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Critical Care > Shock > Flashcards

Shock Flashcards

1
Q

End result of all types of shock

A

*Impaired tissue perfusion/oxygenation
*Impaired cellular metabolism (from the impaired perfusion/oxygenation)

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2
Q

*Names of stages of shock, in order

A

1 - initial
2 - compensatory (early)
3 - progressive (decompensated)
4 - refractory (irreversible)

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3
Q

What occurs during stage 1: Initial stage of shock

A

Subclinical hypoperfusion
*No overt clinical manifestations

Decreased O2 delivery and/or O2 extraction (from hgb)
Decreased CO detectible by hemodynamic monitoring

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4
Q

What occurs with stage II (Compensatory) shock

A

(Body is now trying to improve situation, so will see s/s)

Occurs in response to sustained decreased CO in stage 1
*S/S are evident
Compensatory mechanisms restore tissue perfection
*Shock may be reversed with adequate interventions

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5
Q

During stage 2 of shock, how does the SNS respond?

A

The SNS is activated (Epi and norepi are activated)

Combined action of epi and norepi preserves CO and perfusion to the heart and brain *Temporarily

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6
Q

How does the endocrine system compensate in stage 2 of shock?

A

RAAS activates, ultimately causing
Renin release, which causes body to *hold onto salt and water, which increases fluid volume (increased blood volume)

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7
Q

How does chemical compensation occur during stage 2 of shock?

A

Chemoreceptors detect the decrease in PaO2, causing RR to increase to increase O2
This causes respiratory alkalosis
Also causes cerebral vessels to constrict, resulting in cerebral ischemia

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8
Q

*Cardiovascular clinical manifestations of compensatory shock

A

*SBP > 90
HR 101-150
Pulses weak, rapid
Skin cool, pale, moist

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9
Q

*Neuro clinical manifestations of compensatory shock

A

Decreased LOC (first indication something is wrong)
- Anxious, then restless, then irritable, then lethargic then drowsy

*Pupils dilated but reactive to light (think fight or flight response)

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10
Q

*Respiratory clinical manifestations of compensatory shock

A

RR > 20 / min
Pattern deep and rapid (hyperventilation/hyperpnea), which causes:
* PCO2 <35 mmHg

PO2 < 60 mmHg
HCO3 22-24 (not compensatory yet, so early in process. Can still intervene)

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11
Q

*Renal clinical manifestations of compensatory shock

A

*UOP < 30 mL/hr
Hypernatremia (b/c of RAAS)
Concentrated urine (body trying to hold onto volume to keep BP up)

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12
Q

*GI clinical manifestations of compensatory shock

A

Hypoactive bowel sounds (fight or flight)
Hyperglycemia (caused by counterregulatory hormones)

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13
Q

What occurs during stage 4 of shock (Refractory Shock)?

A

Pooling of blood in capillary beds
Inadequate perfusion of vital organs
Multisystem organ failure (SIDS, MODS)

*Shock is so profound and severe that *Death is imminent

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14
Q

Types of shock

A

Hypovolemia
Cardiogenic
Obstructive
Distributive

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15
Q

Definition of hypovolemic shock

A

Inadequate blood volume to fill intravascular space

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16
Q

External losses causing hypovolemic shock

A

Hemorrhage (Most common cause)
Diarrhea
Vomiting
Massive diuresis (Ex: DI, DKA, HNKS)
Loss of plasma (burns/wounds)

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17
Q

Internal losses causing hypovolemic shock

A

Internal hemorrhage (ex: liver laceration, severe GI bleed)
3rd spacing (ascites)
Increased capillary permeability (sepsis, allergic reaction, burns)

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18
Q

Patho of hypovolemic shock

A

Decreased circulating blood volume
Causes decreased venous return (decreased preload)
Which causes decreased ventricular filling
Which causes decreased stroke volume and cardiac output
Which causes *decreased tissue perfusion
Which causes * impaired cellular metabolism

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19
Q

Symptoms of hypovolemic shock

A

Hypotension
Tachycardia
Oliguria
Cool, pale skin
Decreased cardiac output, CI, PAP, PAWP
Increased systemic vascular resistance

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20
Q

Management of hypovolemic shock

A

*Identify and treat the cause
*Fluid therapy (3:1 rule) (Replace 3 times as much as what was lost)

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21
Q

Prevention of hypovolemic shock

A

Strict I&O (hourly for every pt, esp with foley)
Monitor for bleeding (low hct, hgb, platelets)
Report abnormal findings
Identify patients at risk

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22
Q

What is cardiogenic shock?

