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Principles of Trauma and MCI > Shock > Flashcards

Shock Flashcards

1
Q

Fluid Composition

A

•  The 60-­40­‐20 Rule:
– 60 % of body weight is water
– 40% of body weight is intracellular fluids
– 20% of body weight is extracellular fluid

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2
Q

Stroke Volume

A

Stroke Volume is the amount of blood released from the heart per beat (Beat Volume)

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3
Q

Cardiac Output

A

The amount of blood circulated from the heart in a minute

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4
Q

3 Principle factors that affect Cardiac Output

A

– Preload
– Afterload
– Myocardial contractility

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5
Q

Preload

A

•  Blood delivered to the heart during diastole
•  Measured as LVEDV
– via PCWP (Pulmonary capillary wedge pressure) or CVP
•  Is dependant on venous return
•  Decreased venous return can reduce preload
•  Increased preload = increased stroke volume

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6
Q

Afterload

A
  •   Pressure at which the ventricle pumps against
  •   Blood is ejected only after the resistance is overcome
  •   Dependant on the degree of peripheral arterial vasoconstriction
  •   Vasoconstriction = increased resistance = increased aX\fterload = decreased stroke volume
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7
Q

Myocardial Contractility

A

The force generated by the myocardium on contraction

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8
Q

Blood Pressure

A

The resistance of blood flow by the force of friction between the blood and walls of the vessels

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9
Q

PVR (Peripheral Vascular Resistance)

A

may also be seen as Systemic Vascular Resistance (SVR)

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10
Q

Blood Flow

A
  •   PVR is dependent on internal diameter of vessels and viscosity of blood
  •   Aorta and arteries do not significantly change diameter
  •   Arterioles can change lumen to a factor of 5
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11
Q

Blood pressure Afterload

A
  •   Increased aXerload = ↑ BP

*   Decreased aXerload = ↓ BP

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12
Q

Baroreceptors

A

Sensory fibers located in the aortic and carotid tissues

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13
Q

Baroreceptors

Help control BP by two negative feedback mechanisms:

A

–  Lower BP in response to increased arterial pressure

–  Increase BP in response to decreased arterial pressure

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14
Q

Chemoreceptor Reflexes

A

•  Low arterial pressure stimulates peripheral chemoreceptor cells in
carotid and aortic bodies
•  If oxygen or pH decreases, stimulate vasomotor center of medulla

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15
Q

Venous Systemic pressures

A

 Venous system constricLon increases preload and SV

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16
Q

Arterial Systemic pressures

A

Arterial system constriction increases afterload and BP

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17
Q

Microcirculation

A
  •   Capillary network
  •   Responsive to needs of local tissues
  •   Will adjust to supply/bypass tissues in need/or without need
  •   Utilizes the pre and post capillary sphincters to facilitate these needs
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18
Q

Affects on microcirculation:

A 
–  Local control by tissues 
–  Nervous control of blood flow 
–  Baroreceptors 
–  Chemoreceptors 
–  CNS Ischemia response 
–  Hormonal response 
–  Adrenal-­medullary response 
–  Renin-­angiotensin-­aldosterone mechanism 
–  Vasopressin 
–  Reabsorption of tissue fluid
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19
Q

Oxygen

A
  •   Binds to hemoglobin and diffuses across capillary membrane
  •   97 -­‐ 100 % of hemoglobin are saturated in normal setting
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20
Q

Fick’s principle

A 
– Adequate FiO2 
– Appropriate O2diffusion from blood to capillaries 
– Adequate #’s of RBC’s 
– Proper tissue perfusion 
– Effective tissue off loading
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21
Q

Inadequate Tissue Perfusion (Three basic causes)

A

–  Inadequate cardiac output
–  Inadequate volume
–  Inadequate container

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22
Q

Inadequate cardiac output

A
  •   Inadequate preload
  •   Inadequate stroke volume
  •   Excessive afterload
  •   Inadequate heart rate
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23
Q

