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OBHG Education Subcommittee
ONTARIO
BASE HOSPITAL GROUP
ADVANCED ASSESSMENT
Shock
2007 Ontario Base Hospital Group
QUIT
OBHG Education Subcommittee
AUTHOR(S)
Mike Muir AEMCA, ACP, BHSc
Paramedic Program Manager
Grey-Bruce-Huron Paramedic Base Hospital
Grey Bruce Health Services, Owen Sound
Kevin McNab AEMCA, ACP
Quality Assurance Manager
Huron County EMS
References – Emergency Medicine
REVIEWERS
Rob Theriault EMCA, RCT(Adv.), CCP(F)
Peel Region Base Hospital
Donna L. Smith AEMCA, ACP
Hamilton Base Hospital
2007 Ontario Base Hospital Group
ADVANCED ASSESSMENT
Shock
OBHG Education Subcommittee
Shock
Widespread Tissue Hypoperfusion
Results In
Inadequate oxygenation and supply of nutrients at a cellular level
Inadequate removal of metabolic waste products
Due To
Inadequate circulation of blood
Leads To
Generalized impairment of cellular function
Ultimate cell death
OBHG Education Subcommittee
ENERGY PRODUCTION
Human Body Likes Presence of Oxygen
To Produce Energy
OBHG Education Subcommittee
 Energy production in the setting of
oxygen
 High amount of energy production
 38 Adenosine Tri-phosphate
 Low waste (Acid Production)
Aerobic Metabolism
OBHG Education Subcommittee
 Energy production without oxygen
 Low amount of energy production
 2 Adenosine Tri-phosphate (Glycolysis
Sugar Splitting)
 High acid production
 Pyruvic to Lactic Acid results in metabolic
acidosis
 Cell functions cease due to lack of energy
and acidosis
 Cell death
Anaerobic Metabolism
OBHG Education Subcommittee
S Septic, Spinal
H Hypovolemic
O Obstructive, Mechanical
C Cardiogenic
K Anaphylactic
OBHG Education Subcommittee
 Caused by serious systemic bacterial infection
(usually gram negative bacteria)
 Causes a release of vasoactive agents that affect
microcirculation (arterioles and venules dilate
{increased container size}, capillary leak {loss of
volume}
 Increased container size and loss of volume lead to
inadequate tissue perfusion
Septic Shock
OBHG Education Subcommittee
 Signs and Symptoms
 Fever (may not have fever), tachycardia, tachypnea,
confusion, petechiae around eyes, purpura
 Look for history of recent infection (bladder,
pneumonia)
 Treatment
 Identify and correct infection (antibiotics)
 Manage hypovolemia and acid base imbalance (fluid
therapy, vasoactive and cardiac drugs)
Septic Shock
OBHG Education Subcommittee
 Predominantly causes by Spinal Cord Injury, may
also be caused by head injury, CVA or drug overdose
 Block of sympathetic outflow results in peripheral
vasodilatation
Neurogenic Shock/Spinal Shock
OBHG Education Subcommittee
 Vasomotor paralysis below level of spinal cord injury
 Normal vasomotor tone through sympathetic control
is lost
 Results in vasodilatation, increased container size
 Even normal intravascular volume is insufficient to fill
vascular compartment
 Unable to mount compensatory tachycardia
 Heart rate remains unchanged with hypotension
 Look for line where sympathetic response ends
 Treatment
 Similar to Hypovolemia, caution not to cause fluid
overload
Spinal Shock
OBHG Education Subcommittee
 Blood flow disrupted due to mechanical obstruction
 Examples
 Tension Pnemothorax - Increased intrathoracic
pressure impedes low pressured venous return,
increased pressure can twist and compress heart
 Cardiac Tamponade - Compression of heart due to
accumulation of fluid or in pericardial sac (usually due
to trauma or infection)
Mechanical Shock/Obstructive
OBHG Education Subcommittee
 Examples cont’d
 Pulmonary Embolism - Blockage of blood flow in
