3. Objectives
By the end of this session you should know about
The definition and classification of shock
Approach and management of patient in shock
4. Introduction
• Shock is the failure to meet the metabolic needs of the cell and the
consequences that ensue.
• Shock is the most common and therefore the most important
cause of death among surgical patients
• The initial cellular injury that occurs is reversible; however, the injury will
become irreversible if tissue perfusion is prolonged or severe enough such
that, at the cellular level, compensation is no longer possible
• With insufficient delivery of oxygen and glucose, cells switch from aerobic to
anaerobic metabolism that's why lactate level will be high
5. A central component of shock is decreased tissue perfusion.
This may be a direct consequence of the etiology of shock, such as in
hypovolemic/hemorrhagic, cardiogenic, or neurogenic etiologies, or
It may be secondary to elaborated or released molecules or cellular
products that result in endothelial/ cellular activation, such as in
septic shock or traumatic shock.
Hemodynamic parameters such as blood pressure and heart rate are
relatively insensitive measures of shock, and additional
considerations must be used to help aid in early diagnosis and
treatment of patients in shock
7. cont.…
Regardless of etiology, the initial physiologic responses in shock are
driven by tissue hypoperfusion and the developing cellular energy
deficit.
Many of the organ-specific responses are aimed at maintaining
perfusion in the cerebral and coronary circulation.
Our body tries to preserve the most vital organ and this process is
called diving reflex
8. These are regulated at multiple levels including
Stretch receptors and baroreceptors in the heart and
vasculature (carotid sinus and aortic arch)
chemoreceptor
cerebral ischemia responses
release of endogenous vasoconstrictors
shifting of fluid into the intravascular space and
RAAS
Posterior pituitary –ADH/Vasopressin
Adrenal cortex-cortisol
9. The goal of the neuroendocrine response to hemorrhage is to maintain
perfusion to the heart and the brain, even at the expense of other organ
system
The magnitude of the neuroendocrine response is based on both the
volume of blood lost and the rate at which it is lost
Afferent impulses transmitted from the periphery are processed within
the central nervous system (CNS) and activate the reflexive effector
responses or efferent impulses.
These effector responses are designed to expand plasma volume,
maintain peripheral perfusion and tissue O2 delivery, and restore
homeostasis
10. Ischemia-reperfusion syndrome
The acid and potassium load that has built up during shock can lead to
direct myocardial depression, vascular dilatation and further hypotension.
The cellular and humoral activated by the hypoxia (complement,
neutrophils, microvascular thrombi) are flushed back into the circulation
where they cause further endothelial injury to organs such as the lungs and
kidneys.
This leads to acute lung injury, acute renal injury, multiple organ failure
and death.
Reperfusion injury can currently only be attenuated by reducing
the extent and duration of tissue hypoperfusion.
11. Stages of shock
Compensated shock
Vital organ function maintained
BP remains normal
Uncompensated shock
Microvascular perfusion becomes marginal
Organ and cellular function deteriorates
Hypotension developed
Irreversible shock
Multi-organ system dysfunction with end organ injury.
12. Classification of shock
Hypovolemic
Haemorrhage
Severe burns
Severe dehydration secondary to GI losses
Cardiogenic
Myocardial infarction
Congestive heart failure
Valve problems
Cardiomyopathy
Distributive
Sepsis
Anaphylaxis
Neurogenic shock
Acute adrenal insufficiency
Obstructive
Cardiac tamponade
Tension pneumothorax
Massive pulmonary embolism
13.
14. 1. HYPOVOLEMIC
The most common cause of shock in the surgical or trauma patient is
loss of circulating volume from hemorrhage
Acute blood loss results in reflexive decreased baroreceptor
stimulation from stretch receptors in the large arteries, resulting in
decreased inhibition of vasoconstrictor centers in the brain stem,
increased chemoreceptor stimulation of vasomotor centers, and
diminished output from atrial stretch receptors.