Inadequate volume

A

Hypovolemia
– Hemorrhagic
– Fluid loss

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24
Q

Inadequate container

A
  •   Over-­‐dilation

*   Excessive increase in SVR

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25
Q

Three true classifications of shock

A

– Anaphylactic
– Distributive
– Obstructive

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26
Q

Types of shock

A
  •   Psychogenic D
  •   Neurogenic D
  •   Respiratory D
  •   Hypovolemic D
  •   Hemorrhagic D
  •   Cardiogenic O / D
  •   Metabolic D
  •   Septic D
  •   Anaphylactic A
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27
Q

Psychogenic shock

A

•  Relative hypovolemia due to severe vasodilation
– Vasal vagal type response
•  Caused by sudden and temporary sympathetic nervous system failure.

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28
Q

Neurogenic shock

A
  •   Also know as Spinal Shock
  •   Massive Relative hypovolemia due to severe vasodilation
  •   Damage caused to the nervous system inhibiting its involuntary/voluntary control of homeostasis
  •   Sudden loss of sympathetic tone to the smooth muscles of the vessels below the point of injury
  •   Without constant stimulation widespread relaxation of these muscles causes a decrease in PVR and a drop in BP
29
Q

Respiratory shock

A
  •   Airway obstruction
  •   Hypoventilation
  •   Toxic inhalation
  •   Severe pulmonary edema
  •   Exacerbation COPD
  •   Multi-­lobe bilateral pneumonia (septic also)
30
Q

Hypovolemic Shock

A 
•  Inadequate perfusion of tissues caused by a volume deficiency other than blood. 
•  AKA third space loss 
•  Severe dehydration 
– diarrhea / vomiting 
–   peritonitis 
–   heat exhaustion 
–   severe burns
31
Q

Cardiogenic Shock

A
  •   Failure of the pump to supply O2tissues
  •   Potentially a combination shock ( like anaphylaxis ) depending on the etiology i.e.
  •   Massive AMI
  •   Valvular insufficiency
  •   Lethal dysrhythmia
  •   Cardiac arrest
  •   60 -­‐ 90 % mortality rate
32
Q

Metabolic Shock

A 
Shock as the result of a change in the chemistry of the endocrine system of the body. 
–  Insulin shock 
– Diabetic ketoacidosis 
– Adrenal gland failure 
– Thyroid gland failure 
– Pituitary gland failure 
– Renal failure 
– Toxic ingestion
33
Q

Septic Shock

A
  •   Massive infection and toxin production resulting in inability of the cell to exchange O2/CO2 resulting in cellular death
  •   Relative hypovolemia due to pool of blood in extremities
  •   1 month mortality rate 35 -­‐ 45 %
34
Q

Hemorrhagic Shock

A
  •   Internal/external hemorrhage resulting in hypovolemia and a systemic reduction in tissue perfusion.
  •   Mortality rate dependent on etiology, early recognition, and aggressive intervention
35
Q

Progression of shock

A
  •   Follows a sequence of stages related to changes in capillary perfusion and cellular necrosis
  •   The following examples given are for hemorrhagic shock (blood loss)
36
Q

Classifications of hemorrhage •  Class I (Vasoconstriction)

A

–  15 % blood loss (500 -­750 mls)
•  Healthy body can easily accommodate for the loss
•  No effect on BP, Pulse pressure or renal output

37
Q

Classifications of hemorrhage •  Class I (Vasoconstriction)

Compensation

A

•  Catecholamine release
•  RR
–  Normal ranges (may show slight increase to maintain O2 supplies with increased HR)
•  HR
–  Mild tachycardia to maintain CO due to reduced SV
•  B/P
–  Possible orthostatic hypotension (should appear within normal limits since CO is maintained)
•  Cap Refill
–  Normal
•  CNS
–  Mild anxiety

38
Q

ClassificaLons of hemorrhage •  Class II (Capillary and Venule Opening)

A

–  15 -­25 % blood loss (750 -­1250 mls)

39
Q

Classifications of hemorrhage Class II (Capillary and Venule Opening)
Compensation