pulmonary circulation (fat, air, thrombus)
 Aortic Dissection - Blood flow obstructed distal to left
ventricle (Dissection of Aortic Arch= b/p right arm
greater than left)
 Treatment
 Correct cause of obstruction
Mechanical Shock/Obstructive
OBHG Education Subcommittee
 Cardiac action cannot deliver circulating blood
volume adequate for tissue perfusion
 Examples
 Massive M.I
 Rhythm Disturbance (fast or slow)
 Cardiac Contusion
 Treatment
 Improving pumping action of the heart and
managing cardiac rhythm irregularities
(medications, electrical therapy, fluid)
 Treat associated problems ex. CHF
Cardiogenic Shock
OBHG Education Subcommittee
•Heart Damage >50% Muscle Damage
→ Decreased Circulating Volume
→ Increased Compensatory Heart Rate
→ Damaged ISCHEMIC Heart Has Increased Workload,
Increased Oxygen Demand
→ FURTHUR Damage To Heart Muscle
→ B/p Doesn’t Change Or Drops
→ CON’T Cycle Till Complete Failure
→ >90% Mortality Rate
Cardiogenic Shock - VISCIOUS CYCLE
OBHG Education Subcommittee
 Severe systemic allergic reaction due exposure to an
allergen
 (ex. food,drugs,insect bites)
 Causes exaggerated release of chemical mediators
(HISTAMINE, serotonin, kinins)
Anaphylactic Shock
OBHG Education Subcommittee
 Respiratory
 Upper airway obstruction secondary to edema
 Severe bronchiole constriction
 Integumentary
 Hives
 Local Swelling (capillary leak)
 Gastrointestinal
 Nausea and vomiting, Abdominal pain, Diarrhea
Multi-System Involvement
OBHG Education Subcommittee
 Circulatory
 Hypotension (Capillary leak, vessel dilation)
 Treatment
 remove exposure of allergen, epinephrine,
bronchodilators, antihistamines, fluid therapy
Multi-System Involvement
OBHG Education Subcommittee
 Hemorrhagic
 Internal blood loss, eg. G.I bleed
 External blood loss, laceration
 Non-Hemorrhagic
 G.I losses prolonged severe vomiting and diarrhea
 Renal losses excessive use of diuretics (^urine
prod.)
 Cutaneous losses heat exhaustion and burns
(3rd spaced shift)
Hypovolemic Shock (Loss of
Circulating Volume)
OBHG Education Subcommittee
TREATMENT
Correct circulatory deficit and cause, surgery,
volume replacement
OBHG Education Subcommittee
Adult = 70 ml/kg
Pediatric = 80 ml/kg
Infant = 90 ml/kg
Normal Circulating Volumes
OBHG Education Subcommittee
1st Stage: 0-15 % of blood volume
2nd Stage: 15-30% of blood volume
3rd Stage: 30-40% of blood volume
4th Stage: >40%
Stages of Shock
OBHG Education Subcommittee
 Altered LOA, confusion, agitation
 Normal possible slight increase in blood pressure
 Tachycardia
 Pale, moist skin
Early Signs & Symptoms of Shock
OBHG Education Subcommittee
 Hypotension
Late Sign
OBHG Education Subcommittee
3 STAGES OF SHOCK
OBHG Education Subcommittee
 Some decreased tissue perfusion, but bodies
compensatory mechanisms overcome
 Cardiac output and systolic b/p maintained by
catecholamine release
 Mild tachycardia, altered LOA, agitation, delayed cap
refill, cool skin, b/p normal or slightly elevated
 Continued compensatory leads to acidosis as
perfusion decreases (chemoreceptors respond with
increased respiratory rate)
1 Compensated Shock
OBHG Education Subcommittee
 Unable to maintain systolic blood pressure
 Systolic and diastolic blood pressure drops, pulse
pressure narrows till non existent (pulse pressure
systolic minus diastolic)
 Compensatory mechanisms begin to fail, cerebral
blood flow decreases even with blood being shunted
to vital organs
 Moderate tachycardia, confusion → unconsciousness
 Delayed cap refill, cold extremities, cyanosis,
hypotension
