Sepsis/Shock/MODS Flashcards

1
Q

What two things determine blood pressure?

A

Systemic vascular resistance
Cardiac output

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2
Q

How is cardiac output determined?

A

Heart rate x stroke volume

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3
Q

what factors affect stroke volume?

A

heart size
fitness level
gender
contractility
preload and afterload

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4
Q

what factors affect heart rate?

A

hormones
fitness level
age

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5
Q

Shock begins when…

A

the cardiovascular system fails to function properly
and alteration of AT LEAST ONE of four circulatory components

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6
Q

What are the 4 circulatory components?

A

Blood volume
Myocardial contractility
blood flow
vascular resistance

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7
Q

Types of shock

A

cardiogenic
distributive
hypovolemic
obstructive

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8
Q

What physiological alteration causes cardiogenic shock and example?

A

inadequate myocardial contractility

Heart attack

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9
Q

What physiological alteration causes distributive shock? Examples

A

inadequate vascular tone
Sepsis
anaphylaxis

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10
Q

What is physiological alteration causes hypovolemic shock?

A

inadequate intravascular volume

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11
Q

Shock: Stage I Initiation
Explain.

A

Decreases perfusion
inadequate delivery of oxygen
No obvious signs
Decreased CO can occur

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12
Q

Shock Stage II: Compensatory
Explain.

A

Body tries to compensate for reduction of perfusion

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13
Q

Shock Stage II Compensatory: Neural compensation

A

baroreceptors and chemoreceptors send signals to sympathetic nervous system

VASOCONSTRICTION > INCREASE HR
REDISTRIBUTES BLOOD TO VITAL ORGANS
BRONCHODILATION > RESP RATE GOES UP

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14
Q

Shock Stage II Compensatory:
Endocrine compensation

A

Renin-angiotensin-aldosterone-system is ACTIVTED
renal reabsorption of sodium and water
Blood glucose levels increase

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15
Q

Shock stage II compensatory clinical presentation

A

Increased HR
Thirst
Cool, moist skin
oliguria
diminished bowel sounds
restlessness
hyperglycemia
rapid and deep respirations
decreased creatinine

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16
Q

Shock Stage III Progressive
Explain

A

Hypoperfusion not corrected and compensatory mechanisms have failed
ischemia in extremities

Cells > anaerobic metabolism > lactic acid > metabolic acidosis

Failure of sodium-potassium pump > cell swelling

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17
Q

Shock stage III progressive: Clinical signs

A

Decrease BP
Dysrhythmias
Tachypnea
cold clammy skin
decreased capillary refill
mottling
Anuria
absent bowel sounds
lethargy

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18
Q

Shock stage III: progressive
What can you expect labs to look like?

A

High BUN, Creatinine Potassium
Respiratory and metabolic acidosis

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19
Q

Shock Stage IV: Refractory
Explain

A

Severe tissue hypoxia with ischemia and necrosis
worse acidosis
SIRS
MODS

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20
Q

Shock stage IV Refractory
Clinical presentation

A

Severe dysrhythmias and hypotension
respiratory and metabolic acidosis
acute respiratory failure
DIC
ARDS
hepatic dysfunction or failure
AKI
heart failure
brain ischemia

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21
Q

What is SIRS?

A

Systemic inflammatory response syndrome
balance between proinflammatory and anti-inflammatory processes are disrupted

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22
Q

CNS assessment for shock

A

Early signs are anxiety and restlessness
Late signs are confusion and lethargy/coma

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23
Q

Cardiovascular assessment for shock

A

Blood pressure will be increased INITIALLY
HR is increased
check capillary refill
Assess for JVD
Check pulse rate and quality

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24
Q

Respiratory assessment for shock

A

Early : rapid and deep breathing
late: shallow
ABGs
pulse ox

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25
Q

Renal Assessment for shock

A

Decreased GFR
oliguria (< 0.5 mL/kg/hr)

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26
Q

GI assessment for shock

A

slowed intestinal activity
decreased bowel sounds
N/V
constipation

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27
Q

Hepatic Assessment for shock

A

Altered liver enzymes
DIC
liver can’t detoxify

28
Q

Hematological assessment for shock

A

decreased platelet
messed up clotting factors

29
Q

Skin assessment for shock

A

skin mottling around knees
may see cyanosis

30
Q

What does fluid challenge mean?

A

performed to assess patient’s response to fluids
rapid infusion of 250 mL of a crystalloid solution (NS or LR)

31
Q

What are some complications of fluid challenging?

