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2. Definition of shock
Pathophysiology of shock
Types of shock
Clinical features of shock
Approach to the patient with shock
Management principles
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Outline
3. Shock
The clinical condition of organ dysfunction resulting from an
imbalance between cellular oxygen supply and demand.
There are a multitude of heterogeneous disease processes that
can lead to shock.
Shock is initially reversible, if not treated immediately results
in irreversible phase and death from multisystem organ
dysfunction (MSOD).
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4. The cellular oxygen imbalance of shock is most commonly
related to impaired oxygen delivery in the setting of
circulatory failure.
Shock can also develop during states of increased oxygen
consumption or impaired oxygen utilization.
In the setting of insufficient oxygen supply, the cell is no
longer able to support aerobic metabolism
Without sufficient oxygen supply, the cell is forced into
anaerobic metabolism, in which pyruvate is metabolized to
lactate with much less ATP generation
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Pathophysiology
5. DETERMINANTS OF OXYGEN DELIVERY
The two major components of DO2 are :
Cardiac output (CO)
Arterial oxygen content(CaO2):
DO2 = CO × CaO2
A disease process that affects these variables:
o HR, preload, contractility, SVR, SaO2, or Hb
Has the potential to reduce oxygen delivery and cause
cellular hypoxia.
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6. There are three stages of shock
Compensatory(pre shock)
In this stage the body utilize a variety of physiological mechanisms,
including
Neural
Hormonal and
Bio-chemical mechanisms in an attempt to reverse the condition.
At first blood pressure will decrease, which happens because of the
decrease in CO and narrowing of the pulse pressure.
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7. The baroreceptor in the arteries detect the resulting hypotension, and
cause the release of epinephrine and norepinephrine
Causing vasoconstriction and
Increase in heart rate ;
The combined effect results in an increase in blood pressure.
Renin-angiotensin aldosterone axis is activated and vasopressin
(antidiuretic hormone; ADH) is released to conserve fluid via the
kidneys.
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8. Decompensated Shock
During shock, the compensatory mechanisms become
overwhelmed, and signs and symptoms of organ dysfunction
appear including:
Symptomatic tachycardia, dyspnea
Restlessness, diaphoresis
Metabolic acidosis, hypotension
Oliguria, cool
Clammy skin.
Continued decreased cellular perfusion and resulting altered
capillary permeability are the distinguishing features of this
stage.
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9. Refractory/Irreversible/ shock
Failure of vital organs
Brain damage and cell death are occurring,
Death will occur imminently.
One of the primary reasons that shock is irreversible at this point is
that much cellular ATP has been degraded into adenosine in the
absence of oxygen.
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11. Hypovolemic shock
Hypovolemic shock is caused by a reduced
Circulating volume
Reduced CO, elevated SVR, low CVP and PCWP
Hemorrhagic cause-
Trauma, upper or lower gastrointestinal bleeding.
Non hemorrhagic processes-
Profound emesis or diarrhea, renal losses, skin loss
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12. Cardiogenic shock
Characterized by high preload (CVP) with low CO.
Cardiogenic shock is due to primary failure of the heart to
pump blood to the tissues.
Causes of cardiogenic shock include
Myocardial infarction
Cardiac dysrhythmias
Valvular heart disease
Blunt myocardial injury and
Cardiomyopathy
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13. Obstructive
shock
Obstructive shock is due to obstruction of blood flow
outside of the heart.
Common causes of obstructive shock include
Cardiac tamponade
Tension pneumothorax
Massive pulmonary embolus
Air embolus
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14. Distributive
shock
Distributive shock is due to impaired utilization of oxygen
and thus production of energy by the cell.
There are different types of distributive shock
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a. Septic shock
b. Pancreatitis
c. Severe burns
d. Anaphylactic shock
e. Neurogenic shock
f. Endocrine shock
i. Adrenal crisis
15. 1) septic shock
Sepsis is a dysregulated host response to infection resulting
in life-threatening organ dysfunction.
Septic shock occurs most often in the very old and the very
young.
It also occurs in people who have other illnesses.
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16. For the diagnosis of septic shock
First, SIRS (systemic inflammatory response syndrome) must
be diagnosed by finding at least any two of the following
Tachypnea (high respiratory rate) > 20 breaths per minute
WBC count either significantly low, < 4000 cells/mm³ or
elevated > 12000 cells/mm³
Heart rate > 90 beats per minute
Temperature: fever > 38.5 °C (101.3 °F) or hypothermia
< 35.0 °C (95.0 °F)
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17. Second, there must be sepsis
Third, signs of end-organ dysfunction are required such as
Renal failure
Liver dysfunction
Changes in mental status, or
Elevated serum lactate.