2 Uncompensated Shock
OBHG Education Subcommittee
 Progression of cellular ischemia and necrosis with
subsequent organ death, despite restoration of
oxygenation and perfusion
 Membrane pump fails and various organelles
breakdown inside of cell
 Bradycardia, dysrhythmia, coma, Frank Hypotension
 Results in death even if volume corrected
3 Irreversible Shock
OBHG Education Subcommittee
COMPENSATORY MECHANISMS
IN SHOCK
OBHG Education Subcommittee
 Autonomic (Sympathetic, Fight or Flight)
 Rapid onset
 Increased heart rate (chronotropic), increased force
of contraction (inotropic), increased conduction
(dromotropic) Beta 1
 Stimulates Adrenal Medulla to secrete
Norepinepherine and Epinephrine
 Nor Epinephrine-Alpha 1 peripheral vasoconstriction,
Epinephrine- Beta 2 dilate vessels to coronary and
skeletal muscle, bronchodilation
Neurogenic Compensation (Central
Nervous System)
OBHG Education Subcommittee
 Controls rapid moment to
moment B/P
  in blood pressure causes
baroreceptors (stretch) to
send fewer impulses to the
cardiovascular center in the
CNS
 Response  Sympathetic
output
Cardiac Output
Vasoconstriction
= in blood pressure
Baroreceptors and the Sympathetic
Nervous System
OBHG Education Subcommittee
 Decreased Po2 sensed by peripheral
chemoreceptors, increased acidosis sensed by
central chemoreceptors
 Stimulates increased respiratory rate, maximizes
FiO2, compensates for acid base imbalance
Chemical Compensation (Respiratory
System)
OBHG Education Subcommittee
 Epinephrine and Nor Epinephrine as above
 Renin-Angiotensin System
 Anti-diuretic Hormone
 ACTH – Adrenocorticotropic Hormone
Hormonal Compensation
OBHG Education Subcommittee
 Decreased blood flow to Kidneys-> Hypoprofusion
sensed by Juxtaglomerular Cells, causes kidneys secrete
renin->Renin acts on Angiotensinogen (protein from
liver)->Angiotensine 1->at lungs converted to
Angiotensine 2 by ACE-> Angiotensine 2 powerful
vasoconstrictor and stimulates Adrenal Cortex to secrete
Aldosterone
 Aldosterone stimulates kidneys to retain sodium with that
water overall increasing fluid volume
Renin-Angiotensin System
OBHG Education Subcommittee
Liver
Kidney
Angiotesinogen
Renin
Angiotesin I
Angiotesin
Converting
Enzyme
Angiotesin II
Adrenal
Aldosterone
Na+ and H2O Absorption
Peripheral
Vasoconstriction
Renin/Angiotensin System
OBHG Education Subcommittee
 Secreted by posterior pituitary if stimulated by
hypothalamus (Senses increased osmotic pressure)
 volume =  Tonicity (sodium)
 Causes tubules of kidney to be more permeable to
water therefore more volume retained
Anti-diuretic Hormone - ADH
OBHG Education Subcommittee
 Hypothalamus stimulates anterior pituitary to secrete
ACTH
 ACTH stimulates metabolism of carbohydrates,
proteins and fats
 Decreases permeability of capillary walls helping
prevent loss of intravascular fluid
ACTH - Adrenocorticotropic Hormone
OBHG Education Subcommittee
SPECIAL ASSESMENT CASES
OBHG Education Subcommittee
 Hypotension is usually defined as blood pressure
less than 90 or 100 mmhg (average person)
 Patients who have Hypertension will have
decompensatory drop in blood pressure, their drop of
30 or 40 mmHg may only put them in the 110,100
systolic range they are just as hypotensive though as
the person normal tensive with blood pressure of
80mmHg
 This is called relative hypotension
Relative Hypotension
OBHG Education Subcommittee
 Will not have compensatory increase in heart rate
Beware of Beta Blocked Patient
OBHG Education Subcommittee
 Compensate until point of failure
 Shock may be present despite normal blood pressure
