Nur144 Exam 2:shock

Front 1

Shock
I. Definition--syndrome characterized by ↓--------- perfusion and impaired --------------- (imbalance btw supply and demand for O2 and nutrients)

Back 1

Shock
I. Definition--syndrome characterized by ↓tissue perfusion and impaired cellular metabolism (imbalance btw supply and demand for O2 and nutrients)

Front 2

Shock
II. Low Blood Flow Shock
A. Cardiogenic--systolic/diastolic myocardium dysfunction compromised CO cell hypoperfusion
1. Types (mortality rates 50-______%)
a. Systolic--heart can’t pump blood _________ (L ventricle problem)
b. Diastolic--heart can’t relax and get enough preload (cardiac tamppnade)

Back 2

Shock
II. Low Blood Flow Shock
A. Cardiogenic--systolic/diastolic myocardium dysfunction compromised CO cell hypoperfusion
1. Types (mortality rates 50-80%)
a. Systolic--heart can’t pump blood forward (L ventricle problem)

Front 3

Shock
II. Low Blood Flow Shock
A. Cardiogenic--systolic/diastolic myocardium dysfunction compromised CO cell hypoperfusion
1. Types (mortality rates 50-80%)
a. Systolic--heart can’t pump blood forward (L ventricle problem)
b. Diastolic--heart can’t relax and get enough ---------- (cardiac -----------)
**Can have occurance w/ ---------- ventricle if it is severe enough

Back 3

Shock
II. Low Blood Flow Shock
A. Cardiogenic--systolic/diastolic myocardium dysfunction compromised CO cell hypoperfusion
1. Types (mortality rates 50-80%)
a. Systolic--heart can’t pump blood forward (L ventricle problem)
b. Diastolic--heart can’t relax and get enough preload (cardiac tamppnade)
**Can have occurance w/ R ventricle if it is severe enough

Front 4

Shock
II. Low Blood Flow Shock
A. Cardiogenic-
2. Causes
a. MI--dysrhythmias and ------------- muscles rupture (5-______% pts develop shock w/in 48hrs)
b. Cardiomyopathy--viral --------- failure

Back 4

Shock
II. Low Blood Flow Shock
A. Cardiogenic-
2. Causes
a. MI--dysrhythmias and papillary muscles rupture (5-10% pts develop shock w/in 48hrs)
b. Cardiomyopathy--viral heart failure

Front 5

Shock
II. Low Blood Flow Shock
A. Cardiogenic-
2. Causes
c. ----------- (L ventricular dysfunction) or ------------ (R ventricular dysfunction) HTN
d. Blunt -------------- injury--briusing of heart

Back 5

Shock
II. Low Blood Flow Shock
A. Cardiogenic-
2. Causes
c. Systemic (L ventricular dysfunction) or Pulmonary (R ventricular dysfunction) HTN
d. Blunt cardiac injury--briusing of heart

Front 6

Shock
II. Low Blood Flow Shock
A. Cardiogenic-
2. Causes
e. Myocardial ------------ from sepsis--inflammatory markers release (TNF) ↓--------, ↓--------

Back 6

Shock
II. Low Blood Flow Shock
2. Causes
e. Myocardial depression from sepsis--inflammatory markers release (TNF) ↓SV, ↓CO

Front 7

Shock
II. Low Blood Flow Shock
A. Cardiogenic-
3. Clinical Manifestations--similar to ----------- failure

Back 7

Shock
II. Low Blood Flow Shock
3. Clinical Manifestations--similar to acute heart failure

Front 8

Shock
II. Low Blood Flow Shock
A. Cardiogenic-
3. Clinical Manifestations--similar to acute heart failure
a. ↑----------, ↓---------- w. narrowed pulse pressure

Back 8

Shock
II. Low Blood Flow Shock
3. Clinical Manifestations--similar to acute heart failure
a. ↑HR, ↓BP w. narrowed pulse pressure
b. Tachypneic w/ crackles on auscultation

Front 9

Shock
II. Low Blood Flow Shock
A. Cardiogenic-
3. Clinical Manifestations--similar to acute heart failure
b. -------------- w/ crackles on auscultation

Back 9

Shock
II. Low Blood Flow Shock
3. Clinical Manifestations--similar to acute heart failure
b. Tachypneic w/ crackles on auscultation

Front 10

Shock
II. Low Blood Flow Shock
A. Cardiogenic-
3. Clinical Manifestations--similar to acute heart failure
c. Signs of peripheral ------------- (cyanosis, -----------, ↓cap refill)

Back 10

Shock
II. Low Blood Flow Shock
3. Clinical Manifestations--similar to acute heart failure
c. Signs of peripheral hypoperfusion (cyanosis, pallor, ↓cap refill)

Front 11

Shock
II. Low Blood Flow Shock
A. Cardiogenic-
3. Clinical Manifestations--similar to acute heart failure
d. Hemodynamic findings (↑----------, ↑PVR, ↓-------, ↑-------: due to body clamping down)

Back 11

Shock
II. Low Blood Flow Shock
3. Clinical Manifestations--similar to acute heart failure
d. Hemodynamic findings (↑PAWP, ↑PVR, ↓CO, ↑SVR-due to body clamping down)

Front 12

Shock
II. Low Blood Flow Shock
A. Cardiogenic-
3. Clinical Manifestations--similar to acute heart failure
e. ↓------- output (↓-------- perfusion)

Back 12

Shock
II. Low Blood Flow Shock
3. Clinical Manifestations--similar to acute heart failure
e. ↓Urine output (↓renal perfusion)

Front 13

Shock
II. Low Blood Flow Shock
A. Cardiogenic-
3. Clinical Manifestations--similar to acute heart failure
f. ---------- and water retention (renin-_________-aldosterone activation)

Back 13

Shock
II. Low Blood Flow Shock
3. Clinical Manifestations--similar to acute heart failure
f. Na and water retention (renin-angiotensin-aldosterone activation)

Front 14

Shock
II. Low Blood Flow Shock
A. Cardiogenic-
3. Clinical Manifestations--similar to acute heart failure
g. Confusion and ----------

Back 14

Shock
II. Low Blood Flow Shock
3. Clinical Manifestations--similar to acute heart failure
g. Confusion and anxiety

Front 15

Shock
II. Low Blood Flow Shock
A. Cardiogenic-
3. Diagnostic Studies
a. Cardiac _________
b. E_______

Back 15

Shock
II. Low Blood Flow Shock
3. Diagnostic Studies
a. Cardiac enzymes
b. EKG

Front 16

Shock
II. Low Blood Flow Shock
A. Cardiogenic-
3. Diagnostic Studies
c. C______
d. _________--valular dysfunction and EF

Back 16

Shock
II. Low Blood Flow Shock
3. Diagnostic Studies
c. CXR
d. ECHO--valular dysfunction and EF

Front 17

Shock
II. Low Blood Flow Shock
A. Cardiogenic-
3. Diagnostic Studies
e. Insertion of _________--monitor fluid status
f. Emergent __________

Back 17

Shock
II. Low Blood Flow Shock
A. Cardiogenic-
3. Diagnostic Studies
e. Insertion of PA catheter--monitor fluid status
f. Emergent catheterization

Front 18

Shock
II. Low Blood Flow Shock
B. ____________--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.

Back 18

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.

Front 19

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss ------------- to rapid blood loss (internal or external) low blood flow ↓---------- return ↓tissue ------------/impaired cell met.

Back 19

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.

Front 20

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
1. -------------- loss--true loss of fluid from vascular space (hemorrhage, vomiting, diarrhea)

Back 20

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
1. Absolute loss--true loss of fluid from vascular space (hemorrhage, vomiting, diarrhea)

Front 21

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
1. Absolute loss--true loss of fluid from vascular space (-----------, vomiting, ----------)

Back 21

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
1. Absolute loss--true loss of fluid from vascular space (hemorrhage, vomiting, diarrhea)

Front 22

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
2. Relative loss--fluid there but moved elsewhere from ↑---------- in burn/sepsis (---------- spacing)

Back 22

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
2. Relative loss--fluid there but moved elsewhere from ↑cap perm. in burn/sepsis (2nd spacing)

Front 23

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
3. Ability to compensate (if <---------% loss body is able to compensate w/out ---------- symptoms)

Back 23

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
3. Ability to compensate (if <15% loss body is able to compensate w/out outward symptoms)

Front 24

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
3. Ability to compensate (if <15% loss body is able to compensate w/out outward symptoms)
a. 15-______%--sympathetic venous system response
b. >_____% loss--volume must be replaced with blood

Back 24

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
3. Ability to compensate (if <15% loss body is able to compensate w/out outward symptoms)
a. 15-30%--sympathetic venous system response
b. >30% loss--volume must be replaced with blood

Front 25

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
3. Ability to compensate (if <15% loss body is able to compensate w/out outward symptoms)
a. 15-30%--sympathetic ------------ system response
b. >30% loss--volume must be replaced with -----------

Back 25

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
3. Ability to compensate (if <15% loss body is able to compensate w/out outward symptoms)
a. 15-30%--sympathetic venous system response
b. >30% loss--volume must be replaced with blood

Front 26

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
3. Ability to compensate (if <15% loss body is able to compensate w/out outward symptoms)
c. >_____% loss--irreversible damage to tissues

Back 26

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
3. Ability to compensate (if <15% loss body is able to compensate w/out outward symptoms)
c. >40% loss--irreversible damage to tissues

Front 27

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
3. Ability to compensate (if <15% loss body is able to compensate w/out outward symptoms)
c. >40% loss--irreversible damage to --------

Back 27

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
3. Ability to compensate (if <15% loss body is able to compensate w/out outward symptoms)
c. >40% loss--irreversible damage to tissues

Front 28

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
3. Causes
a. _______--external penetrating
b. Severe ______ bleeding--2nd main cause

Back 28

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
3. Causes
a. Trauma--external penetrating
b. Severe GI bleeding--2nd main cause

Front 29

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
3. Causes
c. ----------- pregnancy
d. ------------ fracture

Back 29

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
3. Causes
c. Ectopic pregnancy
d. Pelvic fracture

Front 30

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
3. Causes
d. Pelvic fracture
e. ---------- obstruction--fluid in colon
f. Ascites due to --------- dysfunction

Back 30

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
3. Causes
d. Pelvic fracture
e. Colon obstruction--fluid in colon
f. Ascites due to liver dysfunction

Front 31

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
4. Clinical Manifestations--result of ------------- mechanisms (can support BP if <---------% loss)

