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SHOCK
Assoc. Prof. Dr. SEVGİ BİLGEN
DEPARTMENT OF ANESTHESIOLOGY AND
REANIMATION
YEDITEPE UNIVERSITY SCHOOL OF MEDICINE
2016-2017
The definition of shock
Mechanism of shock
Basic Physiology
Patient assessment
Types of shock
Shock treatment
The definition of shock
Shock represents an imbalance between
oxygen demand and delivery
The definition of shock
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.
Imbalance between oxygen delivery and oxygen
consumption which leads to cell death, end organ
damage, multi-system organ failure, and death.
The definition of shock
The effect of shock are initially reversible, but rapidly
become irreversible,
resulting in multiorgan failure (MOF) and death.
Shock must be recognized and treated immediately to
prevent progression to irreversible organ dysfunction.
The definition of shock
Undifferentiated shock refers to the situation where
shock is recognized but the cause is unclear.
When a patient presents with undifferentiated shock;
it is important that the clinician immediately initiate
therapy
while rapidly identifying the etiology so that definitive
therapy can be administered to reverse shock and
prevent MOF and death.
The definition of shock
Shock is defined as a state of cellular and tissue hypoxia
due to reduced oxygen delivery and/or increased oxygen
consumption or inadequate oxygen utilization
This most commonly occurs when there is circulatory
failure manifested as hypotension
(reduced tissue perfusion)
But, hypotension is not a requirement
Shock can occur with a normal blood pressure and
hypotension can occur without shock
The definition of shock
Inadequate oxygen delivery leading to shock can
occur despite the patient being hypertensive or
normotensive.
Clinicians should not wait for the presence of
hypotension before aggressively attempting to
reverse shock and restore adequate tissue
perfusion.
Mechanism of shock
Cellular hypoxia occurs as a result of reduced tissue
perfusion/oxygen delivery and/or increased oxygen
consumption or from inadequate oxygen utilization.
Cellular hypoxia, in turn,
causes cell membrane ion pump dysfunction,
intracellular edema,
leakage of intracellular contents into the extracellular space,
inadequate regulation of intracellular pH.
Mechanism of shock
These biochemical processes, when unchecked,
progress to the systemic level,
resulting in acidosis, and endothelial dysfunction,
as well as further stimulation of inflammatory and antiinflammatory cascades.
Mechanism of shock
Serum lactate levels, when elevetated, have traditionally
been used as surrogates for hypoperfusion and tissue
hypoxia.
Elevations in serum lactate level are useful riskstratification tools in undifferentiated shock.
Basic Physiology
In order to treat shock appropriately, it must first be
recognized, then identify the cause.
In order to recognize it, it is important to understand
some of the physiology of the disease process
Basic Physiology
The major physiologic determinants of tissue perfusion
(and systemic blood pressure [BP]) are cardiac output
(CO) and systemic vascular resistance (SVR).
BP= CO X SVR
CO is the product of heart rate (HR) and stroke
volume (SV).
CO= HR X SV
Basic Physiology
The stroke volume is a determined by
Preload
Afterload
Myocardial Contractility
SVR is governed by
o
o
o
Vessel length
Blood viscosity
Vessel diameter (ie, vessel tone)
Basic Physiology
Biologic processes that change any one of these
physiologic parameters can result in hypotension and
shock.
Common to most from of shock is diminished CO
and/or SVR.
Basic Physiology
In general, severe hypovolemia, cardiogenic shock, and
late stage obstructive shock are characterized by a low
CO and compensatory increase in the SVR to
maintain perfusion to vital organs.
Distributive shock is classically associated with reduced
SVR and compensatory increase in the CO.
However, the CO may be normal in the early phases of
hypovolemic and obstructive shock.
Basic Physiology
Some form of shock have normal CO and SVR.
Patients with profound mitochondrial dysfunction
(inheritable mitochondrial disease, carbon monoxide,
and cyanide poisoning) are shock state that occur
despite normal CO, SVR, and tissue perfusion.
Because they are due to inadequate oxygen utilization.
Patient Assessment
When a patient is suspected of having shock,
diagnostic evaluation should occur at the same time as
resuscitation.
Resuscitative efforts should NOT be delayed for
history, physical examination, laboratory testing, or
imaging.
Patient Assessment
Clinical signs and symptoms depends on
the severity of the shock
Patient Assessment
In hypovolemic shock, clinical signs and symptoms are
associated with a 20 to 25 percent reduction in arterial
blood volume,
In cardiogenic shock, a fall in the cardiac index to less
than 2.5 L/min/m2 is required before signs and
symptoms appear.
Patient Assessment
Obvious and immediately detectable manifestations of the shock state include:
tachycardia,
hypotension,
cool extremities,
weak peripheral pulses,
prolonged capillary refill (>2 seconds),
narrowing of the pulse pressure (<25 mmHg), and
altered mental status.
Patient Assessment
Tachycardia, a modest change in systemic blood
pressure (increase or decrease), or mild to moderate
hyperlactatemia, may be the only clinical signs of early
shock.
During shock, the compensatory mechanisms become
overwhelmed,
Signs and symptoms of organ dysfunction appear