 Look For:
 Altered LOA, diminished peripheral pulses, delayed cap
refill, Tachycardia, check temperature of extremities
 Late signs: Bradycardia, hypotension
Beware of the Pediatric Patient
OBHG Education Subcommittee
 30-40% blood volume increase
 Only 15-20% increase in hematocrit (functionally
anemic)
 Present in shock like picture without deficit
{Functional Hyperventilation, PaCO2 30mmhg, Lower
b/p, Increased heart rate 10-30bpm
 Will appear in class 2 or 3 shock without injury
Shock in Pregnant Female
OBHG Education Subcommittee
 Burn patient with 2nd and 3rd degree burns have
large amount of fluid loss due to third space shift
 Damage causes fluid to shift from intracellular space
to interstitial space
 Leads to hypotension and large amounts of swelling
in burned area
 Parkland Formula
 Ideal fluid replacement (4ml/kg X % of area burned)
 1st half over 8 hours, 2nd half over next 16 hours
Burn Patient
OBHG Education Subcommittee
 Body unable to compensate for drop in blood
pressure while in sitting or standing position
 Lying flat allows body to maintain somewhat normal
blood pressure
 Sitting patient up will cause change in blood pressure
and heart rate
 Drop of 20mmHg systolic or 10 mmHg diastolic is
significant
 Increase of heart rate 20 per minute is significant
 Patient must be in sitting position for 1-2 min
 Do not do on patients exhibiting signs of
hypoperfusion (dizziness lying flat)
 Done to rule out positional change in vitals
Orthostatic Vitals
OBHG Education Subcommittee
ONTARIO
BASE HOSPITAL GROUP
Ontario Base Hospital Group
Self-directed Education Program
Well Done!
START QUIT

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015_OBHG_Shock-12_-_2006.ppt

  • 1. OBHG Education Subcommittee ONTARIO BASE HOSPITAL GROUP ADVANCED ASSESSMENT Shock 2007 Ontario Base Hospital Group QUIT
  • 2. OBHG Education Subcommittee AUTHOR(S) Mike Muir AEMCA, ACP, BHSc Paramedic Program Manager Grey-Bruce-Huron Paramedic Base Hospital Grey Bruce Health Services, Owen Sound Kevin McNab AEMCA, ACP Quality Assurance Manager Huron County EMS References – Emergency Medicine REVIEWERS Rob Theriault EMCA, RCT(Adv.), CCP(F) Peel Region Base Hospital Donna L. Smith AEMCA, ACP Hamilton Base Hospital 2007 Ontario Base Hospital Group ADVANCED ASSESSMENT Shock
  • 3. OBHG Education Subcommittee Shock Widespread Tissue Hypoperfusion Results In Inadequate oxygenation and supply of nutrients at a cellular level Inadequate removal of metabolic waste products Due To Inadequate circulation of blood Leads To Generalized impairment of cellular function Ultimate cell death
  • 4. OBHG Education Subcommittee ENERGY PRODUCTION Human Body Likes Presence of Oxygen To Produce Energy
  • 5. OBHG Education Subcommittee  Energy production in the setting of oxygen  High amount of energy production  38 Adenosine Tri-phosphate  Low waste (Acid Production) Aerobic Metabolism
  • 6. OBHG Education Subcommittee  Energy production without oxygen  Low amount of energy production  2 Adenosine Tri-phosphate (Glycolysis Sugar Splitting)  High acid production  Pyruvic to Lactic Acid results in metabolic acidosis  Cell functions cease due to lack of energy and acidosis  Cell death Anaerobic Metabolism
  • 7. OBHG Education Subcommittee S Septic, Spinal H Hypovolemic O Obstructive, Mechanical C Cardiogenic K Anaphylactic
