2.Shock (1).ppt management and it's causes ppt

Shock lecture

1. Shock
Dr Yohannis C.(Assistant Professor of General Surgery)
Prepared for:C1 Medical students
April,2024
JUMC,Jimma,Ethiopia
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2. Outline
•Overview
•Pathophysiology
•Clinical approach
•General Management Principle
•Types of shock
•End points of Resuscitation
•References
2

3. Overview
•Shock, regardless of the etiology, is the failure to meet the metabolic needs of
the cell and the consequences that ensue
•Modern definition: inadequate tissue perfusion marked by decreased delivery of required
metabolic substrates and inadequate removal of cellular waste products
•Six types of shock:
•Hypovolemic
•Septic (vasodilatory)
•Neurogenic
•Cardiogenic
•Obstructive
•Pulmonary embolism, tension pneumothorax, and cardiac tamponade
•Traumatic shock
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4. Pathophysiology of Shock
•The initial physiologic responses in shock are driven by tissue
hypoperfusion and the developing cellular energy deficit
•This imbalance between cellular supply and demand leads to
neuroendocrine and inflammatory responses.
•Many of the organ-specific responses are aimed at maintaining perfusion
in the cerebral and coronary circulation
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5. Cont.
5

6. Cont.
3 phases of shock
•Compensated phase: compensation though the neuroendocrine
response
•Decompensated phase: cellular death and ongoing tissue injury
•Microcirculatory dysfunction, parenchymal tissue damage, and inflammatory
cell activation
•The “vicious cycle of shock”
•Irreversible phase: hemodynamic derangements and cardiovascular
collapse as a result of persistent hypoperfusion
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7. Cont.
•The “vicious cycle of shock”
•Regardless of the etiology, decreased tissue perfusion and shock results in a
feed-forward loop that can exacerbate cellular injury and tissue dysfunction
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8. Cont.
•Types of responses
•Neuroendocrine response
•SNS
•Hormonal (cortisol, glucagon, RAAS, ADH)
•Immunologic and inflammatory response
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9. Neuroendocrine responses to shock
•The goal of the neuroendocrine response to shock is to maintain
perfusion to the heart and the brain.
•The mechanisms include:
•Autonomic control of peripheral vascular tone and cardiac contractility
•Hormonal response to stress and volume depletion
•Local microcirculatory mechanisms that are organ specific and regulate regional
blood flow
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10. Cont.
•Afferent impulses transmitted from the periphery are processed within the
CNS and activate the reflexive effector responses or efferent impulses
•The effector responses are designed to expand plasma volume, maintain
peripheral perfusion and tissue O
2 delivery, and restore homeostasis
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11. Afferent Signals
•Afferent stimuli
•Baroreceptors
•Loss of circulating blood volume
•Chemoreceptors
•Hypoxemia
•Hypercarbia
•Acidosis
•Osmoreceptors
•Osmolality
•Pain receptors
•Pain
•Change in temperature
•Hypoglycemia
•Emotional arousal
•Infection/inflammation
•Mediated by a variety of protein and nonprotein mediators that are produced at the site of injury
•Cytokines, histamine, eicosanoids, and endothelins
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12. Efferent Signals
•Neural responses
•Hormonal responses
•Immune and inflammatory responses
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13. Immune and inflammatory responses to shock
13

14. Effects of Shock
14
•Cellular Hypoperfusion
•Microcirculations are affected
•Vasoconstrictions
•Capillary dysfunction
•Metabolic effects-glycolysis,gluconeogenesis,lipolysis,insulin
resistance.