including symptomatic tachycardia, dyspnea,
restlessness, diaphoresis, metabolic acidosis,
hypotension, oliguria, and cool, clammy skin.
Patient Assessment
Progressive shock leads to irreversible organ damage,
multiorgan failure (MOF), and death.
During this stage, anuria and acute renal failure develop,
acidemia further depresses CO,
hypotension becomes severe and recalcitrant to therapy,
hyperlactatemia often worsens, and
restlessness evolves into obtundation and coma.
Death is common in this phase of shock.
Patient Assessment
Airway: includes brief evaluation of mental status
Breathing: If patient is conversing with you, A & B
are fine
Circulation: Vitals (HR, BP). Includes placement of
adequate IV access
Disability: identification of gross neurologic injury
Exposure: ensures complete exam
Patient Assessment
Laboratory
Hgb, WBC, platelets
PT/PTT
Electrolytes
Arterial blood gases
BUN, Cr
Serum lactate
Mixed venous oxygen saturation (SVO2)
ECG
Patient Assessment
Invasive monitoring
Arterial pressure catheter
CVP monitoring
Pulmonary artery catheter
Mixed or central venous oxygen
saturation (SvO2/ScvO2)
Oxygen delivery(DO2) and
oxygen consumption(VO2)
As indicated
o Chest x-ray
o Pelvic x-ray
o Abd/pelvis CT
o Chest CT
o GI endoscopy
o Bronchoscopy
o Vascular radiology
Types of shock
The main types of shock include:
1.Distributive shock
2.Cardiogenic shock
3.Hypovolemic shock
4.Obstructive shock
Types of shock
Septic shock, a form of distributive shock, is the most
common form of shock among patients admitted to
the intensive care unit,
followed by cardiogenic and hypovolemic shock,
obstructive shock is rare.
1.Distributive Shock
Distributive shock is characterized by severe peripheral
vasodilatation (vasodilatory shock).
Classically associated with reduced SVR and
compensatory increase in the CO.
1.Distributive shock
Septic shock
Systemic inflamatuary response syndrome (SIRS)
Neurogenic shock
Anaphylactic shock
Drug and toxin-induced shock
Endocrin shock
1.Distributive shock/Septic shock
Sepsis, defined as a dysregulated host response to infection
resulting in life-threatening organ dysfunction.
Sepsis is the most common cause of distributive shock.
The type of pathogen causing sepsis varies with the
population studied.
Septic shock is a subset of sepsis associated with mortality in
the 40 to 50 percent range,
It can be identified by the use of vasopressor therapy and
the presence of elevated lactate levels (>2mmol/L) despite
adequate fluid resuscitation.
1.Distributive shock/
Systemic inflammatory response syndrome (SIRS)
SIRS is a clinical syndrome that is characterized by a
robust inflammatory response,
Usually induced by a major body insult that can be
infectious and noninfectious.
1.Distributive shock/
Systemic inflammatory response syndrome (SIRS)
Noninfectious conditions that can be complicated by SIRS:
Pancreatitis
Burns
Hypoperfusion caused by trauma
Significant blunt trauma and crush injury
Amniotic fluid embolism
Fat embolism
Post successful return of spontaneous circulation after a cardiac
arrest, myocardial infarction, or cardio-pulmonary bypass
1.Distributive shock/Neurogenic shock
Hypotension and in some cases, shock are common in
patients with severe traumatic brain injury and spinal
cord injury.
Interruption of autonomic pathways, causing decreased
vascular resistance and altered vagal tone, is thought to
be responsible for distributive shock in patients with
spinal cord injury.
Hypovolemia from blood loss and myocardial
depression may also contribute to shock in this
population.
1.Distributive shock/Anaphylactic shock
Shock from anaphylaxis is most commonly
encountered in patients with severe, immunoglobulinE mediated, allergic reactions to insect stings, food,
and drugs.
1.Distributive shock/
Drug and toxin-induced shock
Drug overdoses
Snake bites
Insect bites including scorpion envenomation and spider bites
Transfusion reactions
Heavy metal poisoning including arsenic, iron, and thallium
Infections associated with toxic shock syndrome
Cyanide and carbon monoxide cause shock from mitochondrial
dysfunction
1.Distributive shock/Endocrine shock
Addisonian crisis and myxedema can be associated
with hypotension and state of shock.
In state of mineralocorticoid deficiency, vasodilation
can occur due to altered vascular tone and aldosteronedeficiency-mediated hypovolemia.
2.Cardiogenic shock
Cardiogenic shock is due to intracardiac causes of
cardiac pump failure that result in reduced cardiac
output (CO).
Causes of cardiac pump failure are diverse, but can be
divided into three categories;
Cardiomypathic
Arrhythmic
Mechanical
2.Cardiogenic shock/Cardiomyopathic
Cardiomyopathic causes of shock include;
myocardial infarction involving greater than 40 percent of the left ventricular
myocardium,
myocardial infarction of any size if accompanied by severe extensive ischemia
due to multivessel coronary artery disease,
severe right ventricular infarction,
acute exacerbation of heart failure in patients with severe underlying dilated
cardiomyopathy,
stunned myocardium following cardiac arrest,
prolonged ischemia or cardiopulmonary bypass,
myocardial depression due to advanced septic or neurogenic shock, and
myocarditis.
2.Cardiogenic shock/Arrhythmic
Both atrial and ventricular tachyarrhythmias and
bradyarrhythmias may induce hypotension, often
contributing to states of shock.
2.Cardiogenic shock/Mechanical
Mechanical causes of cardiogenic shock include;

