtrate. The depletion of renal
ATP stores that occurs with prolonged renal hypoperfusion contributes to subsequent
impairment of renal function

Metabolic Derangements

During shock, there is disruption of the normal cycles of carbohydrate, lipid, and
protein metabolism. Through the citric acid cycle, alanine in conjunction with lactate,
which is converted from pyruvate in the periphery in the presence of oxygen
deprivation enhances the hepatic production of glucose. With reduced availability of
oxygen, the breakdown of glucose to pyruvate, and ultimately lactate, represents an
inefficient cycling of substrate with minimal net energy production. An elevated
plasma lactate/pyruvate ratio is preferable to lactate alone as a measure of anaerobic
metabolism and reflects inadequate tissue perfusion. Decreased clearance of
exogenous triglycerides coupled with increased hepatic lipogenesis causes a
significant rise in serum triglyceride concentrations. There is increased protein
catabolism as energy substrate, a negative nitrogen balance, and, if the process is
prolonged, severe muscle wasting.

Inflammatory Responses

Activation of an extensive network of proinflammatory mediator systems by the

innate immune system plays a significant role in the progression of shock and
contributes importantly to the development of multiple organ injury, dysfunction
(MOD), and failure (MOF). In those surviving the acute insult, there is a prolonged
endogenous counterregulatory response to "turn off" or balance the excessive
proinflammatory response. If balance is restored, the patient does well. If the response
is excessive, adaptive immunity is suppressed and the patient is highly susceptible to
secondary nosocomial infections, which may then drive the inflammatory response
and lead to delayed MOF.

Multiple humoral mediators are activated during shock and tissue injury. The
complement cascade, activated through both the classic and alternate pathways,
8

generates the anaphylatoxins C3a and C5a. Direct complement fixation to injured
tissues can progress to the C5-C9 attack complex, causing further cell damage.
Activation of the coagulation cascade causes microvascular thrombosis, with
subsequent fibrinolysis leading to repeated episodes of ischemia and reperfusion.
Components of the coagulation system (e.g., thrombin), are potent proinflammatory
mediators that cause expression of adhesion molecules on endothelial cells and
activation of neutrophils, leading to microvascular injury. Coagulation also activates
the kallikrein-kininogen cascade, contributing to hypotension.

Eicosanoids are vasoactive and immunomodulatory products of arachidonic acid

metabolism that include cyclooxygenase-derived prostaglandins (PGs) and
thromboxane A2, as well as lipoxygenase-derived leukotrienes and lipoxins.
Thromboxane A2 is a potent vasoconstrictor that contributes to the pulmonary
hypertension and acute tubular necrosis of shock. PGI2 and PGE2 are potent
vasodilators that enhance capillary permeability and edema formation. The cysteinyl
leukotrienes LTC4 and LTD4 are pivotal mediators of the vascular sequelae of
anaphylaxis, as well as of shock states resulting from sepsis or tissue injury. LTB 4 is a
potent neutrophil chemoattractant and secretagogue that stimulates the formation of
reactive oxygen species. Platelet-activating factor, an ether-linked, arachidonyl-
containing phospholipid mediator, causes pulmonary vasoconstriction,
bronchoconstriction, systemic vasodilation, increased capillary permeability, and the
priming of macrophages and neutrophils to produce enhanced levels of inflammatory
mediators.

Tumor necrosis factor (TNF-), produced by activated macrophages, reproduces many

components of the shock state, including hypotension, lactic acidosis, and respiratory
failure. Interleukin 1 (IL-1), originally defined as "endogenous pyrogen" and
produced by tissue-fixed macrophages, is critical to the inflammatory response. Both
are significantly elevated immediately following trauma and shock. IL-6, also
produced predominantly by the macrophage, has a slightly delayed peak response but
is the best single predictor of prolonged recovery and development of MOF following
shock. Chemokines such as IL-8 are potent neutrophil chemoattractants and activators
that upregulate adhesion molecules on the neutrophil to enhance aggregation,
adherence, and damage to the vascular endothelium. While the endothelium normally
produces low levels of NO, the inflammatory response stimulates the inducible
isoform of NO synthase (iNOS), which is overexpressed and produces toxic nitrosyl-
and oxygen-derived free radicals that contribute to the hyperdynamic cardiovascular
response and tissue injury in sepsis.