Peripheral vasoconstriction is prominent, while lack of sympathetic
effects on cerebral and coronary vessels and local auto regulation
promote maintenance of cardiac and CNS blood flow
15. Shock in a trauma patient or postoperative patient should be presumed
to be due to hemorrhage until proven otherwise.
substantial volumes of blood may be lost before the classic clinical
manifestations of shock are evident at least 25% to 30%
16. Serum lactate and base deficit are measurements that are helpful to
both estimate and monitor the extent of bleeding and shock
It must be noted that lack of a depression in the initial hematocrit does
not rule out substantial blood loss or ongoing bleeding
Blood loss sufficient to cause shock is generally of a large volume, and
there are a limited number of sites that can harbor sufficient
extravascular blood volume to induce hypotension (e.g., external,
intrathoracic, intra-abdominal, retroperitoneal, and long bone
fractures)
Intraperitoneal hemorrhage is probably the most common source of
blood loss that induces shock. Intraperitoneal blood may be rapidly
identified by diagnostic ultrasound or diagnostic peritoneal lavage
17. Cont.…
Causes
Loss of fluid from all body compartments
reduced fluid intake
3rd spacing of fluid eg. burns
large GI losses eg. pyloric stenosis, high ouput ileostomy
large renal losses eg. diabetes insipidus
Acute loss of blood volume
e.g. trauma (haemorrhagic shock)
19. 2. TRAUMATIC
The hypoperfusion deficit in traumatic shock is magnified by the
proinflammatory activation that occurs following the induction of
shock
At the cellular level, this may be attributable to the release of cellular
products termed damage associated molecular patterns (DAMPs) that
activate the same set of cell surface receptors as bacterial products,
initiating similar cell signaling
These receptors are termed pattern recognition receptors (PRRs) and
include the TLR family of proteins.
Examples of traumatic shock include small volume hemorrhage
accompanied by soft tissue injury (femur fracture, crush injury)
20. 3.SEPTIC (VASODILATORY )
Vasodilatory shock is the result of dysfunction of the endothelium and
vasculature secondary to circulating inflammatory mediators and cells
or as a response to prolonged and severe hypoperfusion
Vasodilatory shock is characterized by peripheral vasodilation with
resultant hypotension and resistance to treatment with vasopressors
In septic shock, the vasodilatory effects are due, in part, to the
upregulation of the inducible isoform of nitric oxide synthase (iNOS or
NOS 2) in the vessel wall.
iNOS produces large quantities of nitric oxide for sustained periods of
time. This potent vasodilator suppresses vascular tone and renders the
vasculature resistant to the effects of vasoconstricting agents.
21. BASIC TERMS
Systemic inflammatory response syndrome (SIRS) - Any 2 of:
To >380C or <360C;
RR>24 BPM;
PR>90 BPM;
WBC>12,000/l or < 4000 /l or > 10% bands
Sepsis: SIRS with suspected or proven microbial etiology
Severe Sepsis or sepsis syndrome: Sepsis with organ dysfunction
including hypotension, Hypoperfusion, or organ dysfunction
Septic shock: Sepsis with hypotension for > 1hr despite adequate fluid
resuscitation or requiring vasopressors to keep SBP > 90 mmHg
/MAP> 70 mmHg
Refractory Septic Shock: Septic shock lasting for > 1 hour and doesn’t
respond to fluid and vasopressors
22. 3.CARDIOGENIC
Cardiogenic shock is defined clinically as circulatory pump failure
leading to diminished forward flow and subsequent tissue hypoxia, in
the setting of adequate intravascular volume.
Hemodynamic criteria include sustained hypotension (i.e., SBP <90
mmHg for at least 30 minutes), reduced cardiac index (<2.2 L/min per
square meter), and elevated pulmonary artery wedge pressure (>15
mmHg).
Mortality rates for cardiogenic shock are 50% to 80%.
Acute, extensive MI is the most common cause of cardiogenic shock
23. 4. OBSTRUCTIVE
Although obstructive shock can be caused by a number of different
etiologies that result in mechanical obstruction of venous return in
trauma patients this is most commonly due to the presence of tension
pneumothorax and cardiac tamponade.
With either cardiac tamponade or tension pneumothorax, reduced
filling of the right side of the heart from either increased intrapleural
pressure secondary to air accumulation (tension pneumothorax) or
increased intrapericardial pressure precluding atrial filling secondary
to blood accumulation (cardiac tamponade) results in decreased
cardiac output associated with increased central venous pressure.
Beck’s triad consists of hypotension, muffled heart
tones, and neck vein distention. Unfortunately, absence of these
clinical findings may not be sufficient to exclude cardiac injury
and cardiac tamponade
24. 5.Neurogenic
Neurogenic shock refers to diminished tissue perfusion as a result of
loss of vasomotor tone to peripheral arterial beds.