A

When >40% of LV function is lost, results in pump failure; cardiac output cannot meet tissue demands

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23
Q

Causes of cardiogenic shock

A

*MI (most common cause)
Post-cardiac surgery
Dysrhythmias
Valvular heart disease
Cardiomyopathy

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24
Q

Patho of cardiogenic shock

A
  • Myocardial damage: compensatory mechanisms cause further detriment to myocardium
  • Decreased pumping ability
  • Decreased stroke volume and decreased cardiac output
    (Volume is normal, but heart can’t pump to perfuse properly)
  • *Decreased tissue perfusion
  • *Impaired cellular metabolism
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25
Q

Symptoms of cardiogenic shock

A

Hypotension
Tachycardia
Tachypnea
Oliguria
Cool, pale skin
Decreased cardiac output, decreased cardiac index
*Increased Pulmonary artery pressure, increased PAWP
Increased SVR

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26
Q

Management of cardiogenic shock

A

Goal = restore force of contraction: Improve CO and decrease workload

Positive inotropic agents (mid-range dopamine)
Afterload reducing agents (vasodilators: nitros)
Preload reducing agents (diuretic: furosemide)
Mechanical assist devices (rarely)

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27
Q

Prevention of cardiogenic shock

A

Minimize size of infarct
PTCA
Fibrinolytics not recommended anymore
CABG

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28
Q

What is obstructive shock?

A

AKA extracardiac obstructive shock
Occurs as result of physical impairment to adequate blood flow
Obstruction of heart or great vessels impedes venous return or prevents effective pumping action

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29
Q

Three categories of obstructive shock

A

Impaired diastolic filling (causes decreased CO)
Increased RV afterload (has to work harder to push blood into lungs)
Increased LV afterload (aortic valve malfunction)

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30
Q

Causes of impaired diastolic filling leading to obstructive shock

A

Tamponade (pericardial sac has increase in pericardial fluid)
Tension pneumo
Pericarditis
Compression of great veins

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31
Q

Causes of increased RV afterload, leading to obstructive shock

A

PE
Pulmonary HTN
PEEP

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32
Q

Causes of increased LV afterload leading to obstructive shock

A

Aortic dissection
Aortic stenosis
Abdominal distention
Systemic embolization

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33
Q

Patho of obstructive shock

A

Mechanical obstruction
Causes decreased ventricular filling or pumping
Which causes decreased cardiac output
Which causes hypotension
Which causes *Decreased tissue perfusion
And *impaired cellular metabolism

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34
Q

Symptoms of obstructive shock

A

Hypotension
Tachycardia
Tachypnea
Oliguria
Decreased CO
Increased PAP
Increased PCWP
Decreased SvO2

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35
Q

Management of obstructive shock

A

Relieve obstruction (according to cause)
Ex: pericardiocentesis or needle thoracentesis

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36
Q

Prevention of obstructive shock

A

Early reduction of long-bone fracture (femur)
TEDs
SCDs
Prophylactic anticoagulant therapy

37
Q

What is distributive shock?

A

AKA Vasogenic
Widespread *vasodilation and *decreased SVR
Causing abnormal distribution of intravascular volume and relative hypovolemia

38
Q

Three types of distributive shock

A

Neurogenic
Anaphylactic
Septic

39
Q

What is neurogenic shock?

A

Nervous system disturbance effecting vasomotor center, creating SNS disruption.
Results in:
- vasodilation
- loss of vasomotor tone
- impaired thermoregulation

40
Q

Etiology of neurogenic shock

A

High *SCI
Deep general anesthesia
Spinal anesthesia

41
Q

Venous patho of neurogenic shock

A

Massive vasodilation so:
- decreased venous return
- decreased filling (preload)
- decreased cardiac output
- *decreased tissue perfusion
- *impaired cellular metabolism

42
Q

Arterial patho of neurogenic shock

A

Massive vasodilation so:
- decreased SVR (afterload)
- decreased BP
- *decreased tissue perfusion
- *impaired cellular metabolism

43
Q

Symptoms of neurogenic shock

A

Hypotension
*Bradycardia
*Hypothermia
Decreased CO
Decreased PAP, decreased PAWP
*Decreased SVR

44
Q

Management of neurogenic shock

A

*Maintain airway, immobilize pt
*ID and correct problem:
- intubate and ventilate (high SCI)
- vasopressors (to decrease vessel size)
- atropine (for bradycardia)
- slow rewarming (too fast will cause vasodilation)
- DVT prophylaxis (b/c lots of blood pooling, high risk for clots)

45
Q

Prevention of neurogenic shock

A

Properly immobilize spine (of spinal injury pt)
Elevate HOB with spinal anesthesia

46
Q

What is anaphylactic shock?