Back 31

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
4. Clinical Manifestations--result of compensatory mechanisms (can support BP if <30% loss)

Front 32

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
4. Clinical Manifestations--result of compensatory mechanisms (can support BP if <30% loss)
a. Initial symptoms--_________
i. ↑______ (careful b/c some meds keep HR lower than expected--blunting effect)

Back 32

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
4. Clinical Manifestations--result of compensatory mechanisms (can support BP if <30% loss)
a. Initial symptoms--compensating
i. ↑HR (careful b/c some meds keep HR lower than expected--blunting effect)

Front 33

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
4. Clinical Manifestations--result of compensatory mechanisms (can support BP if <30% loss)
a. Initial symptoms--compensating
ii. ↑--------
iii. ↑------- (not a pump problem)

Back 33

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
4. Clinical Manifestations--result of compensatory mechanisms (can support BP if <30% loss)
a. Initial symptoms--compensating
ii. ↑RR
iii. ↑CO (not a pump problem)

Front 34

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
4. Clinical Manifestations--result of compensatory mechanisms (can support BP if <30% loss)
a. Initial symptoms--compensating
iv. ↓-------- (due to ↑HR) and ↓----------

Back 34

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
4. Clinical Manifestations--result of compensatory mechanisms (can support BP if <30% loss)
a. Initial symptoms--compensating
iv. ↓SV (due to ↑HR) and ↓PCWP

Front 35

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
4. Clinical Manifestations--result of compensatory mechanisms (can support BP if <30% loss)
b. Later symptoms--as compensatory mechanisms fail
i. ↓---------
ii, ↓-------- output
iii. Skin --------, cool, clammy

Back 35

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
4. Clinical Manifestations--result of compensatory mechanisms (can support BP if <30% loss)
b. Later symptoms--as compensatory mechanisms fail
i. ↓CO
ii, ↓urine output
iii. Skin pale, cool, clammy

Front 36

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
5. Diagnostic Studies
a. Hg/______--initially normal (get ________) ↓ after give fluids (reflection of actual values)

Back 36

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
5. Diagnostic Studies
a. Hg/Ht--initially normal (get baseline) ↓ after give fluids (reflection of actual values)

Front 37

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
5. Diagnostic Studies
a. Hg/Ht--initially normal (get baseline) ↓ after give ------------ (reflection of ----------- values)

Back 37

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
5. Diagnostic Studies
a. Hg/Ht--initially normal (get baseline) ↓ after give fluids (reflection of actual values)

Front 38

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
5. Diagnostic Studies
b. Urine--↓--------- output (↓------------ perfusion), ↑specific ---------- (renin-aldosterone release)

Back 38

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
5. Diagnostic Studies
b. Urine--↓urine output (↓kidney perfusion), ↑specific gravity (renin-aldosterone release)

Front 39

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
5. Diagnostic Studies
c. Elevated lactic acid levels--acidotic due to ----------- metabolism in tissue from ↓--------

Back 39

Shock
II. Low Blood Flow Shock
B. Hypovolemic--intravascular fluid volume loss secondary to rapid blood loss (internal or external) low blood flow ↓venous return ↓tissue perfusion/impaired cell met.
5. Diagnostic Studies
c. Elevated lactic acid levels--acidotic due to anaerobic metabolism in tissue from ↓O2

Front 40

Shock
III. Misdistribution of Blood Flow Shock
A. ____________--hemodynamic phenomenon that occurs after spinal cord injury at or above T5 resulting in massive vasodilation w/out compensation (onset can occur in 30min and last up to 6 weeks)

Back 40

Shock
III. Misdistribution of Blood Flow Shock
A. Neurogenic--hemodynamic phenomenon that occurs after spinal cord injury at or above T5 resulting in massive vasodilation w/out compensation (onset can occur in 30min and last up to 6 weeks)

Front 41

Shock
III. Misdistribution of Blood Flow Shock
A. Neurogenic--hemodynamic phenomenon that occurs after ------------- injury at or above --------- resulting in massive vasodilation w/out compensation (onset can occur in --------min and last up to 6 weeks)

Back 41

Shock
III. Misdistribution of Blood Flow Shock
A. Neurogenic--hemodynamic phenomenon that occurs after spinal cord injury at or above T5 resulting in massive vasodilation w/out compensation (onset can occur in 30min and last up to 6 weeks)

Front 42

Shock
III. Misdistribution of Blood Flow Shock
A. Neurogenic--
1. Causes--loss of ----------- vasoconstrictor tone pooling of blood in vessels

Back 42

Shock
III. Misdistribution of Blood Flow Shock
A. Neurogenic--
1. Causes--loss of SNS vasoconstrictor tone pooling of blood in vessels

Front 43

Shock
III. Misdistribution of Blood Flow Shock
A. Neurogenic--
1. Causes--loss of SNS vasoconstrictor tone pooling of blood in vessels
a. ----------- injury
b. ----------- anesthesia
c. Drugs: --------------

Back 43

Shock
III. Misdistribution of Blood Flow Shock
A. Neurogenic--
1. Causes--loss of SNS vasoconstrictor tone pooling of blood in vessels
a. Spinal cord injury
b. Spinal anesthesia
c. Drugs--benzodiazepines

Front 44

Shock
III. Misdistribution of Blood Flow Shock
A. Neurogenic--
2. Clinical Manifestations
a. H_________
b. ↓________ (no compensation) ↓_____ (PNS takes over b/c no SNS stimulation)

Back 44

Shock
III. Misdistribution of Blood Flow Shock
A. Neurogenic--
2. Clinical Manifestations
a. Hypotension
b. ↓HR (no compensation) ↓CO (PNS takes over b/c no SNS stimulation)

Front 45

Shock
III. Misdistribution of Blood Flow Shock
A. Neurogenic--
2. Clinical Manifestations
c. ---------------- (take on room’s temp) due to hypothalamic dysfunction (can’t regulate)

Back 45

Shock
III. Misdistribution of Blood Flow Shock
A. Neurogenic--
2. Clinical Manifestations
c. Poikilpthermia (take on room’s temp) due to hypothalamic dysfunction (can’t regulate)

Front 46

Shock
III. Misdistribution of Blood Flow Shock
A. Neurogenic--
2. Clinical Manifestations
c. Poikilpthermia (take on room’s temp) due to hypothalamic dysfunction (can’t regulate)
i. Massive ----------- (often cold)

Back 46

FIX





i. Massive dilation (often cold)

Front 47

Shock
III. Misdistribution of Blood Flow Shock
B. Septic--presence of sepsis w/ ----------- despite fluid resuscitation w/ presence of tissue ---------- abnormalities (mortality rates 28-50%)

Back 47

Shock
III. Misdistribution of Blood Flow Shock
B. Septic--presence of sepsis w/ hypotension despite fluid resuscitation w/ presence of tissue perfusion abnormalities (mortality rates 28-50%)

Front 48

Shock
III. Misdistribution of Blood Flow Shock
B. Septic--presence of sepsis w/ hypotension despite fluid resuscitation w/ presence of tissue perfusion abnormalities (mortality rates 28-____%)

Back 48

Shock
III. Misdistribution of Blood Flow Shock
B. Septic--presence of sepsis w/ hypotension despite fluid resuscitation w/ presence of tissue perfusion abnormalities (mortality rates 28-50%)

Front 49

Shock
III. Misdistribution of Blood Flow Shock
B. Septic--presence of sepsis w/ hypotension despite fluid resuscitation w/ presence of tissue perfusion abnormalities (mortality rates 28-50%)
1. Sepsis--systemic inflammatory response to a documented/suspected --------

Back 49

Shock
III. Misdistribution of Blood Flow Shock
B. Septic--presence of sepsis w/ hypotension despite fluid resuscitation w/ presence of tissue perfusion abnormalities (mortality rates 28-50%)
1. Sepsis--systemic inflammatory response to a documented/suspected infection

Front 50

Shock
III. Misdistribution of Blood Flow Shock
2. Pathophysiology--caused mostly --------- (-) bacteria (higher ---------- rates)

Back 50

Shock
III. Misdistribution of Blood Flow Shock
2. Pathophysiology--caused mostly gram (-) bacteria (higher mortality rates)

Front 51

Shock
III. Misdistribution of Blood Flow Shock
2. Pathophysiology--
a. Release of --------- inflammatory response ↑cap ------------ and vasodilation

Back 51

Shock
III. Misdistribution of Blood Flow Shock
2. Pathophysiology--
a. Release of endotoxins inflammatory response ↑cap permeability and vasodilation

Front 52

Shock
III. Misdistribution of Blood Flow Shock
2. Pathophysiology--
b. Microthrombi ------------- intravascular ------------- (DIC)

Back 52

Shock
III. Misdistribution of Blood Flow Shock
2. Pathophysiology--
b. Microthrombi disseminated intravascular coagulation (DIC)

Front 53

Shock
III. Misdistribution of Blood Flow Shock
2. Pathophysiology--
c. Pts are in---------------- state (like burns)

Back 53

Shock
III. Misdistribution of Blood Flow Shock
2. Pathophysiology--
c. Pts are in hypermetabolic state (like burns)

Front 54

Shock
III. Misdistribution of Blood Flow Shock
3. Clinical Manifestations--systemic response (everything just starts to ----------)

Back 54

Shock
III. Misdistribution of Blood Flow Shock
3. Clinical Manifestations--systemic response (everything just starts to shut down)

Front 55

Shock
III. Misdistribution of Blood Flow Shock
a. Alteration in --------- status (early)

Back 55

Shock
III. Misdistribution of Blood Flow Shock
a. Alteration in mental status (early)

Front 56

Shock
III. Misdistribution of Blood Flow Shock
b. Skin warm and flushed--due to --------------- (early)

Back 56

Shock
III. Misdistribution of Blood Flow Shock
b. Skin warm and flushed--due to vasodilation (early)

Front 57

Shock
III. Misdistribution of Blood Flow Shock
d. Significant ↑_______--overcompensation (early)

Back 57

Shock
III. Misdistribution of Blood Flow Shock
d. Significant ↑CO--overcompensation (early)

Front 58

Shock
III. Misdistribution of Blood Flow Shock
e. ↑_______2--tissues not properly utilizing available O2 seen w/ pulmonary catheter (early)

Back 58

Shock
III. Misdistribution of Blood Flow Shock
e. ↑SvO2--tissues not properly utilizing available O2 seen w/ pulmonary catheter (early)