A 
–  First line compensatory mechanisms can no longer maintain BP 
•  Secondary mechanisms now employed 
–  Early decompensation 
•  RR
–  Tachypnea 
•  HR 
–  Tachycardia 
•  B/P 
–  Hypotension may be prevalent (decreased pulse pressures) 
•  CR
–  Delayed 
•  CNS 
–  Anxiety 
•  Other 
–  Pale, Cool and Clammy Skin (due to peripheral shutdown and catecholamine releases)
40
Q

Capillary Washout

A

•  Accumulated cellular waste products cause post-­capillary sphincter to relax
•  Waste products, cellular contents, and coagulated cells dumped into venous circulation
– Profound metabolic acidosis
– Release of microscopic emboli
•  Body moves quickly towards death

41
Q

Classifications of hemorrhage

•  Class III (Disseminated Intravascular Coagulation)

A

–  25 -­‐ 35 % blood loss (1250 -­‐ 1750 mls)

42
Q

Classifications of hemorrhage
•  Class III (Disseminated Intravascular Coagulation)
Compensation

A 
–  Compensatory mechanisms unable to cope 
–  Late decompensation 
•  Without intervention, patient survival unlikely 
•  RR 
–  Tachypnea 
•  HR 
–  Tachycardia 
•  B/P 
–  Moderate/severe hypotension (narrowing pulse pressures) 
•  CR 
–  Delayed 
•  CNS 
–  Anxiety / confusion
43
Q

What is DIC ?

A

•  DisseminaLng Intravascular Coagulopathy
–  Phospholipids released due to injured/lysed cells
–  Prolonged low CO also triggers phospholipids release due to endothelium injury

44
Q

What is the result of DIC

A

–  Systemic coagulation
–  Diffuse fibrin formation (results in multiple microscopic emboli)
–  Exhaustion of clotting factors
–  Fibrinolytic system activate due to coagulation activation

45
Q

Classifications of hemorrhage

•  Class IV (Multiorgan Dysfunction Syndrome)

A

–  >35% blood loss (>1750 mls)

46
Q

Classifications of hemorrhage
•  Class IV (Multiorgan Dysfunction Syndrome)
Irreversible Shock

A 
•  Survival unlikely 
•  RR 
–  Tachypnea 
•  HR 
–  Thready, rapid pulse 
•  B/P 
–  Severe hypotension 
•  CR 
–  Delayed 
•  CNS 
–  Unresponsive 
•  Other 
–  Decreased to absent urine output
47
Q

Why dose this sequale occur?

A
  •   Glycogen and fat metabolized anaerobically
  •   Cell membrane permeability increases
  •   Na+& H2O enter the cell causing overhydration
  •   K++ leaks out and Ca+enters cell
  •   Lactic acid and CO2 levels increase and cell ruptures
48
Q

Physiological Response to Shock

A 
  Variations and determining factors 
– Age and relative health 
– Older adults 
– Children 
– General physical condition 
– Preexisting disease 
– Ability to activate compensatory mechanisms 
– Medications 
– Specific organ system affected
49
Q

Assessing Shock

A
  •   Early recognition is a key to patient survival
  •   Look for subtle signs both initially and ongoing
  •   Frequent ongoing assessments and trending
50
Q

Shock Assessment

A
  •   Scene assessment
  •   Primary assessment
  •   Focused history and secondary
  •   Detailed secondary assessment
  •   Ongoing assessment
51
Q

Shock Management

A
  •   Airway and breathing
  •   Hemorrhage control
  •   Fluid resuscitation
  •   Temperature control
  •   Pharmacological intervention
52
Q

Differential Shock Assessment Findings

A

Assumed to be Hypovolemic until proven otherwise

53
Q

Differential Shock Assessment Findings
Cardiogenic shock
–  Differentiate from Hypovolemic shock by:

A 
•  Chief complaint 
–  Chest pain 
–  Dyspnea 
–  Tachycardia 
•  Heart rate  
•  Signs of congestive heart failure  
•  Dysrhythmias
54
Q

Differential Shock Assessment Findings
•  Distributive shock
– Differentiate from Hypovolemic shock by:

A 
•  Mechanism suggesting vasodilatation 
–  Spinal cord injury 
–  Drug overdose 
–  Sepsis 
–  Anaphylaxis 
•  Warm, flushed skin  
•  Lack of tachycardia response (not reliable)
55
Q