severe aortic or mitral valve insufficiency,

acute valvular defects due to rupture of a papillary muscle or chordae
tendineae (mitral valve defect),

retrograde dissection of the ascending aorta,

an abscess of the aortic ring.
Additional causes include;

severe ventricular septal defects;

acute rupture of the intraventricular septum,

atrial myxomas,

a ruptured ventricular free wall aneurysm.
3.Hypovolemic shock
Hypovolemic shock is due to reduced intravascular
volume (ie, reduced preload), which, in turn, reduces
CO.
In response to baroreceptor stimulation, the heart rate
increases to maintain cardiac output.
3.Hypovolemic shock
Hypovolemic shock can be divided into two categories
Hemorrhagic
Nonhemorrahagic
The most common cause of hypovolemic shock is
major blood loss, such as occurs with trauma, surgery,
or massive gastrointestinal hemorrhage.
3.Hypovolemic shock/
Hemorrhagic shock
Reduced intravascular volume from blood loss can
result in shock.
There are multiple causes of hemorrhagic shock.
Blunt or penetrating trauma (includes multiple
fractures without vessel injury)
Upper or lower gastrointestinal
bleeding
3.Hypovolemic shock/
Hemorrhagic shock
Less common causes:
Intraoperative or postoperative bleeding
Ruptured abdominal aortic or left ventricle aneurysm
Hemorrhagic pancreatitis
Iatrogenic (inadvertent biopsy of arteriovenous malformation)
Postpartum hemorrhage
Uterine or vaginal hemorrhage from other causes (infection,
tumors)
Ruptured hematoma
3.Hypovolemic shock/
Nonhemorrhagic shock
Reduced intravascular volume from fluid loss other
than blood can cause shock.
Volume depletion from loss of sodium and water occur
from a number of anatomic sites.
3.Hypovolemic shock/
Nonhemorrhagic shock
Gastrointestinal losses
(diarrhea, vomiting, external drainage)
Skin losses (heat stroke, burns, severe dermatologic
conditions including Stevens-Johnson syndrome)
Renal losses (excessive drug-induced or osmotic
diuresis, hypoaldesteronism)
Third space losses into the extravascular space or body
cavities (postoperative and trauma, intestinal
obstruction, crush injury, pancreatitis, cirrhosis)
4. Obstructive shock
Obstructive shock is mostly due to extracardiac causes
of cardiac pump failure.
Often associated with poor right ventricle output.
The causes of obstructive shock can be divided into the
following two categories:
 Pulnonary vascular
 Mechanical
4. Obstructive shock/
Pulmonary vascular
Most cases of obstructive shock are due to right
ventricular failure from,
 hemodynamically significant pulmonary embolism,
 severe pulmonary hypertension.
 Patients with severe stenosis or with acute obstruction
of the pulmonary or tricuspid valve may also fall into
this category
4. Obstructive shock/Mechanical
Patients in this category present clinically as hypovolemic shock
because their primary physiologic disturbance is decreased
preload, rather than pump failure (eg, reduced venous return to
the right atrium or inadequate right ventricle filling).
Mechanical causes of obstructive shock include the following:

Tension pneumothorax

Pericardial tamponade

Constrictive pericarditis

Restrictive cardiomyopathy
Treatment
Identify & reverse the cause
Restore tissue perfusion
Restore organ function
Treatment of Shock
General Management
•
•
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•
ABCDE
Airway
control work of Breathing
optimize Circulation
assure adequate oxygen Delivery
achieve End points of resuscitation
Airway
• Determine need for intubation but remember:
intubation can worsen hypotension
• Sedatives can lower blood pressure
• Positive pressure ventilation decreases preload
• May need volume resuscitation prior to
intubation to avoid hemodynamic collapse
Control Work of Breathing
• Respiratory muscles consume a significant amount of oxygen
• Resting ventilatory muscles will permit diversion of cardiac
output to other hypo perfused organs
• Mechanical ventilation and sedation decrease WOB and
improves survival
Optimizing Circulation
• Unless there are signs of intravascular volume overload
initial resuscitation with IV fluids is generally indicated.
• Isotonic crystalloids
• Titrated to:
• CVP 8-12 mm Hg
• Urine output 0.5 ml/kg/hr. (30 ml/hr.)
• Improving heart rate
• May require 4-6 L of fluids
• No outcome benefit from colloids
• Vasopressor medications should be selected based on
the cause of shock
Maintaining Oxygen Delivery
• Decrease oxygen demands
• Provide analgesia and anxiolytics to relax muscles and avoid
shivering
• Maintain arterial oxygen saturation/content
• Give supplemental oxygen
• Maintain Hemoglobin > 10 g/dL
End Points of Resuscitation
• Goal of resuscitation is to maximize survival and
minimize morbidity
• Use objective hemodynamic and physiologic values to
guide therapy
• Goal directed approach
•
•
•
•
•
•
MAP: above 65mmHg or
Systolic blood pressure: above 90 mmHg
Heart rate: between 60-100/min
Urine output: > 0.5 mL/kg/hr
CVP: 8-12 mmHg
Central venous oxygen concentration: > 70%
Hypovolemic shock /Treatment
Treatment of hypovolemic shock involves restoration of
circulation blood volume and
treatment of the underlying cause of the hypovolemia.
Treatment of the underlying cause of the hypovolemic shock
can be undertaken only when adequate intravenous access
and aggressive fluid therapy are achieved.
Vasopressor therapy may be used to increase systemic blood
pressor,
But it will probably be unsuccessful until intravascular
volume is restored.
Cardiogenic shock/Treatment
The goals in treatment of cardiogenic shock are to
improve cardiac output and decrease afterload.
These interventions allow;
 the ventricle to eject more efficiently,
 decrease myocardial work,
 lower myocardial oxygen consumption, and
 reverse the dangerous spiral of cardiac failure.
Cardiogenic shock/Treatment
Depending on the type of cardiac failure and ventricular filling
conditions, diuretics are generally indicated,
But must be used judiciously to avoid worsening the
hypotension.
Afterload and preload can be reduce with vasodilatators and
venodilatators such as;
nicardipin, nitroglycerin, or nitropurisside.
Dobutamine improves cardiac output and reduces afterload
with a minimal increase in myocardial oxygen demand.
Distributive shock/Treatment
Treatment involves initial intravenous fluid therapy until
adequate preload is established, typically at a central venous
pressure of approximately 8 to 12 cmH2O.
Vasopressors (phenylephrine, dopamine, epinephrine,
norepinephrine) are added if the patient remains hypotensive.
The choice of drug depends on the specific clinical situation.
The underlying cause of the disorder should be treated as soon as
possible.
Inotropic drugs and vasopressors
Dopamine
Epinephrine
Norepinephrine
Phenylephrine
Dobutamine
Vasopressin
Dopamine
Clinically, dopamine is regarded as a relatively weak vasopressor
and is useful in mild hypotensive states.
It is pharmacologic action varies with dose and within individuals
as well.
With small doses (0 to 5 µg/kg/min) dopamine causes dilatation
of the renal arterioles and promotes diuresis (dopamine-1 receptor
agonist activity).
At moderate doses (5 to 10 µg/kg/min) dopamine causes an
increase in myocardial contractility, heart rate, and cardiac output
(ß1-adrenergic effect).
At large doses (10 to 20 µg/kg/min) dopamine acts to increase
vascular smooth muscle tone, which increases systemic vascular
resistance (α1-agonist effect).
Epinephrine
Epinephrine causes direct stimulation of α1, ß1, and ß2 receptors.
Main indications for epinephrine are;