15. Summary of Hemodynamic responses
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16. Clinical approach to shock
•Symptoms
•History that suggests the cause
•Volume loss, infection, trauma, cardiac illness, anaphylaxis
•Orthostatic light headedness
•Weakness
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17. Cont.
•Signs
•PR
•
Usually elevated (bradycardia in neurogenic shock)
•Decrease in pulse volume
•Pulsus paradoxus
•Decrease in SBP with inspiration (Present in cardiac tamponade)
•BP
•Orthostatic hypotension
•Fall in DBP >15 to 20 mm Hg when the patient is sitting or standing
•Hypotension
•Shock may occur with a normal BP, and hypotension may occur without shock
•Shock index (HR/SBP): elevated in volume loss and LV dysfunction (normal is 0.5 to 0.7)
•RR
•Elevated
•Tempreature
•Hypothermia or fever
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18. Cont.
•Respiratory system
•Tachypnea
•Increased MV and dead space
•Respiratory failure
•ARDS
•Cardiovascular system
•Neck veins…..distended or flattened
•Tachycardia and week pulse
•Decreaed capillary refill
•Muffled heart sounds
•Arrhythmias
•Murmurs
•Splanchnic organs
•Ileus
•GI bleeding
•Acute cholecystitis
•Mesenteric ischemia
•Pancreatitis
•Renal
•Decreased GFR and oliguria
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19. Cont.
•Skin
•Pallor
•Duskiness/cyanosis
•Sweating
•Altered temperature
•MSS
•Ischemia/gangrene
•CNS
•Restlessness, disorientation, confusion, coma
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20. General Management Principle
•Core principles in the management of the critically ill or injured patient
include:
•Definitive control of the airway
•Control of active hemorrhage
•Volume resuscitation with blood products (red blood cells, plasma, and platelets)
with limited volume of crystalloid
•Excessive fluid resuscitation may exacerbate bleeding
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21. Mgt..
•Establish airway and deliver oxygen
•Secure venous access with large bore cannula and start infusion of fluids
•Patient positioning
•Prevention of hypothermia
•Correcting acid-base and electrolyte disturbances
•DVT prophylaxis (for high risk patients)
•GI prophylaxis
•Analgesics (preferably IV narcotics)
•Treatment of specific causes of shock
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22. Monitoring
•Minimum
•Electrocardiogram
•Pulse oximetry
•Blood pressure
•Urine output
•Additional modalities
•Invasive blood pressure
•Central venous pressure
•Base deficit and serum lactate
•Cardiac output
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23. Specific Types of shock
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24. Hypovolemic/Hemorrhagic
•The most common cause of shock in the surgical or trauma patient
•Shock in a trauma patient or postoperative patient should be presumed to be due to
hemorrhage until proven otherwise
•Etiology
•Non-haemorrhagic
•Poor fluid intake
•Excessive fluid loss
•Vomiting, diarrhoea, urinary loss (e.g. diabetes)
•Third-spacing
•Hemorrhagic
•Most common cause of shock in the surgical or trauma patient
•Trauma: external, intrathoracic, intra-abdominal, retroperitoneal, and long bone fractures
•Non-trauma: GI bleeding, hemoptysis, urinary tract bleeding, and gynecologic bleeding
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25. Cont.
•The clinical signs of shock may be evidenced by agitation, cool clammy
extremities, tachycardia, weak or absent peripheral pulses, and
hypotension
•Such apparent clinical shock results from at least 25% to 30% loss of the blood
volume
•However, substantial volumes of blood may be lost before the classic clinical
manifestations of shock are evident
•This is especially true in young healthy patients with vigorous compensatory mechanisms
•Elderly patients have an overall poor physiologic reserve
•They may also be taking medications that either promote bleeding (e.g., warfarin or aspirin) or
mask the compensatory responses to bleeding (e.g., β-blockers)
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26. Cont.
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27. Cont.
•Evaluation
•Clinical examination
•A systolic blood pressure (SBP) of less than 110 mmHg is a clinically relevant definition of
hypotension and hypoperfusion
•Hematocrit
•It must be noted that lack of a depression in the initial hematocrit does not rule out substantial
blood loss or ongoing bleeding
•Lactate and base deficit
•Serum lactate and base deficit are measurements that are helpful to both estimate and monitor
the extent of bleeding and shock
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28. Cont.
•Treatment
•Secure the airway and provide adequate ventilation
•Control the source of blood loss (ASAP)
•The probability of death is increased by approximately 1% for each 3 minutes in the emergency
department in patients requiring emergency laparatomy
•Attempts to stabilize an actively bleeding patient anywhere but in the OR are inappropriate
•IV volume resuscitation
•Damage control resuscitation
•Begins in the emergency department, continues into the OR, and into the ICU