  • 8. OBHG Education Subcommittee  Caused by serious systemic bacterial infection (usually gram negative bacteria)  Causes a release of vasoactive agents that affect microcirculation (arterioles and venules dilate {increased container size}, capillary leak {loss of volume}  Increased container size and loss of volume lead to inadequate tissue perfusion Septic Shock
  • 9. OBHG Education Subcommittee  Signs and Symptoms  Fever (may not have fever), tachycardia, tachypnea, confusion, petechiae around eyes, purpura  Look for history of recent infection (bladder, pneumonia)  Treatment  Identify and correct infection (antibiotics)  Manage hypovolemia and acid base imbalance (fluid therapy, vasoactive and cardiac drugs) Septic Shock
  • 10. OBHG Education Subcommittee  Predominantly causes by Spinal Cord Injury, may also be caused by head injury, CVA or drug overdose  Block of sympathetic outflow results in peripheral vasodilatation Neurogenic Shock/Spinal Shock
  • 11. OBHG Education Subcommittee  Vasomotor paralysis below level of spinal cord injury  Normal vasomotor tone through sympathetic control is lost  Results in vasodilatation, increased container size  Even normal intravascular volume is insufficient to fill vascular compartment  Unable to mount compensatory tachycardia  Heart rate remains unchanged with hypotension  Look for line where sympathetic response ends  Treatment  Similar to Hypovolemia, caution not to cause fluid overload Spinal Shock
  • 12. OBHG Education Subcommittee  Blood flow disrupted due to mechanical obstruction  Examples  Tension Pnemothorax - Increased intrathoracic pressure impedes low pressured venous return, increased pressure can twist and compress heart  Cardiac Tamponade - Compression of heart due to accumulation of fluid or in pericardial sac (usually due to trauma or infection) Mechanical Shock/Obstructive
  • 13. OBHG Education Subcommittee  Examples cont’d  Pulmonary Embolism - Blockage of blood flow in pulmonary circulation (fat, air, thrombus)  Aortic Dissection - Blood flow obstructed distal to left ventricle (Dissection of Aortic Arch= b/p right arm greater than left)  Treatment  Correct cause of obstruction Mechanical Shock/Obstructive
  • 14. OBHG Education Subcommittee  Cardiac action cannot deliver circulating blood volume adequate for tissue perfusion  Examples  Massive M.I  Rhythm Disturbance (fast or slow)  Cardiac Contusion  Treatment  Improving pumping action of the heart and managing cardiac rhythm irregularities (medications, electrical therapy, fluid)  Treat associated problems ex. CHF Cardiogenic Shock
  • 15. OBHG Education Subcommittee •Heart Damage >50% Muscle Damage → Decreased Circulating Volume → Increased Compensatory Heart Rate → Damaged ISCHEMIC Heart Has Increased Workload, Increased Oxygen Demand → FURTHUR Damage To Heart Muscle → B/p Doesn’t Change Or Drops → CON’T Cycle Till Complete Failure → >90% Mortality Rate Cardiogenic Shock - VISCIOUS CYCLE
  • 16. OBHG Education Subcommittee  Severe systemic allergic reaction due exposure to an allergen  (ex. food,drugs,insect bites)  Causes exaggerated release of chemical mediators (HISTAMINE, serotonin, kinins) Anaphylactic Shock
  • 17. OBHG Education Subcommittee  Respiratory  Upper airway obstruction secondary to edema  Severe bronchiole constriction  Integumentary  Hives  Local Swelling (capillary leak)  Gastrointestinal  Nausea and vomiting, Abdominal pain, Diarrhea Multi-System Involvement
  • 18. OBHG Education Subcommittee  Circulatory  Hypotension (Capillary leak, vessel dilation)  Treatment  remove exposure of allergen, epinephrine, bronchodilators, antihistamines, fluid therapy Multi-System Involvement