Multiple inflammatory cells, including neutrophils, macrophages, and platelets, are

major contributors to inflammation-induced injury. Margination of activated
neutrophils in the microcirculation is a common pathologic finding in shock, causing
secondary injury due to the release of toxic oxygen radicals, lipases, primarily PLA2,
and proteases. Release of high levels of reactive oxygen intermediates/species
(ROI/ROS) rapidly consumes endogenous essential antioxidants and generates diffuse
oxygen radical damage. Newer efforts to control ischemia/reperfusion injury include
treatment with carbon monoxide, hydrogen sulfide, or other agents to reduce oxidant
stress. Tissue-fixed macrophages produce virtually all major mediators of the
inflammatory response and orchestrate the progression and duration of the
inflammatory response. A major source of activation of the monocyte/macrophage is
9

through the highly conserved membrane toll-like receptors (TLRs) that recognize
DAMPs such as HMGB-1, and pathogen-associated molecular patterns (PAMPs) such
as endotoxins released following tissue injury, and by pathogenic microbial
organisms, respectively. Toll-like receptors also appear important for the chronic
inflammation seen in Crohn's disease, ulcerative colitis, and transplant rejection. The
variability in individual responses is a genetic predisposition that, in part, is due to
single nucleotide polymorphisms (SNPs) in genetic sequences affecting the function
and production of various inflammatory mediators.(1)

Tabel II

Hypovolemic Shock

This most common form of shock results either from the loss of red blood cell mass
and plasma from hemorrhage or from the loss of plasma volume alone due to
extravascular fluid sequestration or GI, urinary, and insensible losses. The signs and
symptoms of nonhemorrhagic hypovolemic shock are the same as those of
hemorrhagic shock, although they may have a more insidious onset. The normal
physiologic response to hypovolemia is to maintain perfusion of the brain and heart
while attempting to restore an effective circulating blood volume. There is an increase
in sympathetic activity, hyperventilation, collapse of venous capacitance vessels,
release of stress hormones, and an attempt to replace the loss of intravascular volume
through the recruitment of interstitial and intracellular fluid and by reduction of urine
output.

Mild hypovolemia (20% of the blood volume) generates mild tachycardia but
relatively few external signs, especially in a supine young patient (Table 270-5). With
10

moderate hypovolemia (2040% of the blood volume), the patient becomes

increasingly anxious and tachycardic; although normal blood pressure may be
maintained in the supine position, there may be significant postural hypotension and
tachycardia. If hypovolemia is severe (40% of the blood volume), the classic signs of
shock appear; the blood pressure declines and becomes unstable even in the supine
position, and the patient develops marked tachycardia, oliguria, and agitation or
confusion. Perfusion of the central nervous system is well maintained until shock
becomes severe. Hence, mental obtundation is an ominous clinical sign. The transition
from mild to severe hypovolemic shock can be insidious or extremely rapid. If severe
shock is not reversed rapidly, especially in elderly patients and those with comorbid
illnesses, death is imminent. A very narrow time frame separates the derangements
found in severe shock that can be reversed with aggressive resuscitation from those of
progressive decompensation and irreversible cell injury.

Table 2705. Hypovolemic Shock

Mild (<20% Blood Moderate (2040% Blood Severe (>40% Blood

Volume) Volume) Volume)
Cool extremities Same, plus: Same, plus:

Increased capillary Tachycardia Hemodynamic instability

refill time
Tachypnea Marked tachycardia
Diaphoresis
Oliguria Hypotension
Collapsed veins
Postural changes Mental status deterioration
Anxiety (coma)

Diagnosis

Hypovolemic shock is readily diagnosed when there are signs of hemodynamic

instability and the source of volume loss is obvious. The diagnosis is more difficult
when the source of blood loss is occult, as into the GI tract, or when plasma volume
alone is depleted. Even after acute hemorrhage, hemoglobin and hematocrit values do
not change until compensatory fluid shifts have occurred or exogenous fluid is
administered. Thus, an initial normal hematocrit does not disprove the presence of
significant blood loss. Plasma losses cause hemoconcentration, and free water loss
leads to hypernatremia. These findings should suggest the presence of hypovolemia.