Finally, septic shock is diagnosed if there is refractory
hypotension (low blood pressure that does not respond to
treatment).
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18. 2) Anaphylactic shock
Massive vasodilation resulting from an allergic reaction
resulting in the release of histamines and other related
substances.
Caused by
Allergic reaction to insect venom
Blood transfusions
Medications, and
Dyes used in radiologic studies
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19. 3)Neurogenic Shock
Interruption of sympathetic nervous system;
Failure of arteriolar resistance leading to massive
vasodilation and pooling of blood
The causes include
Exposure to unpleasant circumstances
Extreme pain
Spinal cord injury
Head injury
High spinal anesthesia
Vasomotor depression
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20. Clinical features of shock
The general signs for all types of shock are
Low blood pressure
Decreased urine output
Confusion and
A fast heart rate
Specific subtypes of shock may have additional
symptoms.
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22. .
• Shock is life threatening emergency.
• Diagnosis, evaluation and management most
often occur simultaneously and speed in
evaluation is important to achieve a good
outcome.
• The two most important goals of clinical
approach:
- The need to initiate therapy before shock
causes irreversible damage to organs
- The need to perform a diagnostic
evaluation to determine the cause of the shock
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23. HISTORY
• Obtained from the patient , relatives or available medical
records
Hx of body fluid loss
hematemesis, hematochezia, melena ,vomiting ,diarrhea and
abdominal pain.
Family history of bleeding disorder , cardiac disease ,HTN , renal
disease.
Hx of recent trauma
Site of trauma
Amount of bleeding
Length of time after the trauma has occurred
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24. Hx of shortness of breath ,chest pain , palpitation and body swelling.
Constitutional SSxs such as fever, loss of appetite, headache, easy
fatigability
Hx of decreased urine output
• Any Hx of allergic reaction.
Drug use
Insect bite.. snake
Allergic skin reaction, allergic rhinitis.
– Catheterization, antibiotics
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25. PHYSICAL EXAMINATION
Physical examination should be efficient and directed toward
uncovering the type, severity, and cause of the shock.
Vital signs
HEENT:
Scleral icterus
Dry conjunctivae
Dry mucous membranes
Pinpoint pupils
Fixed/dilated pupils
Nystagmus
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33. Cont.
Blood culture with sensitivity at least two in 24
hours
Base deficit(arterial blood gas analysis).
Serum lactate and electrolytes test like Na , K
ECHO
CT scan to assess the head , chest or abdominal
bleeding
CXR
Ultrasound
Lumbar puncture
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34. General principles of management
The management of shock contains
1.General approach
2.Etiologic based approach
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35. Early recognition and prompt intervention are extremely important
in the management of all forms of shock .
The initial assessment and treatment :it includes
Stabilization of ABCs.
Depending on the severity of shock, further airway intervention,
including intubation and mechanical ventilation
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36. Hypovolemic shock
Primary goal is to restore the blood volume, tissue perfusion
and oxygenation to normal .
Stop blood or plasma loss
Fluid replacement is the primary concern
The rate of fluid replacement and the type of fluid is an issue to
be considered.
Crystalloids used to replace blood loss , Ringer lactate is
primary choice
Patients who don’t respond to 2-4L of electrolyte solution and
remain hypotensive generally require blood transfusion
Vasopressers are rarely used in patients who fail to respond,
despite adequate resuscitation and control of hemorrhage.
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37. Cardiogenic shock
Overly vigorous fluid challenge esp in the elderly should be
avoided.
Pharmacologic support
Sympathomimetic inotropes. E.g. dopamine
Norepinephrine (for refractory hypotension)
Reperfusion/revascularization: PCI, coronary bypass graft
Anticoagulant therapy: IV heparine, aspirin
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38. Distributive shock
Anaphylactic shock
Epinephrine administration
Large amount of fluid resuscitation
Antihistamines
Neurogenic shock
Maintaining the ability to breath
Immobilizing neck to prevent further spinal cord
damage
Avoid possible complications,such as stool or urine
retention , respiratory or cardiovascular difficulty and
formation deep vein clots in the extremities.