Front 59

Shock
III. Misdistribution of Blood Flow Shock
e. ↑SvO2--tissues not properly utilizing available --------2 seen w/ ---------- catheter (early)

Back 59

Shock
III. Misdistribution of Blood Flow Shock
e. ↑SvO2--tissues not properly utilizing available O2 seen w/ pulmonary catheter (early)

Front 60

Shock
III. Misdistribution of Blood Flow Shock
f. ↓_____--dilation

Back 60

Shock
III. Misdistribution of Blood Flow Shock
f. ↓SVR--dilation

Front 61

Shock
III. Misdistribution of Blood Flow Shock
g. H_________
h. GI bleeding/_________ ileus

Back 61

Shock
III. Misdistribution of Blood Flow Shock
g. Hypotension
h. GI bleeding/paralytic ileus

Front 62

Shock
III. Misdistribution of Blood Flow Shock
i. Hypoxemia w/ resp failure/ARDS (_____% will go on to resp failure and ______% to ARDS)

Back 62

Shock
III. Misdistribution of Blood Flow Shock
i. Hypoxemia w/ resp failure/ARDS (85% will go on to resp failure and 40% to ARDS)

Front 63

Shock
III. Misdistribution of Blood Flow Shock
i. ---------- w/ resp failure/ARDS (85% will go on to resp failure and 40% to ARDS)

Back 63

Shock
III. Misdistribution of Blood Flow Shock
j. ↓------- (late) ↓---------- output; skin cool (clamping down) and mottled (very late)

Front 64

Shock
III. Misdistribution of Blood Flow Shock
C. Anaphylactic--acute, life-threatening - (allergic) reaction to sensitizing substance resulting in massive ------------, release of vasoactive -------------, and ↑-------------- permeability

Back 64

III. Misdistribution of Blood Flow Shock
C. Anaphylactic--acute, life-threatening hypersensitivity (allergic) reaction to sensitizing substance resulting in massive vasodilation, release of vasoactive mediators, and ↑capillary permeability

Front 65

Shock
III. Misdistribution of Blood Flow Shock
C. Anaphylactic
1. Causes--Drug (also IV drug infusions), ------------, vaccine, --------, or insect ---------

Back 65

III. Misdistribution of Blood Flow Shock
C. Anaphylactic
1. Causes--Drug (also IV drug infusions), chemical, vaccine, food, or insect venom

Front 66

Shock
III. Misdistribution of Blood Flow Shock
C. Anaphylactic
2. Clinical Manifestations--sudden onset
a. Hypotension, ----------

Back 66

III. Misdistribution of Blood Flow Shock
C. Anaphylactic
2. Clinical Manifestations--sudden onset
a. Hypotension, chest pain

Front 67

Shock
III. Misdistribution of Blood Flow Shock
C. Anaphylactic
2. Clinical Manifestations--sudden onset
b. Swelling of ------- and --------

Back 67

III. Misdistribution of Blood Flow Shock
C. Anaphylactic
2. Clinical Manifestations--sudden onset
b. Swelling of lips and tongue

Front 68

Shock
III. Misdistribution of Blood Flow Shock
C. Anaphylactic
2. Clinical Manifestations--sudden onset
c. Wheezing and stridor due to ------------ edema and --------------- resp distress

Back 68

III. Misdistribution of Blood Flow Shock
C. Anaphylactic
2. Clinical Manifestations--sudden onset
c. Wheezing and stridor due to laryngeal edema and bronchoconstriction resp distress

Front 69

Shock
III. Misdistribution of Blood Flow Shock
C. Anaphylactic
2. Clinical Manifestations--sudden onset
d. Skin--flushing, ----------, --------

Back 69

III. Misdistribution of Blood Flow Shock
C. Anaphylactic
2. Clinical Manifestations--sudden onset
d. Skin--flushing, pruritus, uticaria

Front 70

Shock
III. Misdistribution of Blood Flow Shock
C. Anaphylactic
2. Clinical Manifestations--sudden onset
e. A________
f. Edema from fluid leaking into _______

Back 70

III. Misdistribution of Blood Flow Shock
C. Anaphylactic
2. Clinical Manifestations--sudden onset
e. Angioedema
f. Edema from fluid leaking into interstitial space

Front 71

Shock
III. Misdistribution of Blood Flow Shock
C. Anaphylactic
3. Patient education--find cause of -----------, carry -------- pen, and wear --------- bracelet

Back 71

III. Misdistribution of Blood Flow Shock
C. Anaphylactic
3. Patient education--find cause of allergy, carry epi pen, and wear med alert bracelet

Front 72

Shock
IV. Stages
A. Initial Stage--body responding at cellular level by utilizing ---------- metabolism (no outward signs)

Back 72

Shock
IV. Stages
A. Initial Stage--body responding at cellular level by utilizing anaerobic metabolism (no outward signs)

Front 73

Shock
IV. Stages
B. Compensatory Stage--activation of compensatory mechanisms in attempt to maintain ---------

Back 73

Shock
IV. Stages
B. Compensatory Stage--activation of compensatory mechanisms in attempt to maintain homeostasis

Front 74

Shock
IV. Stages
B. Compensatory Stage--activation of compensatory mechanisms in attempt to maintain homeostasis
1. If recovery occurs at this stage little ---------- done

Back 74

Shock
IV. Stages
B. Compensatory Stage--activation of compensatory mechanisms in attempt to maintain homeostasis
1. If recovery occurs at this stage little damage done

Front 75

Shock
IV. Stages
B. Compensatory Stage--activation of compensatory mechanisms in attempt to maintain homeostasis
2. Clinical Manifestations--reflect body’s response to imbalance in -----------2 supply and demand (chemo and baroreceptros sense ↓--------- and attempt to raise it)

Back 75

Shock
IV. Stages
B. Compensatory Stage--activation of compensatory mechanisms in attempt to maintain homeostasis
2. Clinical Manifestations--reflect body’s response to imbalance in O2 supply and demand (chemo and baroreceptros sense ↓BP and attempt to raise it)

Front 76

Shock
IV. Stages
B. Compensatory Stage--activation of compensatory mechanisms in attempt to maintain homeostasis
2. Clinical Manifestations--reflect body’s response to imbalance in O2 supply and demand (chemo and baroreceptros sense ↓BP and attempt to raise it)
a. Neurogenic--subtle -----------, agitation, mild -------

Back 76

Shock
IV. Stages
B. Compensatory Stage--activation of compensatory mechanisms in attempt to maintain homeostasis
2. Clinical Manifestations--reflect body’s response to imbalance in O2 supply and demand (chemo and baroreceptros sense ↓BP and attempt to raise it)
a. Neurogenic--subtle restlessness, agitation, mild ALOC

Front 77

Shock
IV. Stages
B. Compensatory Stage--activation of compensatory mechanisms in attempt to maintain homeostasis
2. Clinical Manifestations--reflect body’s response to imbalance in O2 supply and demand (chemo and baroreceptros sense ↓BP and attempt to raise it
b. Cardiovascular--selective ------------ (norepinephrine) ↑-------- and contractility; ß-adrenergic stimulation dilate coronary arteries

Back 77

Shock
IV. Stages
B. Compensatory Stage--activation of compensatory mechanisms in attempt to maintain homeostasis
2. Clinical Manifestations--reflect body’s response to imbalance in O2 supply and demand (chemo and baroreceptros sense ↓BP and attempt to raise it
b. Cardiovascular--selective vasoconstriction (norepinephrine) ↑HR and contractility; ß-adrenergic stimulation dilate coronary arteries

Front 78

Shock
IV. Stages
B. Compensatory Stage--activation of compensatory mechanisms in attempt to maintain homeostasis
2. Clinical Manifestations--reflect body’s response to imbalance in O2 supply and demand (chemo and baroreceptros sense ↓BP and attempt to raise it
b. Cardiovascular--selective vasoconstriction (norepinephrine) ↑HR and contractility; ß----------- stimulation dilate ----------- arteries

Back 78

Shock
IV. Stages
B. Compensatory Stage--activation of compensatory mechanisms in attempt to maintain homeostasis
2. Clinical Manifestations--reflect body’s response to imbalance in O2 supply and demand (chemo and baroreceptros sense ↓BP and attempt to raise it
b. Cardiovascular--selective vasoconstriction (norepinephrine) ↑HR and contractility; ß-adrenergic stimulation dilate coronary arteries

Front 79

Shock
IV. Stages
B. Compensatory Stage--activation of compensatory mechanisms in attempt to maintain homeostasis
2. Clinical Manifestations--reflect body’s response to imbalance in O2 supply and demand (chemo and baroreceptros sense ↓BP and attempt to raise it
c. Respiratory--↑------------ dead space (some areas not leading to gas exchange) ------ mismatch ↑--------- and depth

Back 79

Shock
IV. Stages
B. Compensatory Stage--activation of compensatory mechanisms in attempt to maintain homeostasis
2. Clinical Manifestations--reflect body’s response to imbalance in O2 supply and demand (chemo and baroreceptros sense ↓BP and attempt to raise it
c. Respiratory--↑physiological dead space (some areas not leading to gas exchange) VQ mismatch ↑RR and depth

Front 80

Shock
IV. Stages
B. Compensatory Stage--activation of compensatory mechanisms in attempt to maintain homeostasis
2. Clinical Manifestations--reflect body’s response to imbalance in O2 supply and demand (chemo and baroreceptros sense ↓BP and attempt to raise it
d. GI--constriction ---------------- bowel sounds, ---------

Back 80

Shock
IV. Stages
B. Compensatory Stage--activation of compensatory mechanisms in attempt to maintain homeostasis
2. Clinical Manifestations--reflect body’s response to imbalance in O2 supply and demand (chemo and baroreceptros sense ↓BP and attempt to raise it
d. GI--constriction hypoactive bowel sounds, ileus

Front 81

Shock
IV. Stages
B. Compensatory Stage--activation of compensatory mechanisms in attempt to maintain homeostasis
2. Clinical Manifestations--reflect body’s response to imbalance in O2 supply and demand (chemo and baroreceptros sense ↓BP and attempt to raise it
e. Renal--vasoconstriction ↓------------ release of renin ↑---------

Back 81

Shock
IV. Stages
B. Compensatory Stage--activation of compensatory mechanisms in attempt to maintain homeostasis
2. Clinical Manifestations--reflect body’s response to imbalance in O2 supply and demand (chemo and baroreceptros sense ↓BP and attempt to raise it
e. Renal--vasoconstriction ↓blood flow release of renin ↑aldosterone