Neurogenic shock is usually secondary to spinal cord injuries from
vertebral body fractures of the cervical or high thoracic region that
disrupt sympathetic regulation of peripheral vascular tone
The classic description of neurogenic shock consists of decreased
blood pressure associated with bradycardia (absence of reflexive
tachycardia due to disrupted sympathetic discharge), warm extremities
(loss of peripheral vasoconstriction), motor and sensory deficits
indicative of a spinal cord injury, and radiographic evidence of a
vertebral column fracture.
In a subset of patients with spinal cord injuries from penetrating
wounds, most of the patients with hypotension had blood loss as the
etiology (74%) rather than neurogenic causes, and few (7%) had the
classic findings of neurogenic shock.
25. Overview of different types of shock
Comparison table different types of shock
Hypo-
volaemic
Cardiogenic
Distributive
Sepsis
Distributive
Neurogenic
Obstructive
Peripheries cold cold warm warm cold
Heart rate increased increased increased
may be
bradycardic
increased
Pulse
pressure
reduced
may be
reduced
may be
increased
normal
may be
reduced
(pulsus
paradoxus)
CVP reduced increased reduced reduced increased
Temperature
may be
reduced
normal
may be
increased
normal normal
26. How to approach patient with shock
For trauma patient follow the ATLS principle because
maintaining circulation with out adequate oxygenation is not
important at all
So manage the airway first then breathing , making sure both are
not affected check the circulation
To effectively manage patient with shock focus mainly on the
cause
so take targeted history and try to find common signs of sock
27.
28.
29.
30.
31.
32. Management
Treatment of shock is initially empiric.
A secure airway must be confirmed or established in obtunded patients
The priority is the initiation of volume infusion while the search for the
cause of the hypotension is pursued
Shock in a trauma patient or postoperative patient should be presumed to
be due to hemorrhage until proven otherwise
In management of trauma patients, understanding the patterns of injury of
the patient in shock will help direct the evaluation and management.
33. Hypovolemic
The appropriate priorities in these patients are as follows:
(a) control the source of blood loss, (b) perform IV volume
resuscitation with blood products in the hypotensive patient, and
(c) secure the airway
In trauma, identifying the body cavity harboring active hemorrhage
will help focus operative efforts; however, because time is of the
essence, rapid treatment is essential
Initial resuscitation is limited to keep SBP around 80 to 90 mmHg.
This prevents renewed bleeding from recently clotted vessels
Resuscitation and intravascular volume resuscitation is accomplished
with blood products and limited crystalloids like NS and RL
34. Cont.…
The infusion of 2–3 L of salt solution over 20–30 min should restore
normal hemodynamic parameters
Continued hemodynamic instability implies that shock has not been
reversed and/or that there are significant ongoing blood or volume
losses
Too little volume allowing persistent severe hypotension and
hypoperfusion is dangerous, yet too vigorous of a volume resuscitation
may be just as deleterious
Fluid resuscitation is a major adjunct to physically controlling
hemorrhage in patients with shock
35. In patients with severe hemorrhage, restoration of intravascular
volume should be achieved with blood products ( PRBC is preferred )
In the presence of severe and/or prolonged hypovolemia, inotropic
support with dopamine, vasopressin, or dobutamine may be required
to maintain adequate ventricular performance after blood volume has
been restored
Once hemorrhage is controlled and the patient has stabilized, blood
transfusions should not be continued unless the hemoglobin is
<7g/dL.
36. Generally based the response to initial fluid--can be divided into 3
a. rapid response,
b. transient response, and
c. minimal or no response.
A. RAPID RESPONSE
rapidly to the initial fluid bolus and remain hemodynamically normal
after the initial fluid bolus
usually have lost minimal (less than 20%) blood volume
No further fluid bolus or immediate blood administration
Typed and crosshatched blood should be kept available. Surgical
consultation and evaluation are necessary during initial assessment
and treatment, as operative intervention may still be necessary
37. B. TRANSIENT RESPONSE
respond to the initial fluid bolus.
However, they begin to show deterioration of perfusion indices
as the initial fluids are slowed to maintenance levels, indicating
either an ongoing blood loss or inadequate resuscitation.
Most of these patients initially have lost an estimated 20% to
40% of their blood volume
Transfusion of blood and blood products is indicated, but more
important is the recognition that this patient requires operative
or angiographic control of hemorrhage.
patients who are still bleeding and require rapid surgical
intervention.