•Initial resuscitation is limited to keep SBP around 80 to 90 mmHg for penetrating and around 110 mmHg for
blunt injuries (to prevent secondary TBI) - “Hypotensive resuscitation”
•This prevents renewed bleeding from recently clotted vessels
•Warm patients and prevent coagulopathy
•Treat electrolyte and acid-base disturbances
•Control pain
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29. Septic Shock (Vasodilatory Shock)
•Vasodilatory shock is characterized by peripheral vasodilation with
resultant hypotension and resistance to treatment with vasopressors
•It is the result of dysfunction of the endothelium and vasculature
secondary to circulating inflammatory mediators or as a response to
prolonged and severe hypoperfusion
•Vasodilatory shock seems to represent the final common pathway for profound and
prolonged shock of any etiology
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30. Cont.
•Causes of septic and vasodilatory shock
•Systemic response to infection (the most frequently encountered form of vasodilatory
shock)
•Non-infectious systemic inflammation
•Pancreatitis
•Burns
•Anaphylaxis
•Prolonged, severe hypotension
•Hemorrhagic shock
•Cardiogenic shock
•Metabolic
•Hypoxic lactic acidosis
•Carbon monoxide poisoning
•Acute adrenal insufficiency
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31. Cont.
•Septic shock is a by-product of the body’s response to disruption of the
host-microbe equilibrium, resulting in invasive or severe localized
infection
•Despite advances in intensive care, the mortality rate for severe sepsis
remains at 30% to 50%
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32. Cont.
•Definitions
•SIRS (≥2 of the following)
•Temp (core) >38°C or <36°C
•Heart rate >90 beats/min
•RR >20 breaths/min for patients spontaneously ventilating or a PaCO
2
<32 mm
Hg
•WBC count >12,000 cells/mm
3
or <4000 cells/mm
3
or >10% immature (band)
cells in the peripheral blood smear
•Sepsis
•SIRS with a clearly established focus of infection
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33. Cont.
•Severe Sepsis
•Sepsis associated with organ dysfunction and hypoperfusion
•Systolic blood pressure <90 mm Hg
•>40 mm Hg fall from normal systolic blood pressure
•Acute mental status changes
•Oliguria
•Lactic acidemia
•Septic shock
•Severe sepsis plus
•No response for iv fluid infusion (for at least 1 hr)
•Requiring inotropes or vasoactive agents to maintain SBP ≥90 mmHg or MABP ≥70
mmHg
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34. Sequential organ failure assessment
qSOFA
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35. Cont.
•qSOFA
•Provides simple bedside criteria to identify adult patients with suspected
infection who are likely to have poor outcomes
•Criteria (≥2)
•GCS score of ≤13
•SBP of ≤100 mm Hg
•Respiratory rate of ≥22/min
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36. Cont.
•Sources of infection
•Respiratory (38%)
•Urinary tract (21%)
•Intra-abdominal (16.5%)
•Device (1.3%)
•CNS (0.8%)
•Others (11.3%)
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37. Treatment of Septic shock
•Management of airway and breathing
•Severely obtunded patients and patients whose work of breathing is excessive require
intubation and ventilation to prevent respiratory collapse
•Fluid resuscitation
•It should be at least 30 mL/kg within the first 4 to 6 hours
•Empiric IV antibiotics
•Should be started within the first hour of recognition of severe sepsis
•Mortality increases by 7.6% for each hour delay to appropriate antibiotics
•Source control
•Drainage of infected fluid collections, removal of infected foreign bodies, debridement of
devitalized tissue, and removal/resection of infected organs
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38. Cont.
•Vasopressors
•To maintain MABP ≥65 mmHg
•Catecholamines are the vasopressors used most often, with norepinephrine being the
first-line agent followed by epinephrine
•Dobutamine therapy is recommended for patients with cardiac dysfunction
•Dopamine should not be used for “renal protection”
•Steroids
•Severe sepsis often is associated with adrenal insufficiency or glucocorticoid receptor
resistance
•If SBP remains less than 90 mmHg despite appropriate fluid and vasopressor therapy,
hydrocortisone at 200 mg/d for 7 days in four divided doses or by continuous infusion
should be considered (dose ≤300 mg/d)
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39. Cont.
•Management of end organ dysfunction
•ARDS (Use of lower ventilatory tidal volumes, higher levels of PEEP, alveolar recruitment
maneuvers, and prone positioning)
•Tight glucose management
•Maintenance of blood glucose between 80 and 110 mg/dL (upper blood glucose target of 180 mg/dL)
•Transfusion
•RBCs: when hemoglobin decreases to 7 g/dL
•FFP: when there is bleeding or planned invasive procedures
•Platelets
•Counts are <5000/mm3 regardless of bleeding
•Counts are 5000–30,000/mm3 and there is significant bleeding risk
•Any number with bleeding
•DVT and GI prophylaxis
•Pain control
•Counseling
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40. 40