Front 82

Shock
IV. Stages
B. Compensatory Stage--activation of compensatory mechanisms in attempt to maintain homeostasis
2. Clinical Manifestations--reflect body’s response to imbalance in O2 supply and demand (chemo and baroreceptros sense ↓BP and attempt to raise it
e. Renal--vasoconstriction ↓blood flow release of renin ↑aldosterone
i. Renin --------------- 1 2 (most potent vasoconstrictor in body) Aldosterone (retains -------)

Back 82

Shock
IV. Stages
B. Compensatory Stage--activation of compensatory mechanisms in attempt to maintain homeostasis
2. Clinical Manifestations--reflect body’s response to imbalance in O2 supply and demand (chemo and baroreceptros sense ↓BP and attempt to raise it
e. Renal--vasoconstriction ↓blood flow release of renin ↑aldosterone
i. Renin Angiotensin 1 2 (most potent vasoconstrictor in body) Aldosterone (retains Na)

Front 83

Shock
IV. Stages
B. Compensatory Stage--activation of compensatory mechanisms in attempt to maintain homeostasis
2. Clinical Manifestations--reflect body’s response to imbalance in O2 supply and demand (chemo and baroreceptros sense ↓BP and attempt to raise i
f. Temperature--not -------- finding
g. Skin--pale, ---------- (septic will be warm)

Back 83

Shock
IV. Stages
B. Compensatory Stage--activation of compensatory mechanisms in attempt to maintain homeostasis
2. Clinical Manifestations--reflect body’s response to imbalance in O2 supply and demand (chemo and baroreceptros sense ↓BP and attempt to raise i
f. Temperature--not early finding
g. Skin--pale, cool (septic will be warm)

Front 84

Shock
IV. Stages
B. Compensatory Stage--activation of compensatory mechanisms in attempt to maintain homeostasis
2. Clinical Manifestations--reflect body’s response to imbalance in O2 supply and demand (chemo and baroreceptros sense ↓BP and attempt to raise
h. Labs--↓-----------2 and ------------ (due to ↑resp state)

Back 84

Shock
IV. Stages
B. Compensatory Stage--activation of compensatory mechanisms in attempt to maintain homeostasis
2. Clinical Manifestations--reflect body’s response to imbalance in O2 supply and demand (chemo and baroreceptros sense ↓BP and attempt to raise
h. Labs--↓PaO2 and alkalosis (due to ↑resp state)

Front 85

Shock
IV. Stages
C. Progressive Stage--↓--------------- altered cap perm (begins as comp mechanisms fail)

Back 85

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail)

Front 86

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail)
1. Must be presence of ------------ cause

Back 86

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail)
1. Must be presence of precipitating cause

Front 87

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail)
2. Massive ---------- stimulation (compensatory mechanisms not working)

Back 87

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail)
2. Massive SNS stimulation (compensatory mechanisms not working)

Front 88

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
a. Neurologic--↓-------------- pressure ↓------------- blood flow listless, agitated, ↓ responsiveness to stimuli

Back 88

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
a. Neurologic--↓cerebral perfusion pressure ↓cerebral blood flow listless, agitated, ↓ responsiveness to stimuli

Front 89

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
a. Neurologic--↓cerebral perfusion pressure ↓cerebral blood flow listless, ------------, ↓ -------------- to stimuli

Back 89

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
a. Neurologic--↓cerebral perfusion pressure ↓cerebral blood flow listless, agitated, ↓ responsiveness to stimuli

Front 90

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
b. Respiratory--pulmonary arterioles constriction (to ↑--------) ↑------------ ↓---------- blood flow worsening VQ mismatch ↑cap perm interstitial edema alveolar edema ↓gas exchange tachypnea, crackles, ↓compliance

Back 90

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
b. Respiratory--pulmonary arterioles constriction (to ↑BP) ↑PAP ↓pulm blood flow worsening VQ mismatch ↑cap perm interstitial edema alveolar edema ↓gas exchange tachypnea, crackles, ↓compliance

Front 91

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
b. Respiratory--pulmonary arterioles constriction (to ↑BP) ↑PAP ↓pulm blood flow worsening ---------- mismatch ↑cap perm, -------------, -------- edema ↓gas exchange tachypnea, crackles, ↓compliance

Back 91

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
b. Respiratory--pulmonary arterioles constriction (to ↑BP) ↑PAP ↓pulm blood flow worsening VQ mismatch ↑cap perm interstitial edema alveolar edema ↓gas exchange tachypnea, crackles, ↓compliance

Front 92

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
b. Respiratory--pulmonary arterioles constriction (to ↑BP) ↑PAP ↓pulm blood flow worsening VQ mismatch ↑cap perm interstitial edema alveolar edema ↓gas exchange -----------, ----------, ↓----------

Back 92

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
b. Respiratory--pulmonary arterioles constriction (to ↑BP) ↑PAP ↓pulm blood flow worsening VQ mismatch ↑cap perm interstitial edema alveolar edema ↓gas exchange tachypnea, crackles, ↓compliance

Front 93

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
c. Cardiogenic--↑cap perm ↓-------------- and ↓---------------, progressive tissue --------- ß-adrenergic receptor stimulation CO begins to fail (heart can’t keep up) ↑HR ↓BP ↓peripheral perfusion (MAP) ↓coronary perfusion arrhythmias ischemia potential MI (can be nonatherosclerotic)

Back 93

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
c. Cardiogenic--↑cap perm ↓circulating volume and ↓myocardial function progressive tissue hypoxia ß-adrenergic receptor stimulation CO begins to fail (heart can’t keep up) ↑HR ↓BP ↓peripheral perfusion (MAP) ↓coronary perfusion arrhythmias ischemia potential MI (can be nonatherosclerotic)

Front 94

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
c. Cardiogenic--↑cap perm ↓circulating volume and ↓myocardial function progressive tissue hypoxia ß-adrenergic ------------- stimulation, ------- begins to fail (heart can’t keep up) ↑-------- ↓BP ↓peripheral perfusion (MAP) ↓coronary perfusion arrhythmias ischemia potential MI (can be nonatherosclerotic)

Back 94

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
c. Cardiogenic--↑cap perm ↓circulating volume and ↓myocardial function progressive tissue hypoxia ß-adrenergic receptor stimulation CO begins to fail (heart can’t keep up) ↑HR ↓BP ↓peripheral perfusion (MAP) ↓coronary perfusion arrhythmias ischemia potential MI (can be nonatherosclerotic)

Front 95

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
c. Cardiogenic--↑cap perm ↓circulating volume and ↓myocardial function progressive tissue hypoxia ß-adrenergic receptor stimulation CO begins to fail (heart can’t keep up) ↑HR ↓-------- ↓------------- (MAP) ↓--------- perfusion arrhythmias ischemia potential MI (can be nonatherosclerotic)

Back 95

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
c. Cardiogenic--↑cap perm ↓circulating volume and ↓myocardial function progressive tissue hypoxia ß-adrenergic receptor stimulation CO begins to fail (heart can’t keep up) ↑HR ↓BP ↓peripheral perfusion (MAP) ↓coronary perfusion arrhythmias ischemia potential MI (can be nonatherosclerotic)

Front 96

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
c. Cardiogenic--↑cap perm ↓circulating volume and ↓myocardial function progressive tissue hypoxia ß-adrenergic receptor stimulation CO begins to fail (heart can’t keep up) ↑HR ↓BP ↓peripheral perfusion (MAP) ↓coronary perfusion --------------- ischemia potential ---------- (can be nonatherosclerotic)

Back 96

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
c. Cardiogenic--↑cap perm ↓circulating volume and ↓myocardial function progressive tissue hypoxia ß-adrenergic receptor stimulation CO begins to fail (heart can’t keep up) ↑HR ↓BP ↓peripheral perfusion (MAP) ↓coronary perfusion arrhythmias ischemia potential MI (can be nonatherosclerotic)

Front 97

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
c. Cardiogenic--
i. --------- cannot be maintained (unlike compensatory stage)

Back 97

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
c. Cardiogenic--
i. CO cannot be maintained (unlike compensatory stage)

Front 98

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
d. Renal--↓perfusion to ---------- ↓--------- output ↑------- fxn tests (BUN/CR) ATN ARF ↓ability to excrete acids and absorb bicarb metabolic acidosis

Back 98

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
d. Renal--↓perfusion to kidney ↓urine output ↑renal fxn tests (BUN/CR) ATN ARF ↓ability to excrete acids and absorb bicarb metabolic acidosis

Front 99

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
d. Renal--↓perfusion to kidney ↓urine output ↑renal fxn tests (BUN/CR) ------, -------, ↓ability to excrete ------- and absorb bicarb metabolic acidosis

Back 99

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
d. Renal--↓perfusion to kidney ↓urine output ↑renal fxn tests (BUN/CR) ATN ARF ↓ability to excrete acids and absorb bicarb metabolic acidosis

Front 100

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
d. Renal--↓perfusion to kidney ↓urine output ↑renal fxn tests (BUN/CR) ATN ARF ↓ability to excrete acids and absorb -----, metabolic -------

Back 100

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
d. Renal--↓perfusion to kidney ↓urine output ↑renal fxn tests (BUN/CR) ATN ARF ↓ability to excrete acids and absorb bicarb metabolic acidosis

Front 101

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
e. GI--extended ↓-------------- 2° to vasoconstriction, mucosal ----------, ↓-------- absorption and ulcers/GI bleeding ↑risk of bacteria to blood (sepsis)

Back 101

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
e. GI--extended ↓tissue perfusion 2° to vasoconstriction mucosal barrier ischemia ↓nutrient absorption and ulcers/GI bleeding ↑risk of bacteria to blood (sepsis)

Front 102

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
e. GI--extended ↓tissue perfusion 2° to vasoconstriction mucosal barrier ischemia ↓nutrient absorption and ulcers/------- bleeding ↑risk of -------- to blood (sepsis)

Back 102

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
e. GI--extended ↓tissue perfusion 2° to vasoconstriction mucosal barrier ischemia ↓nutrient absorption and ulcers/GI bleeding ↑risk of bacteria to blood (sepsis)

Front 103

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
f. Hepatic--↓----------- to liver ↓ability to ------------- drugs and waste products ↑-------3 lactate accumulation of bilirubin ↑LFTs (ALT, AST, GGT)

Back 103

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
f. Hepatic--↓perfusion to liver ↓ability to metabolize drugs and waste products ↑NH3 lactate accumulation of bilirubin ↑LFTs (ALT, AST, GGT)