It is essential to distinguish between hypovolemic and cardiogenic shock (Chap. 272)

because, while both may respond to volume initially, definitive therapy differs
significantly. Both forms are associated with a reduced cardiac output and a
compensatory sympathetic mediated response characterized by tachycardia and
elevated systemic vascular resistance. However, the findings in cardiogenic shock of
jugular venous distention, rales, and an S3 gallop distinguish it from hypovolemic
shock and signify that ongoing volume expansion is undesirable and may cause
further organ dysfunction.
11

Treatment: Hypovolemic Shock

Initial resuscitation requires rapid reexpansion of the circulating intravascular blood

volume along with interventions to control ongoing losses. In accordance with
Starling's law (Chap. 224), stroke volume and cardiac output rise with the increase in
preload. After resuscitation, the compliance of the ventricles may remain reduced due
to increased interstitial fluid in the myocardium. Therefore, elevated filling pressures
are frequently required to maintain adequate ventricular performance.

Volume resuscitation is initiated with the rapid infusion of either isotonic saline
(although care must be taken to avoid hyperchloremic acidosis from loss of
bicarbonate buffering capacity and replacement with excess chloride) or a balanced
salt solution such as Ringer's lactate (being cognizant of the presence of potassium
and potential renal dysfunction) through large-bore intravenous lines. Data,
particularly on severe traumatic brain injury (TBI), regarding benefits of small
volumes of hypertonic saline that more rapidly restore blood pressure are variable, but
tend to show improved survival thought to be linked to immunomodulation. No
distinct benefit from the use of colloid has been demonstrated, and in trauma patients
it is associated with a higher mortality, particularly in patients with TBI. The infusion
of 23 L of salt solution over 2030 min should restore normal hemodynamic
parameters. Continued hemodynamic instability implies that shock has not been
reversed and/or there are significant ongoing blood or other volume losses.
Continuing acute blood loss, with hemoglobin concentrations declining to 100 g/L (10
g/dL), should initiate blood transfusion, preferably as fully cross-matched recently
banked (<14 days old) blood. Resuscitated patients are often coagulopathic due to
deficient clotting factors in crystalloids and banked packed red blood cells (PRBCs).
Early administration of component therapy during massive transfusion [fresh-frozen
plasma (FFP) and platelets] approaching a 1:1 ratio of PRBC/FFP appears to improve
survival. In extreme emergencies, type-specific or O-negative packed red cells may be
transfused. Following severe and/or prolonged hypovolemia, inotropic support with
norepinephrine, vasopressin, or dopamine may be required to maintain adequate
ventricular performance but only after blood volume has been restored. Increases in
peripheral vasoconstriction with inadequate resuscitation leads to tissue loss and
organ failure. Once hemorrhage is controlled and the patient has stabilized, blood
transfusions should not be continued unless the hemoglobin is <~7g/dL. Studies have
demonstrated an increased survival in patients treated with this restrictive blood
transfusion protocol.

Successful resuscitation also requires support of respiratory function. Supplemental

oxygen should always be provided, and endotracheal intubation may be necessary to
maintain arterial oxygenation. Following resuscitation from isolated hemorrhagic
shock, end-organ damage is frequently less than following septic or traumatic shock.
This may be due to the absence of massive activation of the inflammatory innate
immune response and consequent nonspecific organ injury and failure.(1)
12

Cardiogenic Shock

Cardiogenic shock (CS) is characterized by systemic hypoperfusion due to severe

depression of the cardiac index [<2.2 (L/min)/m2] and sustained systolic arterial
hypotension (<90 mmHg) despite an elevated filling pressure [pulmonary capillary
wedge pressure (PCWP) >18 mmHg]. It is associated with in-hospital mortality
rates >50%. The major causes of CS are many , a few causes such as Acute
myocardial infarction, Papillary muscle/chordal rupture, Ventricular free wall rupture
with subacute tamponade, and Post cardiac arrest . Circulatory failure based on
cardiac dysfunction may be caused by primary myocardial failure, most commonly
secondary to acute myocardial infarction (MI) , and less frequently by
cardiomyopathy or myocarditis, cardiac tamponade, or critical valvular heart disease.