A

Severe allergic reaction
Caused by repeated exposure to an antigen (normally, but not always)

47
Q

Patho of anaphylactic shock

A

Causes release of vasoactive substances (causes redness and swelling)

Leads to massive vasodilation, causing decrease in BP, decreased tissue perfusion

Capillary permeability increases so intravascular volume decreases

48
Q

Symptoms of anaphylactic shock

A

Hypotension
Tachycardia
Tachypnea and *wheezing
Dyspnea
*Stridor
*Urticaria, *pruritus
*Angioedema
Cyanosis
Decreased CO and CI
Decreased SVR
Decreased SvO2

49
Q

Management of anaphylactic shock

A

Intubate and ventilate
Bronchodilators (albuterol)
Steroids (to decrease edema and inflammation)
Antihistamines (to block chem. mediators causing the prob)
Sympathomimetics (*Epi = drug of choice)

50
Q

Prevention of anaphylactic shock

A

Careful history for allergies
Diligent monitoring for:
- IV antibiotic reactions, esp with first doses
- Monitor for blood transfusion reaction

51
Q

What is septic shock?

A

Component of continuum of progressive clinical insults to include:
SIRS
Sepsis
MODS

52
Q

What is SIRS?

A

(Systemic inflammatory response syndrome)
Exaggerated defense response to noxious stressor to localize and then eliminate the endogenous or exogenous source of the insult

53
Q

Examples of noxious stressors that could cause SIRS

A

Infection
Trauma
Surgery
Acute inflammation
Ischemia
Reperfusion
Malignancy

54
Q

What is sepsis?

A

“Overwhelming infection”
Life threatening organ dysfunction caused by dysregulated host response to infection

55
Q

What is MODS?

A

Organ dysfunction in acutely ill clients

56
Q

What is septic shock?

A

Subset of sepsis where circulation and cellular metabolism are impaired enough to cause increased mortality

57
Q

Causes of septic shock

A

*Gram-negative bacteria (Ex: *E. Coli & *pseudomonas)
Gram-positive bacteria (Ex: strep & staph)
Viruses (Ex: covid)
Fungi

58
Q

Which type of shock can nurses have the biggest impact in preventing?

A

Septic shock (by preventing infection)

59
Q

Screening tools to detect sepsis

A

SIRS criteria
Vital signs
Signs of infection
qSOFA criteria
NEWS
MEWS

60
Q

What is qSOFA criteria?

A

Quick Sequential Organ Failure Assessment

Scoring = 1 point for each of 3 criteria:
(1) respiratory rate ≥ 22 breaths/min
(2) altered mental status
(3) systolic blood pressure (SBP) ≤ 100 mm Hg.

A qSOFA score ≥ 2 is suggestive of sepsis

61
Q

Describe the continuum of sepsis and the S/S in each stage

A

Infection - fever
Sepsis - fever, increased HR, increased RR, increased or decreased WBC
Severe sepsis - hypotension, increased lactate, acute lung injury
Septic shock - vasopressors required, lactate higher
MODS - progressive dysfunction of 2 or more body systems as a result of SIRS

62
Q

*Early symptoms of septic shock
HR, pulse, BP, skin, LOC, UOP, temp

A

Tachycardia
Bounding pulses
BP normal or low
Skin warm, flushed
Hyperpnea
Irritable, confused
Oliguria
*Hyperthermia

63
Q

*Late symptoms of septic shock

A

Tachycardia
Pulses weak/thready
Hypotension
Narrow pulse pressure
Skin cool, pale
Lethargy to coma
Anura
*Hypothermia

64
Q

Hemodynamic symptoms of septic shock in early vs. late phases CO/CI, RAP/PAP/PCWP, SVR, SvO2

A

Early:
- *increased CO/CI
- decreased RAP/PAP/PCWP
- decreased SVR
- increased SvO2

Late:
- *decreased CO
- decreased SvO2

65
Q

Diagnostic assessment cues (lab values) of early vs. late septic shock acid/base bal, PT/PTT, platelets, WBCs, glucose, BUN/Cr, lactate

A

Early:
- *respiratory alkalosis
- increased PT, PTT
- decreased platelets
- *increased WBC count
- increased glucose

Late:
- *metabolic acidosis
- increased PT, PTT
- decreased platelets
- *decreased WBC count
- decreased glucose
- increased BUN, Cr
- *increased lactate

66
Q

What is the surviving sepsis campaign?