Front 104

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
f. Hepatic--↓perfusion to liver ↓ability to metabolize drugs and waste products ↑NH3 lactate accumulation of ---------- ↑---------s (ALT, AST, GGT)

Back 104

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
f. Hepatic--↓perfusion to liver ↓ability to metabolize drugs and waste products ↑NH3 lactate accumulation of bilirubin ↑LFTs (ALT, AST, GGT)

Front 105

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
f. Hepatic--↓perfusion to liver ↓ability to metabolize drugs and waste products ↑NH3 lactate accumulation of bilirubin ↑LFTs (ALT, ------, ------)

Back 105

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
f. Hepatic--↓perfusion to liver ↓ability to metabolize drugs and waste products ↑NH3 lactate accumulation of bilirubin ↑LFTs (ALT, AST, GGT)

Front 106

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
g. Hematologic--platelets and clotting factor consumption ----------, ↑--------, ↑PTT, ↓-------- DIC risk widespread bleeding (GI, lungs, puncture sites)

Back 106

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
g. Hematologic--platelets and clotting factor consumption thrombocytopenia, ↑PT, ↑PTT, ↓fibrinogen DIC risk widespread bleeding (GI, lungs, puncture sites)

Front 107

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
g. Hematologic--platelets and clotting factor consumption thrombocytopenia, ↑PT, ↑-------, ↓fibrinogen ---------- risk widespread bleeding (GI, -------, puncture sites)

Back 107

Shock
IV. Stages
C. Progressive Stage--↓cellular perfusion altered cap perm (begins as comp mechanisms fail))
3. Pathophysiology and Manifestations
g. Hematologic--platelets and clotting factor consumption thrombocytopenia, ↑PT, ↑PTT, ↓fibrinogen DIC risk widespread bleeding (GI, lungs, puncture sites)

Front 108

Shock
IV. Stages
D. Refractory Stage--high likelihood of ------- (can sometimes be reversed)

Back 108

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)

Front 109

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
1. ↓---------- ↓------ anaerobic metabolism ↑-------- acid ↑cap perm interstitial fluid transfer worsens ↓intravascular volume ↓BP worsens myocardial depression worsens ↑HR ischemia further ↓CO ↓ cerebral flow cerebral ischemia

Back 109

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
1. ↓Perfusion ↓CO anaerobic metabolism ↑lactic acid ↑cap perm interstitial fluid transfer worsens ↓intravascular volume ↓BP worsens myocardial depression worsens ↑HR ischemia further ↓CO ↓ cerebral flow cerebral ischemia

Front 110

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
1. ↓Perfusion ↓CO anaerobic ----------- ↑lactic acid ↑cap perm interstitial ------------ worsens ↓---------- volume ↓BP worsens myocardial depression worsens ↑HR ischemia further ↓CO ↓ cerebral flow cerebral ischemia

Back 110

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
1. ↓Perfusion ↓CO anaerobic metabolism ↑lactic acid ↑cap perm interstitial fluid transfer worsens ↓intravascular volume ↓BP worsens myocardial depression worsens ↑HR ischemia further ↓CO ↓ cerebral flow cerebral ischemia

Front 111

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
1. ↓Perfusion ↓CO anaerobic metabolism ↑lactic acid ↑cap perm interstitial fluid transfer worsens ↓intravascular volume ↓--------- worsens myocardial ----------- worsens ↑---------- ischemia further ↓CO ↓ cerebral flow cerebral ischemia

Back 111

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
1. ↓Perfusion ↓CO anaerobic metabolism ↑lactic acid ↑cap perm interstitial fluid transfer worsens ↓intravascular volume ↓BP worsens myocardial depression worsens ↑HR ischemia further ↓CO ↓ cerebral flow cerebral ischemia

Front 112

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
1. ↓Perfusion ↓CO anaerobic metabolism ↑lactic acid ↑cap perm interstitial fluid transfer worsens ↓intravascular volume ↓BP worsens myocardial depression worsens ↑HR ischemia further ↓----------- ↓ ------------ flow cerebral --------

Back 112

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
1. ↓Perfusion ↓CO anaerobic metabolism ↑lactic acid ↑cap perm interstitial fluid transfer worsens ↓intravascular volume ↓BP worsens myocardial depression worsens ↑HR ischemia further ↓CO ↓ cerebral flow cerebral ischemia

Front 113

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
2. Pathophysiology--recovery is -------- (pt will code quickly)

Back 113

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
2. Pathophysiology--recovery is unlikely (pt will code quickly)

Front 114

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
2. Pathophysiology--recovery is unlikely (pt will code quickly)
a. Neurologic--unresponsive, pupils ------------ and dilated, --------- (loss of reflexes)

Back 114

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
2. Pathophysiology--recovery is unlikely (pt will code quickly)
a. Neurologic--unresponsive, pupils nonreactive and dilated, areflexia (loss of reflexes)

Front 115

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
2. Pathophysiology--recovery is unlikely (pt will code quickly)
b. Respiratory--severe refractory ----------- (despite intubation ↑---------2) and resp failure

Back 115

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
2. Pathophysiology--recovery is unlikely (pt will code quickly)
b. Respiratory--severe refractory hypoxemia (despite intubation ↑FiO2) and resp failure

Front 116

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
2. Pathophysiology--recovery is unlikely (pt will code quickly)
c. Cardiogenic--profound ------------ (can’t get it back up), ↓----------, bradycardia

Back 116

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
2. Pathophysiology--recovery is unlikely (pt will code quickly)
c. Cardiogenic--profound hypotension (can’t get it back up), ↓CO, bradycardia

Front 117

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
2. Pathophysiology--recovery is unlikely (pt will code quickly)
i. ---------- can only compensate for so long then if begins to drop

Back 117

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
2. Pathophysiology--recovery is unlikely (pt will code quickly)
i. HR can only compensate for so long then if begins to drop

Front 118

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
2. Pathophysiology--recovery is unlikely (pt will code quickly)
d. Renal--anuria; need ------------ or they will die (everything is shut down)

Back 118

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
2. Pathophysiology--recovery is unlikely (pt will code quickly)
d. Renal--anuria; need dialysis or they will die (everything is shut down)

Front 119

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
2. Pathophysiology--recovery is unlikely (pt will code quickly)
e. GI--_________

Back 119

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
2. Pathophysiology--recovery is unlikely (pt will code quickly)
e. GI--ischemic gut

Front 120

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
2. Pathophysiology--recovery is unlikely (pt will code quickly)
f. Hepatic--accumulation of ----------- products (including ↑---------3 and lactate)

Back 120

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
2. Pathophysiology--recovery is unlikely (pt will code quickly)
f. Hepatic--accumulation of waste products (including ↑NH3 and lactate)

Front 121

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
2. Pathophysiology--recovery is unlikely (pt will code quickly)
g. Skin--mottled and ----------

Back 121

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
2. Pathophysiology--recovery is unlikely (pt will code quickly)
g. Skin--mottled and cyanotic

Front 122

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
3. Residual Deficits (if live through stage)
a. Gangrene and amputations from -----------
b. Kidney and ----------- problems (possibly need transplants)

Back 122

Shock
IV. Stages
D. Refractory Stage--high likelihood of death (can sometimes be reversed)
3. Residual Deficits (if live through stage)
a. Gangrene and amputations from vasoconstriction

Front 123

Shock
V. Diagnostic Studies--no single ---------- test

Back 123

Shock
V. Diagnostic Studies--no single diagnostic test

Front 124

Shock
V. Diagnostic Studies--no single diagnostic test
A. ↑----------- levels and base deficit--from ↓--------- perfusion and anaerobic metabolism

Back 124

Shock
V. Diagnostic Studies--no single diagnostic test
A. ↑lactate levels and base deficit--from ↓tissue perfusion and anaerobic metabolism

Front 125

Shock
V. Diagnostic Studies--no single diagnostic test
B. EKG--if ------------- shock

Back 125

Shock
V. Diagnostic Studies--no single diagnostic test
B. EKG--if cardiogenic shock

Front 126

Shock
V. Diagnostic Studies--no single diagnostic test
C. C______
D. ____________ monitoring

Back 126

Shock
V. Diagnostic Studies--no single diagnostic test
C. CXR
D. Hemodynamic monitoring

Front 127

Shock
V. Diagnostic Studies--no single diagnostic test
E. Continuous--------- oximeter
F. ----------2

Back 127

Shock
V. Diagnostic Studies--no single diagnostic test
E. Continuous pulse oximeter
F. SVO2

Front 128

Shock
V. Diagnostic Studies--no single diagnostic test
G. Labs
1. Electrolytes--↑-------- (↑-----------), early ↓-------- (↑aldoseterone), later ↑K (cells die ↓kidney fxn)

Back 128

Shock
V. Diagnostic Studies--no single diagnostic test
G. Labs
1. Electrolytes--↑Na (↑aldosterone), early ↓K (↑aldoseterone), later ↑K (cells die ↓kidney fxn)

Front 129

Shock
V. Diagnostic Studies--no single diagnostic test
G. Labs
1. Electrolytes--↑Na (↑aldosterone), early ↓K (↑------------), later ↑K (cells die ↓---------- fxn)

Back 129

Shock
V. Diagnostic Studies--no single diagnostic test
G. Labs
1. Electrolytes--↑Na (↑aldosterone), early ↓K (↑aldoseterone), later ↑K (cells die ↓kidney fxn)

Front 130

Shock
V. Diagnostic Studies--no single diagnostic test
G. Labs
2. Blood--↓-------/Hg after volume replacement (if ---------)

Back 130

Shock
V. Diagnostic Studies--no single diagnostic test
G. Labs
2. Blood--↓Ht/Hg after volume replacement (if hemorrhagic)

Front 131

Shock
V. Diagnostic Studies--no single diagnostic test
G. Labs
3. ABGs--late metabolic ----------- (anaerobic ----------)

Back 131

Shock
V. Diagnostic Studies--no single diagnostic test
G. Labs
3. ABGs--late metabolic acidosis (anaerobic metabolism)

Front 132

Shock
V. Diagnostic Studies--no single diagnostic test
G. Labs
4. Renal function tests--↑----------/Cr

Back 132

Shock
V. Diagnostic Studies--no single diagnostic test
G. Labs
4. Renal function tests--↑BUN/Cr

Front 133

Shock
V. Diagnostic Studies--no single diagnostic test
G. Labs
5. LFTs--increased (only in -------------- stages)

Back 133

Shock
V. Diagnostic Studies--no single diagnostic test
G. Labs
5. LFTs--increased (only in progressive stages)

