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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
Three true classifications of shock
– Anaphylactic – Distributive – Obstructive
26
Types of shock
*   Psychogenic D *   Neurogenic D *   Respiratory D *   Hypovolemic D *   Hemorrhagic D *   Cardiogenic O / D *   Metabolic D *   Septic D *   Anaphylactic A
27
Psychogenic shock
•  Relative hypovolemia due to severe vasodilation – Vasal vagal type response •  Caused by sudden and temporary sympathetic nervous system failure.
28
Neurogenic shock
*   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
Respiratory shock
*   Airway obstruction *   Hypoventilation *   Toxic inhalation *   Severe pulmonary edema *   Exacerbation COPD *   Multi-­lobe bilateral pneumonia (septic also)
30
Hypovolemic Shock
``` •  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
Cardiogenic Shock
*   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
Metabolic Shock
``` 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
Septic Shock
*   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
Hemorrhagic Shock
*   Internal/external hemorrhage resulting in hypovolemia and a systemic reduction in tissue perfusion. *   Mortality rate dependent on etiology, early recognition, and aggressive intervention
35
Progression of shock
*   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
Classifications of hemorrhage •  Class I (Vasoconstriction)
–  15 % blood loss (500 -­750 mls) •  Healthy body can easily accommodate for the loss •  No effect on BP, Pulse pressure or renal output
37
Classifications of hemorrhage •  Class I (Vasoconstriction) | Compensation
•  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
ClassificaLons of hemorrhage •  Class II (Capillary and Venule Opening)
–  15 -­25 % blood loss (750 -­1250 mls)
39
Classifications of hemorrhage Class II (Capillary and Venule Opening) Compensation
``` –  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
Capillary Washout
•  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
Classifications of hemorrhage | •  Class III (Disseminated Intravascular Coagulation)
–  25 -­‐ 35 % blood loss (1250 -­‐ 1750 mls)
42
Classifications of hemorrhage •  Class III (Disseminated Intravascular Coagulation) Compensation
``` –  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
What is DIC ?
•  DisseminaLng Intravascular Coagulopathy –  Phospholipids released due to injured/lysed cells –  Prolonged low CO also triggers phospholipids release due to endothelium injury
44
What is the result of DIC
–  Systemic coagulation –  Diffuse fibrin formation (results in multiple microscopic emboli) –  Exhaustion of clotting factors –  Fibrinolytic system activate due to coagulation activation
45
Classifications of hemorrhage | •  Class IV (Multiorgan Dysfunction Syndrome)
–  >35% blood loss (>1750 mls)
46
Classifications of hemorrhage •  Class IV (Multiorgan Dysfunction Syndrome) Irreversible Shock
``` •  Survival unlikely •  RR –  Tachypnea •  HR –  Thready, rapid pulse •  B/P –  Severe hypotension •  CR –  Delayed •  CNS –  Unresponsive •  Other –  Decreased to absent urine output ```
47
Why dose this sequale occur?
*   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
Physiological Response to Shock
```   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
Assessing Shock
*   Early recognition is a key to patient survival *   Look for subtle signs both initially and ongoing *   Frequent ongoing assessments and trending
50
Shock Assessment
*   Scene assessment *   Primary assessment *   Focused history and secondary *   Detailed secondary assessment *   Ongoing assessment
51
Shock Management
*   Airway and breathing *   Hemorrhage control *   Fluid resuscitation *   Temperature control *   Pharmacological intervention
52
Differential Shock Assessment Findings
Assumed to be Hypovolemic until proven otherwise
53
Differential Shock Assessment Findings Cardiogenic shock –  Differentiate from Hypovolemic shock by:
``` •  Chief complaint –  Chest pain –  Dyspnea –  Tachycardia •  Heart rate •  Signs of congestive heart failure •  Dysrhythmias ```
54
Differential Shock Assessment Findings •  Distributive shock – Differentiate from Hypovolemic shock by:
``` •  Mechanism suggesting vasodilatation –  Spinal cord injury –  Drug overdose –  Sepsis –  Anaphylaxis •  Warm, flushed skin •  Lack of tachycardia response (not reliable) ```
55
Differential Shock Assessment Findings •  Obstructive shock – Differentiate from hypovolemic shock by signs and symptoms of:
*   Cardiac tamponade *   Tension pneumothorax *   Pulmonary embolism
56
Detailed Physical Examination
``` •  Vital signs – Pulse – Blood pressure – Orthostatic vital signs •  Evaluate patient’s ECG ```
57
Resuscitation
Restore adequate tissue oxygenation by: – Ensuring adequate oxygenation – Maintaining effective volume-­to-­container size ratio – Rapid transport to appropriate medical facility
58
Red Blood Cell Oxygenation
•  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
Ratio of Volume to Container Size
•  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
Fluid Resuscitation
•  What solutions to use? – Crystalloid – Colloid
61
Key Principles in Managing Shock
*   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
Hypovolemic Shock
Correct circulatory deficit and its causes – Crystalloid fluid replacement for dehydration – Volume replacement for hemorrhage (controversial) – Definitive surgery – Critical care support – Postoperative rehabilitation
63
Hypovolemic Shock
•  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
Cardiogenic Shock
•  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
Neurogenic Shock
•  Treatment similar to hypovolemia – Avoid circulatory overload – Monitor lung sounds for pulmonary congestion •  Vasopressors may be indicated
66
Anaphylactic Shock
``` •  Subcutaneous epinephrine in acute anaphylactic reactions •  Other therapy – Oral, IV, or IM antihistamines – Bronchodilators – Steroids reduce inflammatory response – Crystalloid volume replacement – Airway management ```
67
Septic Shock Treatment
•  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
Integration of Patient Assessment and the Treatment Plan
•  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
Shock Definition
•  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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