A

Performance improvement program that includes sepsis screening for acutely ill/high risk pts
SOP (protocol) for treatment

67
Q

**Possible interventions for septic shock

A

For all pts: isotonic crystalloids (*LR or NS depending on meds)
Vasopressors - Norepi = vasopressor of choice
Antibiotics

Treat hyperglycemia > 180 mg/dL
Stress ulcer prophylaxis (with PPI)
Pharmacologic VTE prophylaxis (Lovenox)

68
Q

**Prevention of septic shock

A

Good hand hygiene
Monitor temp, WBC
Standard precautions
Keep pt clean
Oral & airway care
Catheter and wound care
*ID high risk patients

69
Q

Examples of pts at high risk for sepsis

A

Basically anyone in CC unit, but:
> 65 yrs
Compromised immunity
Co-morbidities

70
Q

*Desired outcomes for pts with septic shock

A

CVP 8-12 mmHg
MAP 65 mmHg *if on vasopressor
UOP > or equal to 0.5 mL/kg/hr
SvO2 65%

71
Q

Possible interventions for Initial Resuscitation of septic shock

A

*Medical emergency

Begin treatment/resuscitation immediately
*At least 30mL/kg crystalloid for hypotension in first 3 hrs (more if Bp is worse)

72
Q

Suggested guidelines for initial resuscitation of septic shock

A

Using dynamic (direct) measure to guide fluid resuscitation
Guiding resuscitation to decrease high lactate
*Using cap refill as adjunct to other measures
Admit to ICU within 6 hrs if required

73
Q

Hemodynamic management of septic shock

A
  • *Crystalloids as first line fluid for everyone (LR or NS)
  • No starches or gelatins (nothing with sugar)
  • Norepinephrine, vasopressin, epi *IN THIS ORDER (add a drug as opposed to escalating the dose)
  • Use peripheral line rather than waiting for central access
  • Invasive BP monitoring (art line instead of BP cuff)
74
Q

Recommendation for ventilation for pts with septic shock

A

*HFNC
If ARDS, follow current guidelines for ARDS

75
Q

When should a pt with septic shock be fed and how?

A

Start enteral feeding if tolerated within 72 hours

76
Q

Long-term outcomes/goals for pts with septic shock

A

Discussion of goals with pt/family within 72 hrs of onset
Palliative care consultation when appropriate
Support group referral as appropriate upon discharge
Written/verbal discharge education

77
Q

VAP bundle for prevention of sepsis

A

HOB elevation 30-45 degrees
Sedation vacations QD
Sedation protocol
Avoid intubation
Toothbrushing daily
Physical conditioning
Early enteral nutrition
Change vent circuit only when necessary

78
Q

5 moments for hand hygiene to prevent sepsis

A

Before pt contact
Before aseptic task
After body fluid exposure
After pt contact
After contact with pt surroundings

79
Q

In general, what are the problems for all types of shock?

A

Decreased tissue perfusion related to decreased circulating blood volume, decreased myocardial contractility, and widespread vasodilation

80
Q

Baseline measurements that should be obtained for all types of shock

A

RAP
PAOP/PCWP

81
Q

When monitoring fluid volume in a patient with shock, which patient responses should be monitored?

A

PA pressures (PA catheter to judge fluid replacement)
Vital signs
Urine output
*Body weight (would be best measurement, but rarely accurate)
*LOC

82
Q

Guidelines for treating shock with crystalloids

A

LR or NS
3:1 rule (replace with 3 mL for every mL of blood loss)

83
Q

Colloids for treatment of shock

A

Hypertonic fluids that pull fluid from 3rd space into vascular space to increase BP
No evidence that colloids are a good treatment

84
Q

Positioning for pts with shock

A

*Avoid trendelenburg position (tricks the baroreceptors!)
HOB 20-30 degrees
FOB elevated
Pt should be turned frequently

85
Q

Types of mechanical interventions for cardiogenic shock

A

Intra-aortic balloon pump
Ventricular assist device

86
Q

Benefits of intra-aortic balloon pump

A

Inflated diastole, deflated systole:
Increased coronary artery perfusion
Decreased afterload

87
Q

Potential complications of intra-aortic balloon pump

A

Thromboembolism
Decreased perfusion to extremities

88
Q

Nursing interventions for ventricular assist device

A

Maximize O2 delivery & reduce O2 consumption (limit activity)
Positioning
Maintenance of body temp
Nutritional support
Maintenance of skin integrity
Psychological support

89
Q

Potential complications for a ventricular assist device

A

Cerebral edema
DIC
Leukopenia
ARDS
Acute renal failure
Decreased liver function
MODS

Critical Care (35 decks)

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