  • 19. OBHG Education Subcommittee  Hemorrhagic  Internal blood loss, eg. G.I bleed  External blood loss, laceration  Non-Hemorrhagic  G.I losses prolonged severe vomiting and diarrhea  Renal losses excessive use of diuretics (^urine prod.)  Cutaneous losses heat exhaustion and burns (3rd spaced shift) Hypovolemic Shock (Loss of Circulating Volume)
  • 20. OBHG Education Subcommittee TREATMENT Correct circulatory deficit and cause, surgery, volume replacement
  • 21. OBHG Education Subcommittee Adult = 70 ml/kg Pediatric = 80 ml/kg Infant = 90 ml/kg Normal Circulating Volumes
  • 22. OBHG Education Subcommittee 1st Stage: 0-15 % of blood volume 2nd Stage: 15-30% of blood volume 3rd Stage: 30-40% of blood volume 4th Stage: >40% Stages of Shock
  • 23. OBHG Education Subcommittee  Altered LOA, confusion, agitation  Normal possible slight increase in blood pressure  Tachycardia  Pale, moist skin Early Signs & Symptoms of Shock
  • 24. OBHG Education Subcommittee  Hypotension Late Sign
  • 25. OBHG Education Subcommittee 3 STAGES OF SHOCK
  • 26. OBHG Education Subcommittee  Some decreased tissue perfusion, but bodies compensatory mechanisms overcome  Cardiac output and systolic b/p maintained by catecholamine release  Mild tachycardia, altered LOA, agitation, delayed cap refill, cool skin, b/p normal or slightly elevated  Continued compensatory leads to acidosis as perfusion decreases (chemoreceptors respond with increased respiratory rate) 1 Compensated Shock
  • 27. OBHG Education Subcommittee  Unable to maintain systolic blood pressure  Systolic and diastolic blood pressure drops, pulse pressure narrows till non existent (pulse pressure systolic minus diastolic)  Compensatory mechanisms begin to fail, cerebral blood flow decreases even with blood being shunted to vital organs  Moderate tachycardia, confusion → unconsciousness  Delayed cap refill, cold extremities, cyanosis, hypotension 2 Uncompensated Shock
  • 28. OBHG Education Subcommittee  Progression of cellular ischemia and necrosis with subsequent organ death, despite restoration of oxygenation and perfusion  Membrane pump fails and various organelles breakdown inside of cell  Bradycardia, dysrhythmia, coma, Frank Hypotension  Results in death even if volume corrected 3 Irreversible Shock
  • 30. OBHG Education Subcommittee  Autonomic (Sympathetic, Fight or Flight)  Rapid onset  Increased heart rate (chronotropic), increased force of contraction (inotropic), increased conduction (dromotropic) Beta 1  Stimulates Adrenal Medulla to secrete Norepinepherine and Epinephrine  Nor Epinephrine-Alpha 1 peripheral vasoconstriction, Epinephrine- Beta 2 dilate vessels to coronary and skeletal muscle, bronchodilation Neurogenic Compensation (Central Nervous System)
  • 31. OBHG Education Subcommittee  Controls rapid moment to moment B/P   in blood pressure causes baroreceptors (stretch) to send fewer impulses to the cardiovascular center in the CNS  Response  Sympathetic output Cardiac Output Vasoconstriction = in blood pressure Baroreceptors and the Sympathetic Nervous System
  • 32. OBHG Education Subcommittee  Decreased Po2 sensed by peripheral chemoreceptors, increased acidosis sensed by central chemoreceptors  Stimulates increased respiratory rate, maximizes FiO2, compensates for acid base imbalance Chemical Compensation (Respiratory System)
  • 33. OBHG Education Subcommittee  Epinephrine and Nor Epinephrine as above  Renin-Angiotensin System  Anti-diuretic Hormone  ACTH – Adrenocorticotropic Hormone Hormonal Compensation