41. Cardiogenic Shock
•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)
•Elevated pulmonary artery wedge pressure (>15 mmHg)
•Reduced cardiac index (<2.2 L/min per square meter)
•Other causes of hypotension must be excluded
•Mortality rates for are 50% to 80%
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42. Cont.
•Acute, extensive MI is the most common cause of cardiogenic shock
•Other causes
•VHD
•Arrhythmia
•End-stage cardiomyopathy
•Myocarditis
•Severe myocardial contusion
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43. Cont.
•Treatment
•Maintenance of adequate oxygenation
•To ensure adequate myocardial O
2
delivery
•Judicious fluid administration
•To avoid fluid overload and development of cardiogenic pulmonary edema
•Inotropic support
•May be indicated to improve cardiac contractility and cardiac output
•Dopamine may be preferable to dobutamine
•Correction of electrolyte abnormalities
•Commonly hypokalemia and hypomagnesemia
•Adequate treatment of pain
•To minimize sympathetic discharge
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44. Obstructive Shock
•Due to etiologies that result in mechanical obstruction of venous return
•Tension pneumothorax
•Pericardial tamponade
•Pulmonary embolus
•IVC obstruction
•Deep venous thrombosis
•Gravid uterus on IVC
•Neoplasm
•Increased intrathoracic pressure
•Excess positive end-expiratory pressure
•Neoplasm
•Reduced filling of the right side of the heart results in decreased cardiac output
associated with increased central venous pressure
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45. Cont.
•Tension pneumothorax
•Most common cause of obstructive shock in trauma patients
•Classic clinical findings
•Respiratory distress (in an awake patient)
•Hypotension
•Diminished breath sounds over one hemithorax
•Hyperresonance to percussion (may be difficult to appreciate in a noisy resuscitation area)
•Jugular venous distention (may be absent in a hypovolemic patient)
•Shift of mediastinal structures to the unaffected side with tracheal deviation (is a late finding
and often is not apparent on clinical examination)
•Practically, 3 findings are sufficient to make the diagnosis
•Respiratory distress or hypotension, decreased lung sounds, and hypertympany to percussion
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46. Cont.
•Chest x-ray findings
•Deviation of mediastinal structures
•Depression of the hemidiaphragm
•Hypo-opacification with absent lung markings
•Treatment
•Definitive treatment of a tension pneumothorax is immediate tube
thoracostomy
•Most recommend placement in the fourth intercostal space (nipple level) at the
anterior axillary line
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47. Cont.
•Cardiac tamponade
•It results from the accumulation of blood within the pericardial sac, usually from
penetrating trauma or chronic medical conditions such as heart failure or uremia
•The hemodynamic abnormalities are due to elevation of intracardiac pressures with
resultant decrease in cardiac output
•Acutely, the pericardium does not distend; thus small volumes of blood may
produce cardiac tamponade
•If the effusion accumulates slowly, the quantity of fluid producing cardiac tamponade may
reach 2000 mL
•Signs
•Beck’s triad: hypotension, muffled heart tones, and neck vein distention
•Pulsus paradoxus: decreased systemic arterial pressure with inspiration
•Elevated CVP
•Elevated right atrial and right ventricular pressure
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48. Cont.
•Diagnosis
•Echocardiography
•It has become the preferred test for the diagnosis
•Pericardiocentesis
•To diagnose pericardial blood and potentially relieve tamponade
•Diagnostic pericardial window
•It represents the most direct method to determine the presence of blood within the
pericardium
•The procedure is best performed in the operating room under general anesthesia
•Rx-Therapeutic pericardiocentesis
•Pericardiotomy
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49. Traumatic Shock
•In traumatic shock, soft tissue and bony injury leads to the activation
of inflammatory cells and the release of circulating factors (DAMPs)
which are recognized by pattern recognition receptors (PRRs)
•Small-volume hemorrhage accompanied by soft tissue injury or any
combination of the other types of shock that precipitates rapidly
progressive pro-inflammatory activation
•Even simple hemorrhage induces pro-inflammatory activation that
results in many of the cellular changes typically ascribed only to septic
shock
•Attributable to the release of cellular products termed DAMPs
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50. Cont.
•Treatment
•Prompt control of hemorrhage
•Adequate volume resuscitation
•Management of injured tissue
•Stabilization of bony injuries
•Appropriate treatment of soft tissue injuries
•Débridement of non-viable tissue
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51. Neurogenic Shock
•It refers to diminished tissue perfusion as a result of loss of vasomotor tone to
peripheral arterial beds
•Loss of vasoconstrictor impulses results in increased vascular capacitance, decreased venous
return, and decreased cardiac output
•It 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
•Other causes
•Spinal cord neoplasm
•Spinal/epidural anesthetic
•Hypotension contributes to the worsening of acute spinal cord injury as the result of
further reduction in blood flow to the spinal cord
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52. Cont.
•Classic description of neurogenic shock
•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
•With or without radiographic evidence of a vertebral column fracture