in the management of cardiac arrest,

severe cardiogenic shock,

anaphylactic and anaphylactoid reactions.
When given as a continuous infusion, the usual range of
epinephrine is between 1 and 20 µg/min.
However, in patients with refractory, life-threatening shock, it may
be necessary to administer epinephrine at even larger doses.
Epinephrine
Increases in heart rate, myocardial activity, and cardiac
output reflect ß1- receptor effects.
The principal ß2- receptor effects are bronchial and
vascular smooth muscle relaxation.
With larger doses, the α1- receptor effects of
epinephrine act to increase systemic vascular resistance
and reduce splanchnic and renal blood flow while
maintaining both cerebral and myocardial perfusion
pressure.
Norepinephrine
It is similar to epinephrine except that norepinephrine lack
the ß2- receptor effect of epinephrine and has much
stronger α1- receptor activity.
Norepinephrine can be used for the treatment of septic
shock.
It is ß1 activity may help offset the myocardial dysfunction
associated with severe sepsis and septic shock.
Norepinephrine must be given by continuous infusion,
The typical dose range is between 1 and 20 µg/min.
Phenylephrine
Phenylephrine is a direct-acting, highly selective α1-receptor agonist
which increases systemic vascular resistance and arterial blood pressure.
Phenylephrine is frequently used for the treatment of septic and other
forms of vasodilatory shock to increase systemic blood pressure.
Phenylephrine is often administered to brain-injured patients to improve
cerebral perfusion pressure.
It does not cross the blood-brain barrier,
It has no effect on the cerebral vasculature.
The typical dosage range for phenylephrine is up to 200µg/min.
Larger doses have little therapeutic effect, with only worsening of
splanchnic ischemia.
Dobutamine
Dobutamine is mixed ß1- and ß2- receptor agonist.
The primary effect of dobutamine is to increase both heart
rate and myocardial contractility.
Dobutamine relaxes vascular smooth muscle via binding at
ß2- receptors.
Dobutamine is typically indicated for the treatment of
patients in cardiogenic shock with high afterload and low
cardiac output.
Dobutamine is given by continuous infusion only, and the
usual dosage range is between 1 and 20µg/kg/min.
Vasopressin
Vasopressin is a potent vasoconstrictor that does not work via the
adrenergic receptor system.
Vasopressin binds to peripheral vasopressin receptors to induce
potent vasoconstriction.
Patients with severe sepsis and septic shock may have a relative
deficiency of vasopressin. This group of patient is remarkably sensitive
to the effects of vasopressin.
For septic shock, the recommendation is to infuse vasopressin at
0.04U/min.
Vasopressin has been successfully used for cardiogenic shock.
In this patients, the dose of vasopressin (0.1U/min) is significantly
larger than that used for septic shock.
Which Pressor should I choose?
Hypovolemic shock
Fluids and Blood
Cardiogenic shock
Dobutamine -β1 agonist)
Neurogenic shock
Fluids, phenylephrine -α1
agonist, norepinephrine -α1 and
β1 agonists, look for another
type of shock if it is persistent
Septic shock
Norepinephrine – α1 and β1
agonists
Anaphylactic shock
Fluids and epinephrine -α1, ß1, and
ß2agonist
Survival and outcomes improve with early
perfusion, adequate oxygenation, and
identification with appropriate treatment of
the cause of shock.