Front 134

Shock
V. Diagnostic Studies--no single diagnostic test
G. Labs
5. LFTs--_________ (only in progressive stages)

Back 134

Shock
V. Diagnostic Studies--no single diagnostic test
G. Labs
5. LFTs--increased (only in progressive stages)

Front 135

Shock
V. Diagnostic Studies--no single diagnostic test
G. Labs
6. Cardiac ---------

Back 135

Shock
V. Diagnostic Studies--no single diagnostic test
G. Labs
6. Cardiac enzymes

Front 136

Shock
V. Diagnostic Studies--no single diagnostic test
G. Labs
7. DIC panel--↓----------, ↓-----------, ↑PT/PTT

Back 136

Shock
V. Diagnostic Studies--no single diagnostic test
G. Labs
7. DIC panel--↓fibrinogen, ↓platelets, ↑PT/PTT

Front 137

Shock
V. Diagnostic Studies--no single diagnostic test
G. Labs
8. Glucose
a. Early--SNS stimulation, liver releases ------------ and stress response releases ----------- to maintain glucose levelsshock continues↓cells responsive to insulin↑glucose

Back 137

Shock
V. Diagnostic Studies--no single diagnostic test
G. Labs
8. Glucose
a. Early--SNS stimulationliver releases glycogen and stress response releases cortisol to maintain glucose levelsshock continues↓cells responsive to insulin↑glucose

Front 138

Shock
V. Diagnostic Studies--no single diagnostic test
G. Labs
8. Glucose
a. Early--SNS stimulationliver releases glycogen and stress response releases cortisol to maintain glucose levelsshock continues↓--------- responsive to insulin↑----------

Back 138

Shock
V. Diagnostic Studies--no single diagnostic test
G. Labs
8. Glucose
a. Early--SNS stimulationliver releases glycogen and stress response releases cortisol to maintain glucose levelsshock continues↓cells responsive to insulin↑glucose

Front 139

Shock
V. Diagnostic Studies--no single diagnostic test
G. Labs
8. Glucose
b. Late--depleted ---------- stores and no --------- from kidney ↓glucose

Back 139

Shock
V. Diagnostic Studies--no single diagnostic test
G. Labs
8. Glucose
b. Late--depleted glycogen stores and no cortisol from kidney ↓glucose

Front 140

Shock
VI. Management
A. Oxygenation and Ventilation--goal is to ↑O2 ----------- and ↓ O2 ---------

Back 140

Shock
VI. Management
A. Oxygenation and Ventilation--goal is to ↑O2 supply and ↓ O2 demand

Front 141

Shock
VI. Management
A. Oxygenation and Ventilation--goal is to ↑O2 supply and ↓ O2 demand
1. Optimize O2 delivery--NR mask, ----------, ↑---------2

Back 141

Shock
VI. Management
A. Oxygenation and Ventilation--goal is to ↑O2 supply and ↓ O2 demand
1. Optimize O2 delivery--NR mask, intubation, ↑FiO2

Front 142

Shock
VI. Management
A. Oxygenation and Ventilation--goal is to ↑O2 supply and ↓ O2 demand
2. Ensure pt has patent -----------
3. Provide ---------- O2

Back 142

Shock
VI. Management
A. Oxygenation and Ventilation--goal is to ↑O2 supply and ↓ O2 demand
2. Ensure pt has patent airway
3. Provide supplemental O2

Front 143

Shock
VI. Management
A. Oxygenation and Ventilation--goal is to ↑O2 supply and ↓ O2 demand
4. Optimize cardiac output--drug therapy (------------, debutamine, -----------)

Back 143

Shock
VI. Management
A. Oxygenation and Ventilation--goal is to ↑O2 supply and ↓ O2 demand
4. Optimize cardiac output--drug therapy (epinephrine, debutamine, levofed)

Front 144

Shock
VI. Management
A. Oxygenation and Ventilation--goal is to ↑O2 supply and ↓ O2 demand
4. Optimize cardiac output--drug therapy (epinephrine, debutamine, ---------)

Back 144

Shock
VI. Management
A. Oxygenation and Ventilation--goal is to ↑O2 supply and ↓ O2 demand
4. Optimize cardiac output--drug therapy (epinephrine, debutamine, levofed)

Front 145

Shock
VI. Management
A. Oxygenation and Ventilation--goal is to ↑O2 supply and ↓ O2 demand
5. Assess labs including ----------/Ht, ---------2

Back 145

Shock
VI. Management
A. Oxygenation and Ventilation--goal is to ↑O2 supply and ↓ O2 demand
5. Assess labs including Hg/Ht, SaO2

Front 146

Shock
VI. Management
A. Oxygenation and Ventilation--goal is to ↑O2 supply and ↓ O2 demand
6. Hemodynamic monitoring to assess ---------2 (assesses ----------- at level of tissues)

Back 146

Shock
VI. Management
A. Oxygenation and Ventilation--goal is to ↑O2 supply and ↓ O2 demand
6. Hemodynamic monitoring to assess SVO2 (assesses oxygenation at level of tissues)

Front 147

Shock
VI. Management
B. Fluid therapy--not ------------- (good volume w/ bad pump) or ---------- (good volume w/ vasodil.)

Back 147

Shock
VI. Management
B. Fluid therapy--not cardiogenic (good volume w/ bad pump) or neurogenic (good volume w/ vasodil.)

Front 148

Shock
VI. Management
B. Fluid therapy--not cardiogenic (good volume w/ bad pump) or neurogenic (good volume w/ vasodil.)
1. Establish ----------- access (14 to -------G)

Back 148

Shock
VI. Management
B. Fluid therapy--not cardiogenic (good volume w/ bad pump) or neurogenic (good volume w/ vasodil.)
1. Establish IV access (14-16G)

Front 149

Shock
VI. Management
B. Fluid therapy--not cardiogenic (good volume w/ bad pump) or neurogenic (good volume w/ vasodil.)
2. Hemodynamic monitoring to assess --------- status

Back 149

Shock
VI. Management
B. Fluid therapy--not cardiogenic (good volume w/ bad pump) or neurogenic (good volume w/ vasodil.)
2. Hemodynamic monitoring to assess fluid status

Front 150

Shock
VI. Management
B. Fluid therapy--not cardiogenic (good volume w/ bad pump) or neurogenic (good volume w/ vasodil.)
3. Fluid choice--think about what has been -------

Back 150

Shock
VI. Management
B. Fluid therapy--not cardiogenic (good volume w/ bad pump) or neurogenic (good volume w/ vasodil.)
3. Fluid choice--think about what has been lost

Front 151

Shock
VI. Management
B. Fluid therapy--not cardiogenic (good volume w/ bad pump) or neurogenic (good volume w/ vasodil.)
3. Fluid choice--think about what has been lost
a. RBCs--give w/ ----------- b/c RBCs do not have ------------ factors (1-2U FFP for 5U RBCs)

Back 151

Shock
VI. Management
B. Fluid therapy--not cardiogenic (good volume w/ bad pump) or neurogenic (good volume w/ vasodil.)
3. Fluid choice--think about what has been lost
a. RBCs--give w/ FFP b/c RBCs do not have clotting factors (1-2U FFP for 5U RBCs)

Front 152

Shock
VI. Management
B. Fluid therapy--not cardiogenic (good volume w/ bad pump) or neurogenic (good volume w/ vasodil.)
3. Fluid choice--think about what has been lost
a. RBCs--give w/ FFP b/c RBCs do not have clotting factors (1-______U FFP for 5_______ RBCs)

Back 152

Shock
VI. Management
B. Fluid therapy--not cardiogenic (good volume w/ bad pump) or neurogenic (good volume w/ vasodil.)
3. Fluid choice--think about what has been lost
a. RBCs--give w/ FFP b/c RBCs do not have clotting factors (1-2U FFP for 5U RBCs)

Front 153

Shock
VI. Management
B. Fluid therapy--not cardiogenic (good volume w/ bad pump) or neurogenic (good volume w/ vasodil.)
3. Fluid choice--think about what has been lost
a. Crystalloid (NS, LR)--2/3rd diffuse into ------------ space (require more -----------)

Back 153

Shock
VI. Management
B. Fluid therapy--not cardiogenic (good volume w/ bad pump) or neurogenic (good volume w/ vasodil.)
3. Fluid choice--think about what has been lost
a. Crystalloid (NS, LR)--2/3rd diffuse into interstitial space (require more volume)

Front 154

Shock
VI. Management
B. Fluid therapy--not cardiogenic (good volume w/ bad pump) or neurogenic (good volume w/ vasodil.)
3. Fluid choice--think about what has been lost
a. Crystalloid (---------, -----------)--2/3rd diffuse into interstitial space (require more volume)

Back 154

Shock
VI. Management
B. Fluid therapy--not cardiogenic (good volume w/ bad pump) or neurogenic (good volume w/ vasodil.)
3. Fluid choice--think about what has been lost
a. Crystalloid (NS, LR)--2/3rd diffuse into interstitial space (require more volume)

Front 155

Shock
VI. Management
B. Fluid therapy--not cardiogenic (good volume w/ bad pump) or neurogenic (good volume w/ vasodil.)
3. Fluid choice--think about what has been lost
b. Colloid (----------, -----------)--large therefore fluids stay in vascular space better

Back 155

Shock
VI. Management
B. Fluid therapy--not cardiogenic (good volume w/ bad pump) or neurogenic (good volume w/ vasodil.)
3. Fluid choice--think about what has been lost
b. Colloid (Albumin, Hespain)--large therefore fluids stay in vascular space better

Front 156

Shock
VI. Management
B. Fluid therapy--not cardiogenic (good volume w/ bad pump) or neurogenic (good volume w/ vasodil.)
3. Fluid choice--think about what has been lost
b. Colloid (Albumin, Hespain)--large therefore fluids stay in --------- space better

Back 156

Shock
VI. Management
B. Fluid therapy--not cardiogenic (good volume w/ bad pump) or neurogenic (good volume w/ vasodil.)
3. Fluid choice--think about what has been lost
b. Colloid (Albumin, Hespain)--large therefore fluids stay in vascular space better

Front 157

Shock
VI. Management
B. Fluid therapy--not cardiogenic (good volume w/ bad pump) or neurogenic (good volume w/ vasodil.)
3. Fluid choice--think about what has been lost
b. Colloid (Albumin, Hespain)--large therefore fluids stay in vascular space better
a. Can be given in concentrated space (esp. w/ ↑------------)--careful w/ -----------