  • 34. OBHG Education Subcommittee  Decreased blood flow to Kidneys-> Hypoprofusion sensed by Juxtaglomerular Cells, causes kidneys secrete renin->Renin acts on Angiotensinogen (protein from liver)->Angiotensine 1->at lungs converted to Angiotensine 2 by ACE-> Angiotensine 2 powerful vasoconstrictor and stimulates Adrenal Cortex to secrete Aldosterone  Aldosterone stimulates kidneys to retain sodium with that water overall increasing fluid volume Renin-Angiotensin System
  • 35. OBHG Education Subcommittee Liver Kidney Angiotesinogen Renin Angiotesin I Angiotesin Converting Enzyme Angiotesin II Adrenal Aldosterone Na+ and H2O Absorption Peripheral Vasoconstriction Renin/Angiotensin System
  • 36. OBHG Education Subcommittee  Secreted by posterior pituitary if stimulated by hypothalamus (Senses increased osmotic pressure)  volume =  Tonicity (sodium)  Causes tubules of kidney to be more permeable to water therefore more volume retained Anti-diuretic Hormone - ADH
  • 37. OBHG Education Subcommittee  Hypothalamus stimulates anterior pituitary to secrete ACTH  ACTH stimulates metabolism of carbohydrates, proteins and fats  Decreases permeability of capillary walls helping prevent loss of intravascular fluid ACTH - Adrenocorticotropic Hormone
  • 39. OBHG Education Subcommittee  Hypotension is usually defined as blood pressure less than 90 or 100 mmhg (average person)  Patients who have Hypertension will have decompensatory drop in blood pressure, their drop of 30 or 40 mmHg may only put them in the 110,100 systolic range they are just as hypotensive though as the person normal tensive with blood pressure of 80mmHg  This is called relative hypotension Relative Hypotension
  • 40. OBHG Education Subcommittee  Will not have compensatory increase in heart rate Beware of Beta Blocked Patient
  • 41. OBHG Education Subcommittee  Compensate until point of failure  Shock may be present despite normal blood pressure  Look For:  Altered LOA, diminished peripheral pulses, delayed cap refill, Tachycardia, check temperature of extremities  Late signs: Bradycardia, hypotension Beware of the Pediatric Patient
  • 42. OBHG Education Subcommittee  30-40% blood volume increase  Only 15-20% increase in hematocrit (functionally anemic)  Present in shock like picture without deficit {Functional Hyperventilation, PaCO2 30mmhg, Lower b/p, Increased heart rate 10-30bpm  Will appear in class 2 or 3 shock without injury Shock in Pregnant Female
  • 43. OBHG Education Subcommittee  Burn patient with 2nd and 3rd degree burns have large amount of fluid loss due to third space shift  Damage causes fluid to shift from intracellular space to interstitial space  Leads to hypotension and large amounts of swelling in burned area  Parkland Formula  Ideal fluid replacement (4ml/kg X % of area burned)  1st half over 8 hours, 2nd half over next 16 hours Burn Patient
  • 44. OBHG Education Subcommittee  Body unable to compensate for drop in blood pressure while in sitting or standing position  Lying flat allows body to maintain somewhat normal blood pressure  Sitting patient up will cause change in blood pressure and heart rate  Drop of 20mmHg systolic or 10 mmHg diastolic is significant  Increase of heart rate 20 per minute is significant  Patient must be in sitting position for 1-2 min  Do not do on patients exhibiting signs of hypoperfusion (dizziness lying flat)  Done to rule out positional change in vitals Orthostatic Vitals
  • 45. OBHG Education Subcommittee ONTARIO BASE HOSPITAL GROUP Ontario Base Hospital Group Self-directed Education Program Well Done! START QUIT