A

Pulmonary edema
transfusion reaction

32
Q

Medications used for shock

A

Norepinephrine
Vasopressin
Dobutamine
Epinephrine

33
Q

What does norepinephrine do?

A

causes vasoconstriction

34
Q

Purpose of vasopressin

A

to restore vascular tone in distributive shock

35
Q

What does dobutamine do?

A

increase cardiac contractility and HR
causes vasodilation in low cardiac output states

36
Q

What are some examples of supportive care for patients with shock?

A

Warm blankets
nutrition-enteral feedings
Turning every 2 hours
barrier creams
elevate heels of the bed

37
Q

What is Hypovolemic shock? Give examples

A

Inadequate fluid volume
EX: bleeding, trauma, diarrhea/vomiting

38
Q

Manifestations of hypovolemic shock

A

Increased HR
decreased BP
Tachypnea
cool, pale skin
oliguria
flat neck veins

39
Q

What is the management/treatment for hypovolemic shock?

A

Give isotonic crystalloids (NS or LR) or blood

40
Q

What is Cardiogenic shock? Give examples

A

Heart fails to pump efficiently
Heart attack, dysrhythmias, severe heart failure

41
Q

Management/ treatment for cardiogenic shock

A

decrease preload and afterload
increase cardiac output

42
Q

Manifestations of cardiogenic shock

A

Increased HR
dysrhythmias
decreased BP
chest pain
tachypnea
decreased mentation

43
Q

Clinical manifestations of distributive shock- Neurogenic

A

PROFOUND bradycardia with hypotension
Hypothermia
warm dry flushed skin

44
Q

Septic shock v sepsis

A

septic shock is a life threatening complication of sepsis
Sepsis is life threatening organ dysfunction caused by response to infection

45
Q

What is the diagnostic criteria for sepsis?

A

2 or more indicators of systemic inflammation
Temp >38.3 or <36
HR > 90
RR > 20
WBC >12 or < 4

46
Q

Diagnosis criteria for septic shock

A

Urine output < 0.05 mL/kg/hr
Creatinine > 0.5
Lactate > 4 or > 2

47
Q

What are the steps in the sepsis bundle

A

obtain blood culture
give broad spectrum antibiotics
rapidly give 30 ml/kg of fluids
give vasopressors if patient is hypotensive

48
Q

What is MODS?

A

Multiple organ dysfunction syndrome
dysfunction of 2 or more organ systems from uncontrolled inflammatory response

49
Q

What is Primary MODS?

A

direct injury to organ from shock, trauma, or burn

50
Q

What is secondary MODS?

A

consequence of widespread systemic inflammation

51
Q

Clinical manifestations of MODS

A

tachypnea/hypoxemia
Petechiae/bleeding
jaundice
abdominal distention
oliguria or anuria
tachycardia
hypotension
LOC change

52
Q

What is DIC?

A

Disseminated Intravascular coagulation
exaggerated microvascular coagulation, depletion of clotting factors and bleeding

53
Q

What is the most common cause of DIC?

A

sepsis

54
Q

DIC Assessment findings

A

overt bleeding
occult bleeding
PLT deficiency
decreased organ perfusion

55
Q

Expected lab findings for DIC

A

Low PLTs
Low fibrinogen
low coag factors
low hgb and hct
HIGH D-dimer

56
Q

How do you know if patient is tolerating fluid replacement?

A

MAP is between 65-70
Urine output is > 0.5 mg/kg/hr

57
Q

What is neurogenic shock?

A

Shock from spinal cord injuries

58
Q

Management for Neurogenic shock

A

Immobilization
IV fluids for hypotension
slow rewarming to prevent further vasodilation

59
Q

Clinical manifestations of anaphylactic

A

Angioedema
High HR and BP
integumentary
tightened airway
wheezing

60
Q

Management of anaphylactic shock

A

epinephrine
protect airway
remove offending agent

61
Q

What organs are the first to fail in MODS?

A

Kidneys

62
Q

What is the management of MODS?

A

antibiotics
provide adequate tissue perfusion
maintain 88%-92% O2 sat
Maintain Hgb 7-9

63
Q

What are some positive outcomes of shock, sepsis, and MODS?

A

Improved tissue perfusion
normotensive
warm, dry skin
adequate urine output
intact skin

64
Q

What can cause DIC?

A

Infection
trauma
obstetric conditions
blood disorders
septic shock
ARDS

65
Q

Nursing management for DIC

A

Assess and prevent
blood products
relieve pain
analyze lab values