Back 157

Shock
VI. Management
B. Fluid therapy--not cardiogenic (good volume w/ bad pump) or neurogenic (good volume w/ vasodil.)
3. Fluid choice--think about what has been lost
b. Colloid (Albumin, Hespain)--large therefore fluids stay in vascular space better
a. Can be given in concentrated space (esp. w/ ↑permeability)--careful w/ CHF

Front 158

Shock
VI. Management
B. Fluid therapy--not cardiogenic (good volume w/ bad pump) or neurogenic (good volume w/ vasodil.)
3. Fluid choice--think about what has been lost
b. Colloid (Albumin, Hespain)--large therefore fluids stay in vascular space better
b. More ---------

Back 158

Shock
VI. Management
B. Fluid therapy--not cardiogenic (good volume w/ bad pump) or neurogenic (good volume w/ vasodil.)
3. Fluid choice--think about what has been lost
b. Colloid (Albumin, Hespain)--large therefore fluids stay in vascular space better
b. More costly

Front 159

Shock
VI. Management
B. Fluid therapy--not cardiogenic (good volume w/ bad pump) or neurogenic (good volume w/ vasodil.)
3. Fluid choice--think about what has been lost
c. Avoid in first 24-_______hrs w/ burn pts

Back 159

Shock
VI. Management
B. Fluid therapy--not cardiogenic (good volume w/ bad pump) or neurogenic (good volume w/ vasodil.)
3. Fluid choice--think about what has been lost
c. Avoid in first 24-48hrs w/ burn pts

Front 160

Shock
VI. Management
B. Fluid therapy--not cardiogenic (good volume w/ bad pump) or neurogenic (good volume w/ vasodil.)
4. Monitor for ------------ (try to get warm fluids)

Back 160

Shock
VI. Management
B. Fluid therapy--not cardiogenic (good volume w/ bad pump) or neurogenic (good volume w/ vasodil.)
4. Monitor for hypothermia (try to get warm fluids)

Front 161

Shock
VI. Management
C. Drug Therapy--goal is to correct decreased ----------

Back 161

Shock
VI. Management
C. Drug Therapy--goal is to correct decreased tissue perfusion

Front 162

Shock
VI. Management
C. Drug Therapy--goal is to correct decreased tissue perfusion
1. Utilized if ------------- replacement does not work

Back 162

Shock
VI. Management
C. Drug Therapy--goal is to correct decreased tissue perfusion
1. Utilized if volume replacement does not work

Front 163

Shock
VI. Management
C. Drug Therapy--goal is to correct decreased tissue perfusion
1. Utilized if volume replacement does not work
a. Good response is seen w/ --------- output of 30-50mL/hr (0.5mL/kg/hr for critical care)

Back 163

Shock
VI. Management
C. Drug Therapy--goal is to correct decreased tissue perfusion
1. Utilized if volume replacement does not work
a. Good response is seen w/ urine output of 30-50mL/hr (0.5mL/kg/hr for critical care)

Front 164

Shock
VI. Management
C. Drug Therapy--goal is to correct decreased tissue perfusion
1. Utilized if volume replacement does not work
a. Good response is seen w/ urine output of 30-______mL/hr (_______mL/kg/hr for critical care)

Back 164

Shock
VI. Management
C. Drug Therapy--goal is to correct decreased tissue perfusion
1. Utilized if volume replacement does not work
a. Good response is seen w/ urine output of 30-50mL/hr (0.5mL/kg/hr for critical care)

Front 165

Shock
VI. Management
C. Drug Therapy--goal is to correct decreased tissue perfusion
2. Types
a. -------------- drugs
b. Vasopressors--cause vasoconstriction

Back 165

Shock
VI. Management
C. Drug Therapy--goal is to correct decreased tissue perfusion
2. Types
a. Sympathomimetic drugs
b. Vasopressors--cause vasoconstriction

Front 166

Shock
VI. Management
C. Drug Therapy--goal is to correct decreased tissue perfusion
2. Types
a. Sympathomimetic drugs
b. Vasopressors--cause ------------

Back 166

Shock
VI. Management
C. Drug Therapy--goal is to correct decreased tissue perfusion
2. Types
a. Sympathomimetic drugs
b. Vasopressors--cause vasoconstriction

Front 167

Shock
VI. Management
C. Drug Therapy--goal is to correct decreased tissue perfusion
2. Types
a. Sympathomimetic drugs
b. Vasopressors--cause vasoconstriction
i. Dobutamine (---------)

Back 167

Shock
VI. Management
C. Drug Therapy--goal is to correct decreased tissue perfusion
2. Types
a. Sympathomimetic drugs
b. Vasopressors--cause vasoconstriction
i. Dobutamine (Dobutrex)

Front 168

Shock
VI. Management
C. Drug Therapy--goal is to correct decreased tissue perfusion
2. Types
a. Sympathomimetic drugs
b. Vasopressors--cause vasoconstriction
ii. D________
iii. E________

Back 168

Shock
VI. Management
C. Drug Therapy--goal is to correct decreased tissue perfusion
2. Types
a. Sympathomimetic drugs
b. Vasopressors--cause vasoconstriction
ii. Dopamine
iii. Epinephrine

Front 169

Shock
VI. Management
C. Drug Therapy--goal is to correct decreased tissue perfusion
2. Types
a. Sympathomimetic drugs
b. Vasopressors--cause vasoconstriction
iv. ---------- (Levophed)
v. _________

Back 169

Shock
VI. Management
C. Drug Therapy--goal is to correct decreased tissue perfusion
2. Types
a. Sympathomimetic drugs
b. Vasopressors--cause vasoconstriction
iv. Norepinephrine (Levophed)
v. Neo-Synephrine

Front 170

Shock
VI. Management
C. Drug Therapy--goal is to correct decreased tissue perfusion
3. ----------Effects--balancing act

Back 170

Shock
VI. Management
C. Drug Therapy--goal is to correct decreased tissue perfusion
3. Detrimental Effects--balancing act

Front 171

Shock
VII. Specific Interventions
A. Cardiogenic--restore blood flow to ----------- by restoring balance between --------2 supply and demand

Back 171

Shock
VII. Specific Interventions
A. Cardiogenic--restore blood flow to myocardium by restoring balance between O2 supply and demand

Front 172

Shock
VII. Specific Interventions
A. Cardiogenic--
1. Hemodynamic goal--decrease ----------- of heart
2. --------- therapy

Back 172

Shock
VII. Specific Interventions
A. Cardiogenic--
1. Hemodynamic goal--decrease workload of heart
2. Drug therapy

Front 173

Shock
VII. Specific Interventions
A. Cardiogenic--
2. Drug therapy
a. ------------ therapy
b. Decrease ---------

Back 173

Shock
VII. Specific Interventions
A. Cardiogenic--
2. Drug therapy
a. Thrombolytic therapy
b. Decrease preload

Front 174

Shock
VII. Specific Interventions
A. Cardiogenic--
2. Drug therapy
i. Nitrates
ii. M_______
iii. D_______

Back 174

Shock
VII. Specific Interventions
A. Cardiogenic--
2. Drug therapy
i. Nitrates
ii. Morphine
iii. Diuretics

Front 175

Shock
VII. Specific Interventions
A. Cardiogenic--
2. Drug therapy
c. Reduce __________--be careful with reducing afterload ↓_________

Back 175

Shock
VII. Specific Interventions
A. Cardiogenic--
2. Drug therapy
c. Reduce afterload--be careful with reducing afterload ↓BP

Front 176

Shock
VII. Specific Interventions
A. Cardiogenic--
2. Drug therapy
i. Inotropic drugs (------------, ------------ Epinephrine)

Back 176

Shock
VII. Specific Interventions
A. Cardiogenic--
2. Drug therapy
i. Inotropic drugs (Dobutamine, Dopamine Epinephrine)

Front 177

Shock
VII. Specific Interventions
A. Cardiogenic--
2. Drug therapy
i. Inotropic drugs (Dobutamine, Dopamine Epinephrine)
ii. N---------

Back 177

Shock
VII. Specific Interventions
A. Cardiogenic--
2. Drug therapy
i. Inotropic drugs (Dobutamine, Dopamine Epinephrine)
ii. Nipride

Front 178

Shock
VII. Specific Interventions
A. Cardiogenic--
2. Drug therapy
d. ß-blockers, ---------: ↓--------- to allow for ↑ filling time

Back 178

Shock
VII. Specific Interventions
A. Cardiogenic--
2. Drug therapy
i. Inotropic drugs (Dobutamine, Dopamine Epinephrine)
ii. Nipride

Front 179

Shock
VII. Specific Interventions
A. Cardiogenic--
3. Correct ---------

Back 179

Shock
VII. Specific Interventions
A. Cardiogenic--
3. Correct arrhythmias

Front 180

Shock
VII. Specific Interventions
A. Cardiogenic--
4. Stents, emergency ----------
5. ------------ assist devices (only in critical care)

Back 180

Shock
VII. Specific Interventions
A. Cardiogenic--
4. Stents, emergency revascularization
5. Circulatory assist devices (only in critical care)

Front 181

Shock
VII. Specific Interventions
A. Cardiogenic--
5. Circulatory assist devices (only in critical care)
a. IABP--↓----------- and ↑---------- blood flow

Back 181

Shock
VII. Specific Interventions
A. Cardiogenic--
5. Circulatory assist devices (only in critical care)
a. IABP--↓afterload and ↑coronary blood flow

Front 182

Shock
VII. Specific Interventions
A. Cardiogenic--
5. Circulatory assist devices (only in critical care)
b. VAD--outside pump ------------ blood (likely need ----------)

Back 182

Shock
VII. Specific Interventions
A. Cardiogenic--
5. Circulatory assist devices (only in critical care)
b. VAD--outside pump diverts blood (likely need transplant)

Front 183

Shock
VII. Specific Interventions
B. Hypovolemic--restore ------------- volume and stop fluid loss restore ----------

Back 183

Shock
VII. Specific Interventions
B. Hypovolemic--restore circulating volume and stop fluid loss restore perfusion

Front 184

Shock
VII. Specific Interventions
B. Hypovolemic--restore circulating volume and stop fluid loss restore perfusion
1. Optimize ----------
2. ---------- cause

Back 184

Shock
VII. Specific Interventions
B. Hypovolemic--restore circulating volume and stop fluid loss restore perfusion
1. Optimize oxygenation
2. Correct cause