Surgery
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39. Septic shock
The treatment of patients with septic shock consists of the
following 3 major goals:
1) Resuscitation using supportive measures to correct
hypoxia, hypotension, and impaired tissue
oxygenation.
2) Identifying the source of infection and treat with
antimicrobial therapy, surgery, or both.
3) Maintain adequate organ system function guided by
cardiovascular monitoring and interrupt the
pathogenesis of multiple organ dysfunction syndrome
(MODS).
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40. Principles in the management of septic shock includes :
Early recognition
Early and adequate antibiotic therapy
Source control
Early hemodynamic resuscitation and continued
support
Corticosteroids (refractory vasopressor-dependent
shock)
Tight glycemic control
Proper ventilator management with low tidal volume
in pts with ARDS
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41. Initial treatment includes support of respiratory and circulatory
function, supplemental oxygen, mechanical ventilation, and volume
infusion.
The resuscitation endpoints include both global (restoration of BP,
heart rate and urine output, lactate, base deficit, mixed venous
oxygen saturation, ventricular end-diastolic volume) and regional
(gastric tonometry) measures
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42. In about 1/3 of pts, hypotension and organ hypoperfusion
respond to fluid resuscitation; the goal is to maintain a
mean arterial BP of >65 mmHg (systolic pressure >90
mmHg)
Resuscitation of the circulation should target a central or
mixed venous oxyhemoglobin saturation (ScvO2 or SvO2,
respectively) of ≥70%
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43. High mixed venous saturation levels (> 70%) are seen in
sepsis and some other forms of distributive shock
Levels lower than this indicates that the patient is not only
in septic shock but also in hypovolemic or cardiogenic
shock
Hypovolemia should be corrected with fluid therapy and
low cardiac output caused by myocardial depression or
failure should be treated with inotropes (dobutamine) to
achieve a mixed venous saturation level of > 70% (normal
for the septic state)
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44. If these guidelines cannot be met by volume infusion, vasopressor
therapy is indicated
Treatment beyond these supportive measures includes
antimicrobial therapy, removal or drainage of the infected foci
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45. ADDITIONAL THERAPIES
Patients with septic shock develop hyperglycemia and
electrolyte abnormalities. Serum glucose should be
maintained in the reference range with insulin infusion
Hypokalemia, hypomagnesemia, and hypophosphatemia
should be measured and corrected if deficient
Glucocorticoids - because the pathogenesis of sepsis
involves an intense and potentially deleterious host
inflammatory response
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46. Nutrition because patients with septic shock generally
have high protein and energy requirements.
The enteral route is preferred for protection of gut
mucosa, avoiding translocation of organisms from the
gastrointestinal (GI) tract, lowering the complication rate
Correction of anemia and coagulopathy
External cooling
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If left untreated, shock transitions from this reversible phase to an irreversible phase and death from multisystem organ dysfunction (MSOF).
The clinician is required to identify the patient with shock promptly, make a preliminary assessment of the type of shock present, and initiate
therapy to prevent irreversible organ dysfunction and death
An example of the impaired oxygen utilization is cyanide poisoning, which causes uncoupling of oxidative phosphorylation.
Maintenance of the homeostatic environment of thecell is dependent on an adequate supply of ATP. ATP-dependent ionpumping systems, such as the Na+/K+ ATPase, consume 20–80%of the cell’s energy. Inadequate oxygen delivery and subsequentdecreased ATP disrupt the cell’s ability to maintain osmotic, ionic, andintracellular pH homeostasis.
The two components of CO are heart rate (HR) and stroke volume(SV), The major determinants of SV are preload, afterload (systemic vascularresistance, SVR), and cardiac contractility. CaO2 = (Hb × 1.39 × SaO2) + (PaO2 × 0.03)
At this point, there are no overt signs of organ dysfunction.
Laboratory evaluation may demonstrate mild organ dysfunction (i.e., elevated creatinine or troponin)
or a mild elevation of lactate
Altered capillary permeability allows leakage of fluid and protein out of the vascular space
in to the surrounding interstitial space causing a decrease in circulating volume and an increase in systemic interstitial edema
Appropriate interventions to restore perfusion and oxygen delivery
during these initial two phases of shock can reverse the organ dysfunction
At this point,the organ dysfunction is permanent and often the patient progressesto MSOF . During this stage, anuria and acute renal failure develop, acidemia further depresses CO,
hypotension becomes severe and recalcitrant(refractory) to therapy, hyperlactemia often worsens,
and restlessness evolves into obtundation and coma.