Pathophysiology

Systolic and diastolyc myocardial disfunction result in a reduction in ardiac output

and often pulmonary congestion. Systemic and coronary hypoperfusion occur
resulting in progressive ischemia. Although a number of compensatory mechanims
are activated in an attempt to support the circulation, these compensatory mechanisms
may become maladaptive and produce a worsening of hemodynamics. *Release of
inflammatory cytokines after myocardial infarction may lead to inducible nitric oxide
expression, excess nitric oxide, and inappropriate vasodilation. This causes further
reduction in systemic and coronary perfusion. A vicious spiral of progressive
myocardial dysfunction occurs that ultimately results in death if it is not interrupted.
LVEDP, left ventricular end diastolic pressure.
13

Table III
14

ALGORITHM Cardiogenic Shock

Revascularization

Early revascularization as shown in the SHould we emergently revascularize

Occluded Coronaries for cardiogenic shocK (SHOCK) trial is the most important
treatment strategy in CS complicating AMI.(3) Although the trial failed to meet the
primary endpoint (superiority of early revascularization over medical therapy on 30-
day mortality) there was a significant mortality reduction at longer follow-up of 1/2,
1, and 6 years.(4) The number needed to save one life by early revascularization in
comparison to initial medical stabilization is <8.
15

In current guidelines, early revascularization by either percutaneous coronary

intervention (PCI) or coronary artery bypass grafting (CABG) is a class 1B
recommendation. Even though application of early revascularization has markedly
increased in clinical practice, rates are still unsatisfactory ranging from 50 to 70% in
registries. Therefore, more efforts are needed to convince clinicians to recognize the
benefit of revascularization even if the associated risk is anticipated to be high such as
in the elderly or following resuscitation.

Fluids, vasopressors, inotropes

Irrespective of early revascularization, the basic treatment measures include initial

stabilization with volume expansion to obtain euvolaemia, vasopressors, and
inotropes plus additional therapy for the prevention or treatment of multiorgan system
dysfunction (MODS). Fluid administration in CS is mainly based on
pathophysiological considerations.

Despite the frequent use of catecholamines which are administered in 90% of

patients in CS,7 there is only limited evidence from randomized trials comparing
catecholamines in CS. Furthermore, despite beneficial effects on haemodynamics,
there are no randomized data showing a prognostic benefit. In a randomized
comparison of 1679 patients with shock including 280 CS patients treatment with
dopamine in comparison to norepinephrine was associated with significantly more
arrhythmic events for the overall study cohort but with a lack of significant reduction
in mortality. The predefined CS subgroupthe percentage of CS due to AMI is not
reportedhad lower mortality with norepinephrine (Figure 1). Therefore, when blood
pressure is low, norepinephrine should be the first choice as vasopressor. In analogy to
septic shock, the target mean blood pressure should be titrated to 6570 mmHg as a
higher blood pressure is not associated with beneficial outcome. The current European
STEMI guidelines are partly confusing and recommend in contrast to current
evidence dopamine (IIa/C recommendation) over norepinephrine (IIb/B
recommendation), whereas on the other hand it is stated that norepinephrine is
preferred over dopamine when the blood pressure is low.
16

Because catecholamines increase myocardial oxygen consumption and

vasoconstrictors may impair microcirculation as well as tissue perfusion, their use
should be restricted to the shortest possible duration and the lowest possible dose.