Front 185

Shock
VII. Specific Interventions
B. Hypovolemic--restore circulating volume and stop fluid loss restore perfusion
3. Volume replacement--warm to prevent ---------

Back 185

Shock
VII. Specific Interventions
B. Hypovolemic--restore circulating volume and stop fluid loss restore perfusion
3. Volume replacement--warm to prevent hypothermia
a. Fresh frozen plasma (FFP)

Front 186

Shock
VII. Specific Interventions
B. Hypovolemic--restore circulating volume and stop fluid loss restore perfusion
3. Volume replacement--warm to prevent hypothermia
a. Fresh ---------- ----------- (FFP)

Back 186

Shock
VII. Specific Interventions
B. Hypovolemic--restore circulating volume and stop fluid loss restore perfusion
3. Volume replacement--warm to prevent hypothermia
a. Fresh frozen plasma (FFP)

Front 187

Shock
VII. Specific Interventions
B. Hypovolemic--restore circulating volume and stop fluid loss restore perfusion
4. Monitor response to --------------- (↑PAWP and central venous pressures from 0 12)

Back 187

Shock
VII. Specific Interventions
B. Hypovolemic--restore circulating volume and stop fluid loss restore perfusion
4. Monitor response to fluid replacement (↑PAWP and central venous pressures from 0 12)

Front 188

Shock
VII. Specific Interventions
B. Hypovolemic--restore circulating volume and stop fluid loss restore perfusion
4. Monitor response to fluid replacement (↑------------ and central venous pressures from 0 to -------)

Back 188

Shock
VII. Specific Interventions
B. Hypovolemic--restore circulating volume and stop fluid loss restore perfusion
4. Monitor response to fluid replacement (↑PAWP and central venous pressures from 0 12)

Front 189

Shock
VII. Specific Interventions
C. Septic--: --------- O2 supply and ------------ O2 demand

Back 189

Shock
VII. Specific Interventions
C. Septic--optimize O2 supply and decrease O2 demand

Front 190

Shock
VII. Specific Interventions
C. Septic--optimize O2 supply and decrease O2 demand
1. Large amounts of fluid replacement (6-______L crystalloids or 2-______L colloids)

Back 190

Shock
VII. Specific Interventions
C. Septic--optimize O2 supply and decrease O2 demand
1. Large amounts of fluid replacement (6-10L crystalloids or 2-4L colloids)

Front 191

Shock
VII. Specific Interventions
C. Septic--optimize O2 supply and decrease O2 demand
1. Large amounts of fluid replacement (6-10L --------- or 2-4L ----------)

Back 191

Shock
VII. Specific Interventions
C. Septic--optimize O2 supply and decrease O2 demand
1. Large amounts of fluid replacement (6-10L crystalloids or 2-4L colloids)

Front 192

Shock
VII. Specific Interventions
C. Septic--optimize O2 supply and decrease O2 demand
1. Large amounts of fluid replacement (6-10L crystalloids or 2-4L colloids)
a. Endotoxins ↑----------- lose lots of fluids to -------- space

Back 192

Shock
VII. Specific Interventions
C. Septic--optimize O2 supply and decrease O2 demand
1. Large amounts of fluid replacement (6-10L crystalloids or 2-4L colloids)
a. Endotoxins ↑cap perm lose lots of fluids to interstitial space

Front 193

Shock
VII. Specific Interventions
C. Septic--optimize O2 supply and decrease O2 demand
2. Optimize ----------

Back 193

Shock
VII. Specific Interventions
C. Septic--optimize O2 supply and decrease O2 demand
2. Optimize CO

Front 194

Shock
VII. Specific Interventions
C. Septic--optimize O2 supply and decrease O2 demand
2. Optimize CO
a. V---------
b. Vasopressors to ↑----------
c. I-----------

Back 194

Shock
VII. Specific Interventions
C. Septic--optimize O2 supply and decrease O2 demand
2. Optimize CO
a. Volume
b. Vasopressors to ↑BP
c. Inotropes

Front 195

Shock
VII. Specific Interventions
C. Septic--optimize O2 supply and decrease O2 demand
3. Correct -----------
4. Antibiotics (------------ before beginning)

Back 195

Shock
VII. Specific Interventions
C. Septic--optimize O2 supply and decrease O2 demand
3. Correct acidosis
4. Antibiotics (cultures before beginning)

Front 196

Shock
VII. Specific Interventions
D. Neurogenic
1. Use ----------- precautions

Back 196

Shock
VII. Specific Interventions
D. Neurogenic
1. Use spinal precautions

Front 197

Shock
VII. Specific Interventions
D. Neurogenic
2. Treatment of ↓BP w/ --------- and --------- therapy

Back 197

Shock
VII. Specific Interventions
D. Neurogenic
2. Treatment of ↓BP w/ fluids and drug therapy
a. Dopamine--↑BP and is (+) cornotrope (↑HR)

Front 198

Shock
VII. Specific Interventions
D. Neurogenic
2. Treatment of ↓BP w/ fluids and drug therapy
a. Dopamine--↑------- and is (+) --------- (↑HR)

Back 198

Shock
VII. Specific Interventions
D. Neurogenic
2. Treatment of ↓BP w/ fluids and drug therapy
a. Dopamine--↑BP and is (+) cornotrope (↑HR)

Front 199

Shock
VII. Specific Interventions
D. Neurogenic
2. Treatment of ↓BP w/ fluids and drug therapy
b. E---------

Back 199

Shock
VII. Specific Interventions
D. Neurogenic
2. Treatment of ↓BP w/ fluids and drug therapy
b. Epinephrine

Front 200

Shock
VII. Specific Interventions
D. Neurogenic
3. Monitor for ---------

Back 200

Shock
VII. Specific Interventions
D. Neurogenic
3. Monitor for hypothermia

Front 201

Shock
VII. Specific Intervention
E. Anaphylactic--can generally be ------------ if treated promptly

Back 201

Shock
VII. Specific Intervention
E. Anaphylactic--can generally be reverse if treated promptly

Front 202

Shock
VII. Specific Intervention
E. Anaphylactic--can generally be reverse if treated promptly
1. Prevention--avoidance of known ---------

Back 202

Shock
VII. Specific Intervention
E. Anaphylactic--can generally be reverse if treated promptly
1. Prevention--avoidance of known allergen
2. Treatment

Front 203

Shock
VII. Specific Intervention
E. Anaphylactic--can generally be reverse if treated promptly
2. Treatment
a. Maintain patient ----------

Back 203

Shock
VII. Specific Intervention
E. Anaphylactic--can generally be reverse if treated promptly
2. Treatment
a. Maintain patient airway
b. Drugs

Front 204

Shock
VII. Specific Intervention
E. Anaphylactic--can generally be reverse if treated promptly
2. Treatment
b. Drugs
i. --------------- (drug of choice)--peripheral vasoconstriction and bronchodilation

Back 204

Shock
VII. Specific Intervention
E. Anaphylactic--can generally be reverse if treated promptly
2. Treatment
b. Drugs
i. Epinephrine (drug of choice)--peripheral vasoconstriction and bronchodilation

Front 205

Shock
VII. Specific Intervention
E. Anaphylactic--can generally be reverse if treated promptly
2. Treatment
b. Drugs
i. Epinephrine (drug of choice)--peripheral ------------ and ------------

Back 205

Shock
VII. Specific Intervention
E. Anaphylactic--can generally be reverse if treated promptly
2. Treatment
b. Drugs
i. Epinephrine (drug of choice)--peripheral vasoconstriction and bronchodilation

Front 206

Shock
VII. Specific Intervention
E. Anaphylactic--can generally be reverse if treated promptly
2. Treatment
b. Drugs
i. Epinephrine (drug of choice)--peripheral vasoconstriction and bronchodilation
ii. Benadryl--blocks release of ---------
iii. IV steroids--↓------------ response

Back 206

Shock
VII. Specific Intervention
E. Anaphylactic--can generally be reverse if treated promptly
2. Treatment
b. Drugs
i. Epinephrine (drug of choice)--peripheral vasoconstriction and bronchodilation
ii. Benadryl--blocks release of histamine
iii. IV steroids--↓allergic response

Front 207

Shock
VII. Specific Intervention
E. Anaphylactic--can generally be reverse if treated promptly
2. Treatment
c. Aggressive --------- replacement (colloids) to combat ----------

Back 207

Shock
VII. Specific Intervention
E. Anaphylactic--can generally be reverse if treated promptly
2. Treatment
c. Aggressive fluid replacement (colloids) to combat hypotension

Front 208

Shock
VIII. Nursing Management
A. Goals
1. Assurance of adequate -------- perfusion
2. Restoration of normal ----------

Back 208

Shock
VIII. Nursing Management
A. Goals
1. Assurance of adequate tissue perfusion
2. Restoration of normal BP

Front 209

Shock
VIII. Nursing Management
A. Goals
3. Return/Recovery of -------- function
4. Avoidance of complications from prolonged states of -----------

Back 209

Shock
VIII. Nursing Management
A. Goals
3. Return/Recovery of organ function
4. Avoidance of complications from prolonged states of hypoperfusion

Front 210

Shock
VIII. Nursing Management
B. Acute Interventions
1. ------------ status
2. ---------- status
3. ----------- status

Back 210

Shock
VIII. Nursing Management
B. Acute Interventions
1. Neurologic status
2. Cardiovascular status
3. Respiratory status

Front 211

Shock
VIII. Nursing Management
B. Acute Interventions
4.-------- status
5. G---------
6. Skin and ----------

Back 211

Shock
VIII. Nursing Management
B. Acute Interventions
4. Renal status
5. GI
6. Skin and temperature

Front 212

Shock
VIII. Nursing Management
B. Acute Interventions
7. Emotional --------- or comfort

Back 212

Shock
VIII. Nursing Management
B. Acute Interventions
7. Emotional support or comfort

Front 213

Shock
VIII. Nursing Management
C. Health Promotion Strategies
1. Prevention--identify patients at -------
2. Interventions aimed at decreasing --------- demand

Back 213

Shock
VIII. Nursing Management
C. Health Promotion Strategies
1. Prevention--identify patients at risk
2. Interventions aimed at decreasing O2 demand

Front 214

Shock
VIII. Nursing Management
C. Health Promotion Strategies
3. Monitoring of ------------ balance to prevent hypovolemic shock
4. Prevention of -------------

Back 214

Shock
VIII. Nursing Management
C. Health Promotion Strategies
3. Monitoring of fluid balance to prevent hypovolemic shock
4. Prevention of infection