•Other causes of shock must be sought and excluded
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53. Cont.
•Difficulties in diagnosis
•Spinal cord injuries often have head injuries that may make identification of motor
and sensory deficits difficult in the initial evaluation
•In the multiply injured patient, other causes of hypotension, including hemorrhage,
tension pneumothorax, and cardiogenic shock may mask neurogenic shock
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54. Cont’d
•Treatment
•Airway and breathing
•Fluid resuscitation
•Most patients with neurogenic shock will respond to restoration of intravascular volume alone
•Vasoconstrictors
•They will improve peripheral vascular tone, decrease vascular capacitance, and increase
venous return
•They should only be considered once hypovolemia is excluded as the cause of the
hypotension
•Stabilize the vertebral fracture
•Restoration of normal blood pressure and adequate tissue perfusion should precede any
operative attempts to stabilize the vertebral fracture
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55. Endpoints in Resuscitation
•The goal in the treatment of shock is restoration of adequate organ
perfusion and tissue oxygenation
•Resuscitation is complete when O
2 debt is repaid, tissue acidosis is corrected, and
aerobic metabolism is restored
•Recognition of subclinical hypoperfusion requires information beyond
vital signs and urinary output
•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 O
2 saturation
55

56. Cont.
•Goals of initial resuscitation
•Mean arterial pressure ≥65mmHg
•Urine output ≥0.5 mL/kg/hr
•Central venous pressure 8–12 mmHg
•Central venous or mixed venous oxygen saturation ≥70% or ≥65%, respectively
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57. Cont.
•Endpoints in resuscitation
•Systemic/global
•Vital signs
•Cardiac output
•Oxygen delivery and consumption
•Lactate
•Base deficit
•Tissue specific
•Gastric tonometry
•Tissue pH, oxygen, carbon dioxide levels
•Near infrared spectroscopy
•Cellular
•Membrane potential
•ATP
57

58. Cont.
•Surrogate parameters have been sought to estimate the O
2 debt
•Lactate
•It is generated by conversion of pyruvate to lactate by lactate dehydrogenase
in the setting of insufficient O2
•Time interval to normalize the serum lactate is important prognostic
indicators for survival
•Base Deficit
•It usually is measured by arterial blood gas analysis in clinical practice as it is
readily and quickly available
•It may be better predictors of mortality than the plasma lactate alone
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59. References
•Schwartz’s principle of surgery 11
th
ed.
•Sabiston Textbook of surgery 21th ed.
•Bailey and Love’s short practice of surgery 27 th ed.
•Uptodate 2018
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