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1. Shock
Moderators
Dr.Belay (MD, Internist)
Presenters
Abduljebar Mohammed C I
Gudeta Noto C I
Samira Gemada C I
Date: 17th January, 2024
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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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10. Classification of shock
Hypovolaemic
Cardiogenic
Obstructive
Distributive
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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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21. APPROACH TO THE
PATIENT WITH SHOCK
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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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26. NECK:
 Jugular venous distention
 Distended neck vein
 Delayed carotid upstroke
 Carotid bruits
 Meningeal signs
Lungs:
 Tachypnea
 Crackles/rales
 Consolidation
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27. Cardiovascular system;
 Arrythmia
 Murmurs or S3 gallop
 Diffuse PMI
 Right or left ventricular heave
 Distant heart sounds
 Rub
 Pulsus paradoxus
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28. Abdomen
 Tenseness
 Distension
 Tenderness
 Rebound/guarding
 Absent bowel sounds
 Pulsitile masses
 Ascites
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29. Rectal:
 Decreased tone
 Blood (hematochezia )
Extremities:
 Calf swelling/palpable cords
 Unequal pulses
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30. Integumentary:
 Cold, clammy
 Warm, hyperemic
 Rashes
 Petechiae
 Urticaria
 Cellulitis
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31. Neurologic
 Agitation
 Confusion
 Delirium
 Obtundation
 Coma
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32. INVESTIGATIONS
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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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47. Obstructive shock
 Tension pneumothorax
 Chest tube , needle decompression
 Cardiac tamponade
 Pericardiocentesis
 Pulmonary embolism
 Heparin ,consider thrombolytics
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48. 48
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Harrison Principles of Medicine 21st edition
Up to date 21.6
References

49. 49
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