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Critical Care <3 > Sepsis/Shock/MODS > Flashcards

Sepsis/Shock/MODS Flashcards

(65 cards)

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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
Renal Assessment for shock
Decreased GFR oliguria (< 0.5 mL/kg/hr)
26
GI assessment for shock
slowed intestinal activity decreased bowel sounds N/V constipation
27
Hepatic Assessment for shock
Altered liver enzymes DIC liver can't detoxify
28
Hematological assessment for shock
decreased platelet messed up clotting factors
29
Skin assessment for shock
skin mottling around knees may see cyanosis
30
What does fluid challenge mean?
performed to assess patient's response to fluids rapid infusion of 250 mL of a crystalloid solution (NS or LR)
31
What are some complications of fluid challenging?
Pulmonary edema transfusion reaction
32
Medications used for shock
Norepinephrine Vasopressin Dobutamine Epinephrine
33
What does norepinephrine do?
causes vasoconstriction
34
Purpose of vasopressin
to restore vascular tone in distributive shock
35
What does dobutamine do?
increase cardiac contractility and HR causes vasodilation in low cardiac output states
36
What are some examples of supportive care for patients with shock?
Warm blankets nutrition-enteral feedings Turning every 2 hours barrier creams elevate heels of the bed
37
What is Hypovolemic shock? Give examples
Inadequate fluid volume EX: bleeding, trauma, diarrhea/vomiting
38
Manifestations of hypovolemic shock
Increased HR decreased BP Tachypnea cool, pale skin oliguria flat neck veins
39
What is the management/treatment for hypovolemic shock?
Give isotonic crystalloids (NS or LR) or blood
40
What is Cardiogenic shock? Give examples
Heart fails to pump efficiently Heart attack, dysrhythmias, severe heart failure
41
Management/ treatment for cardiogenic shock
decrease preload and afterload increase cardiac output
42
Manifestations of cardiogenic shock
Increased HR dysrhythmias decreased BP chest pain tachypnea decreased mentation
43
Clinical manifestations of distributive shock- Neurogenic
PROFOUND bradycardia with hypotension Hypothermia warm dry flushed skin
44
Septic shock v sepsis
septic shock is a life threatening complication of sepsis Sepsis is life threatening organ dysfunction caused by response to infection
45
What is the diagnostic criteria for sepsis?
2 or more indicators of systemic inflammation Temp >38.3 or <36 HR > 90 RR > 20 WBC >12 or < 4
46
Diagnosis criteria for septic shock
Urine output < 0.05 mL/kg/hr Creatinine > 0.5 Lactate > 4 or > 2
47
What are the steps in the sepsis bundle
obtain blood culture give broad spectrum antibiotics rapidly give 30 ml/kg of fluids give vasopressors if patient is hypotensive
48
What is MODS?
Multiple organ dysfunction syndrome dysfunction of 2 or more organ systems from uncontrolled inflammatory response
49
What is Primary MODS?
direct injury to organ from shock, trauma, or burn
50
What is secondary MODS?
consequence of widespread systemic inflammation
51
Clinical manifestations of MODS
tachypnea/hypoxemia Petechiae/bleeding jaundice abdominal distention oliguria or anuria tachycardia hypotension LOC change
52
What is DIC?
Disseminated Intravascular coagulation exaggerated microvascular coagulation, depletion of clotting factors and bleeding
53
What is the most common cause of DIC?
sepsis
54
DIC Assessment findings
overt bleeding occult bleeding PLT deficiency decreased organ perfusion
55
Expected lab findings for DIC
Low PLTs Low fibrinogen low coag factors low hgb and hct HIGH D-dimer
56
How do you know if patient is tolerating fluid replacement?
MAP is between 65-70 Urine output is > 0.5 mg/kg/hr
57
What is neurogenic shock?
Shock from spinal cord injuries
58
Management for Neurogenic shock
Immobilization IV fluids for hypotension slow rewarming to prevent further vasodilation
59
Clinical manifestations of anaphylactic
Angioedema High HR and BP integumentary tightened airway wheezing
60
Management of anaphylactic shock
epinephrine protect airway remove offending agent
61
What organs are the first to fail in MODS?
Kidneys
62
What is the management of MODS?
antibiotics provide adequate tissue perfusion maintain 88%-92% O2 sat Maintain Hgb 7-9
63
What are some positive outcomes of shock, sepsis, and MODS?
Improved tissue perfusion normotensive warm, dry skin adequate urine output intact skin
64
What can cause DIC?
Infection trauma obstetric conditions blood disorders septic shock ARDS
65
Nursing management for DIC
Assess and prevent blood products relieve pain analyze lab values

Critical Care <3 (16 decks)

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