38. C. MINIMAL OR NO RESPONSE
Failure to respond to crystalloid and blood in the ER dictates the
need for immediate, definitive intervention (e.g., operation or
Angioembolization) to control exsanguinating hemorrhage.
So the possible DDX are
blunt cardiac injury
cardiac tamponade
tension pneumothorax
Non hemorrhagic shock
Cardiogenic
Septic
Central venous pressure monitoring and cardiac ultrasonography
help to differentiate between the various causes of shock
39. TRAUMATIC
Follow the ATLS guideline initially
Treatment of traumatic shock is focused on correction of the
individual elements to diminish the cascade of proinflammatory
activation, and includes prompt control of hemorrhage,
adequate volume resuscitation to correct O2 debt, debridement
of nonviable tissue, stabilization of bony injuries, and
appropriate treatment of soft tissue injuries
Supplementation of depleted endogenous antioxidants also
reduces subsequent organ failure and mortality
40. SEPTIC
Because vasodilation and decrease in total peripheral resistance may
produce hypotension, fluid resuscitation and restoration of circulatory
volume with balanced salt solutions is essential.
Fluid resuscitation should begin within the first hour and should be
at least 30 mL/kg for hypotensive patients
Empiric antibiotics must be chosen carefully based on the most likely
pathogens (gram-negative rods, gram-positive cocci, and anaerobes)
because the portal of entry of the offending organism and its identity
may not be evident until culture data return or imaging studies are
completed.
After first-line therapy of the septic patient with antibiotics, IV fluids,
and intubation if necessary, vasopressors may be necessary to treat
patients with septic shock
41. Catecholamine's are the vasopressors used most often, with
norepinephrine being the first-line agent followed by epinephrine
Occasionally, patients with septic shock will develop arterial resistance
to catecholamines.
Arginine vasopressin, a potent vasoconstrictor, is often efficacious in
this setting and is often added to norepinephrine
A single IV dose of 50 mg of hydrocortisone improved mean arterial
blood pressure response relationships to norepinephrine in patients
with septic shock and was most notable in patients with relative
adrenal insufficiency
42. Cardiogenic
Judicious fluid administration to avoid fluid overload and development
of cardiogenic pulmonary edema
Electrolyte abnormalities, commonly hypokalemia and
hypomagnesemia, should be corrected
Dobutamine primarily stimulates cardiac β1- receptors to increase
cardiac output but may also vasodilate peripheral vascular beds, lower
total peripheral resistance, and lower systemic blood pressure through
effects on β2-receptors.
Ensuring adequate preload and intravascular volume is therefore
essential prior to instituting therapy with dobutamine
Dopamine may be preferable to dobutamine in treatment of cardiac
dysfunction in hypotensive patients.
43. Patients whose cardiac dysfunction is refractory to cardiotonics may
require mechanical circulatory support with an intra-aortic balloon
pump.
NEUROGENIC
Most patients with neurogenic shock will respond to restoration of
intravascular volume alone, with satisfactory improvement in perfusion
and resolution of hypotension
Vasoconstrictor should only be considered once hypovolemia is
excluded as the cause of the hypotension and the diagnosis of
neurogenic shock is established
Dopamine may be used first. A pure α-agonist, such as phenylephrine,
may be used primarily or in patients unresponsive to dopamine
44. End point in resuscitation
it is much easier to know when to start resuscitation than when to stop
Even with normalization of blood pressure, heart rate, and urine
output, 80% to 85% of trauma patients have inadequate tissue
perfusion, as evidenced by increased lactate or decreased mixed venous
O2 saturation.
Resuscitation algorithms directed at correcting global perfusion
endpoints (base deficit, lactate, mixed venous oxygen saturation)
rather than traditional endpoints like PR &BP
Resuscitation is complete when O2 debt is repaid, tissue acidosis is
corrected, and aerobic metabolism restored.
45. ADJUNCT THERAPY
The sympathomimetic amines dobutamine, dopamine, and
norepinephrine are widely used in the treatment of all
forms of shock
Arginine-vasopressin (antidiuretic hormone) is also being
used increasingly and may better protect vital organ blood
flow and prevent pathologic vasodilation.
Positioning of the patient may be a valuable adjunct in the
initial treatment of hypovolemic shock.
The NASG and the military antishock trousers (MAST)
Rewarming or avoidance of hypothermia
47. Reference
Schwartz principle of surgery 11 ed
Sabiston textbook of surgery
Baily and love short practice of surgery
Up-to-date 21.6
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