Differential Shock Assessment Findings
•  Obstructive shock
– Differentiate from hypovolemic shock by signs and symptoms of:

A
  •   Cardiac tamponade
  •   Tension pneumothorax
  •   Pulmonary embolism
56
Q

Detailed Physical Examination

A 
•  Vital signs 
– Pulse 
– Blood pressure 
– Orthostatic vital signs 
•  Evaluate patient’s ECG
57
Q

Resuscitation

A

Restore adequate tissue oxygenation by:
– Ensuring adequate oxygenation
– Maintaining effective volume-­to-­container size ratio
– Rapid transport to appropriate medical facility

58
Q

Red Blood Cell Oxygenation

A

•  Need adequate tissue oxygenation
•  For red blood cell oxygenation:
– Patent airway
– Support ventilation with high FiO2
•  If necessary, positive-­pressure ventilation
– Correct airway abnormalities that interfere with adequate ventilation

59
Q

Ratio of Volume to Container Size

A

•  Container must be full of fluid to carry oxygen
•  Accomplish by:
– Decreasing size of container
•  Especially in shock states not associated with hemorrhage
– Vasoactive medications in some distributive shock (Sepsis and Cardiogenic)
– Volume replacement may be needed

60
Q

Fluid Resuscitation

A

•  What solutions to use?
– Crystalloid
– Colloid

61
Q

Key Principles in Managing Shock

A
  •   Open airway
  •   High‐concentration oxygen
  •   Assist ventilation as needed
  •   Control external bleeding (if present)
  •   IV fluid replacement if appropriate
  •   Consider PASG (if protocols allow)
  •   Maintain body temperature
  •   Monitor ECG and oxygen saturation
  •   Reassess vital signs
62
Q

Hypovolemic Shock

A

Correct circulatory deficit and its causes
– Crystalloid fluid replacement for dehydration
– Volume replacement for hemorrhage (controversial)
– Definitive surgery
– Critical care support
– Postoperative rehabilitation

63
Q

Hypovolemic Shock

A

•  Fluid volume replacement
•  Large volume fluid replacement if:
– Systolic BP >100 mmHg AND
–  Isolated head or extremity injuries
– Not for penetrating trauma in urban center
•  Blunt or penetrating trauma in rural area:
–  IV Fluids to maintain systolic BP>90 mm Hg

64
Q

Cardiogenic Shock

A

•  Improve pumping action of heart and manage dysrhythmias
– Fluid replacement
– Drug therapy (if needed)
– Cardiogenic shock due to myocardial ischemia or infarction requires:
•  Reperfusion strategies
•  Possible circulatory support
– Manage tension pneumothorax and cardiac tamponade

65
Q

Neurogenic Shock

A

•  Treatment similar to hypovolemia
– Avoid circulatory overload
– Monitor lung sounds for pulmonary congestion
•  Vasopressors may be indicated

66
Q

Anaphylactic Shock

A 
•  Subcutaneous epinephrine in acute anaphylactic reactions 
•  Other therapy 
– Oral, IV, or IM antihistamines 
– Bronchodilators  
– Steroids reduce inflammatory response 
– Crystalloid volume replacement 
– Airway management
67
Q

Septic Shock Treatment

A

•  Management of hypovolemia (if present)
•  Correction of metabolic acid-­‐base imbalance
•  Prehospital care
– Fluid resuscitation
– Respiratory support
– Vasopressors to improve cardiac output
– Thorough history to find source of sepsis

68
Q

Integration of Patient Assessment and the Treatment Plan

A

•  For severe hemorrhage or shock:
– Rapid recognition
–  Initiation of treatment
– Prevention of additional injury
– Rapid transport to appropriate hospital
– Advance notification to receiving facility

69
Q

Shock Definition

A

•  Shock is a state of inadequate perfusion of the tissues.
– Transitional stage between homeostasis and death
– Underlying killer of all trauma patients
•  Often presents with subtle signs and symptoms

Principles of Trauma and MCI (7 decks)

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