As inotropic agent, dobutamine may be given simultaneously to norepinephrine in an

attempt to improve cardiac contractility which is often performed in clinical practice.
Other inotropes such as levosimendan or phosphodiesterase-inhibitors are of interest
in CS based on their improvement of myocardial contractility without increasing
oxygen requirements and potential for vasodilation. However, as shown in a recent
Cochrane review, the current evidence for inotropes and vasodilators in CS is very
limited. Only four very small studies were eligible for this meta-analysis and three
trials with a total of 63 participants with high overall risk of bias compared
levosimendan to standard treatment (enoximone or dobutamine) or placebo.
Levosimendan showed a borderline survival benefit in comparison with enoximone .
Only small differences in haemodynamics, length of hospital stay, and frequency of
major adverse cardiac events were observed.
Optimal treatment of MODS in the intensive care unit is essential for the treatment of
CS patients since it has a major impact on prognosis. Although not specifically
investigated in CS, multiple measures are generally recommended. If invasive
ventilation is required, lung-protective ventilation should be performed to prevent
pulmonary injury. Urinary production should be measured and continuous renal
replacement therapy be initiated in case of acute renal failure with clinical signs of
uraemia, hydropic decompensation, metabolic acidosis, and/or refractory
hyperkalaemia. Moreover, optimal nutrition, glycaemic control to <11.0 mmol/L by
avoiding hypoglycaemia, as well as thromboembolism and stress ulcer prophylaxis
should be provided. Because much of haemodynamic management depends on
optimal filling pressures pulmonary artery catheters, Pulse Contour Cardiac Output
(PiCCO) or other systems should be used in all complicated courses. However, no
specific randomized trial in CS has been performed with these monitoring systems.
Moderate/severe bleeding is common in patients with CS ranging from 20 to 90%
depending on the definition used and also influenced by concomitant use of
mechanical support devices. Formerly it was generally believed that raising
haemoglobin levels via transfusion will increase oxygen delivery and thus is
beneficial. However, blood transfusions in acute coronary syndromes itself increase
17

mortality. Alterations in erythrocyte nitric oxide biology in stored blood may provide
a partial explanation, leading to initial vasoconstriction, platelet aggregation, and
ineffective oxygen delivery. In addition, bleeding itself as well as transfusion
contribute to inflammation.37Recent trials in non-CS patients with bleeding could
clearly demonstrate that a restrictive transfusion regimen can improve outcome and
general accepted intensive care strategies are to avoid the correction of laboratory
anomalies unless there is a clinical bleeding problem.(5)

Algorythm Hypovolemic Shock

18
19

CHAPTER III

CONCLUSION

Shock is a serious condition that occurs when the cardiovascular system (heart
and blood vessels) are not able to drain blood around the body in sufficient quantity.
Shock is a clinical syndrome which has a characteristic form of hypotension,
tachycardia, skin cold, pale and wet, hyperventilation, changes in mental status and
decreased urine formation. Shock is classified into several groups, namely: (1)
cardiogenic shock (associated with heart defects), (2) hypovolaemic shock (due to
decreased blood volume), (3) Shock anafilaktik (due to allergic reactions), (4) septic
shock (associated with infection), (5) neurogenic shock (due to damage to the
nervous)
The most type of shock that occur is Hypovolaemic shock because of decrease in
intravascular fluid. Treatment of all type shocks is kindly similliar one another, but the
portion is different. Fluid Resuscitation is one of the most important treatment of
shock.

REFERENCES
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1. Kasper DL, Braunwald E, Fauci AS, Hauser SL, Longo DL, Jameson JL,
Loscalzo J (2008). Harrison's principles of internal medicine (17th ed.). New
York: McGraw-Hill Medical Publishing Division.

2. Jean-Louis Vincent, M.D., Ph.D., and Daniel De Backer, M.D.,

Ph.D..Circulatory Shock. In:The New England Journal of Medicine. October
2013; 369: 1726-1734.

3. Hochman JS, Sleeper LA. Early revascularization in acute myocardial infarction

complicated by cardiogenic shock. Shoud We Emergently Revascularize
Occluded Coronaries for Cardiogenic Shock. N Engl J Med 1999;341:625-634.

4. Hocman JS, Sleeper LA. Early revascularization and long-term survival in

cardiogenic shock complicating acute myocardial infraction. JAMA
2006;295:2511-2515.

5. Thiele H, Ohman EM, Desch S. Management of cardiogenic shock. European

Heart Journal 2015;36:1223-1230.