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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
Symptoms of cardiogenic shock
Hypotension Tachycardia Tachypnea Oliguria Cool, pale skin Decreased cardiac output, decreased cardiac index *Increased Pulmonary artery pressure, increased PAWP Increased SVR
26
Management of cardiogenic shock
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)
27
Prevention of cardiogenic shock
Minimize size of infarct PTCA Fibrinolytics not recommended anymore CABG
28
What is obstructive shock?
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
29
Three categories of obstructive shock
Impaired diastolic filling (causes decreased CO) Increased RV afterload (has to work harder to push blood into lungs) Increased LV afterload (aortic valve malfunction)
30
Causes of impaired diastolic filling leading to obstructive shock
Tamponade (pericardial sac has increase in pericardial fluid) Tension pneumo Pericarditis Compression of great veins
31
Causes of increased RV afterload, leading to obstructive shock
PE Pulmonary HTN PEEP
32
Causes of increased LV afterload leading to obstructive shock
Aortic dissection Aortic stenosis Abdominal distention Systemic embolization
33
Patho of obstructive shock
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
34
Symptoms of obstructive shock
Hypotension Tachycardia Tachypnea Oliguria Decreased CO Increased PAP Increased PCWP Decreased SvO2
35
Management of obstructive shock
Relieve obstruction (according to cause) Ex: pericardiocentesis or needle thoracentesis
36
Prevention of obstructive shock
Early reduction of long-bone fracture (femur) TEDs SCDs Prophylactic anticoagulant therapy
37
What is distributive shock?
AKA Vasogenic Widespread *vasodilation and *decreased SVR Causing abnormal distribution of intravascular volume and relative hypovolemia
38
Three types of distributive shock
Neurogenic Anaphylactic Septic
39
What is neurogenic shock?
Nervous system disturbance effecting vasomotor center, creating SNS disruption. Results in: - vasodilation - loss of vasomotor tone - impaired thermoregulation
40
Etiology of neurogenic shock
High *SCI Deep general anesthesia Spinal anesthesia
41
Venous patho of neurogenic shock
Massive vasodilation so: - decreased venous return - decreased filling (preload) - decreased cardiac output - *decreased tissue perfusion - *impaired cellular metabolism
42
Arterial patho of neurogenic shock
Massive vasodilation so: - decreased SVR (afterload) - decreased BP - *decreased tissue perfusion - *impaired cellular metabolism
43
Symptoms of neurogenic shock
Hypotension *Bradycardia *Hypothermia Decreased CO Decreased PAP, decreased PAWP *Decreased SVR
44
Management of neurogenic shock
*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
Prevention of neurogenic shock
Properly immobilize spine (of spinal injury pt) Elevate HOB with spinal anesthesia
46
What is anaphylactic shock?
Severe allergic reaction Caused by repeated exposure to an antigen (normally, but not always)
47
Patho of anaphylactic shock
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
Symptoms of anaphylactic shock
Hypotension Tachycardia Tachypnea and *wheezing Dyspnea *Stridor *Urticaria, *pruritus *Angioedema Cyanosis Decreased CO and CI Decreased SVR Decreased SvO2
49
Management of anaphylactic shock
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
Prevention of anaphylactic shock
Careful history for allergies Diligent monitoring for: - IV antibiotic reactions, esp with first doses - Monitor for blood transfusion reaction
51
What is septic shock?
Component of continuum of progressive clinical insults to include: SIRS Sepsis MODS
52
What is SIRS?
(Systemic inflammatory response syndrome) Exaggerated defense response to noxious stressor to localize and then eliminate the endogenous or exogenous source of the insult
53
Examples of noxious stressors that could cause SIRS
Infection Trauma Surgery Acute inflammation Ischemia Reperfusion Malignancy
54
What is sepsis?
“Overwhelming infection” Life threatening organ dysfunction caused by dysregulated host response to infection
55
What is MODS?
Organ dysfunction in acutely ill clients
56
What is septic shock?
Subset of sepsis where circulation and cellular metabolism are impaired enough to cause increased mortality
57
Causes of septic shock
*Gram-negative bacteria (Ex: *E. Coli & *pseudomonas) Gram-positive bacteria (Ex: strep & staph) Viruses (Ex: covid) Fungi
58
Which type of shock can nurses have the biggest impact in preventing?
Septic shock (by preventing infection)
59
Screening tools to detect sepsis
SIRS criteria Vital signs Signs of infection qSOFA criteria NEWS MEWS
60
What is qSOFA criteria?
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
Describe the continuum of sepsis and the S/S in each stage
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
*Early symptoms of septic shock HR, pulse, BP, skin, LOC, UOP, temp
Tachycardia Bounding pulses BP normal or low Skin warm, flushed Hyperpnea Irritable, confused Oliguria *Hyperthermia
63
*Late symptoms of septic shock
Tachycardia Pulses weak/thready Hypotension Narrow pulse pressure Skin cool, pale Lethargy to coma Anura *Hypothermia
64
Hemodynamic symptoms of septic shock in early vs. late phases CO/CI, RAP/PAP/PCWP, SVR, SvO2
Early: - *increased CO/CI - decreased RAP/PAP/PCWP - decreased SVR - increased SvO2 Late: - *decreased CO - decreased SvO2
65
Diagnostic assessment cues (lab values) of early vs. late septic shock acid/base bal, PT/PTT, platelets, WBCs, glucose, BUN/Cr, lactate
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
What is the surviving sepsis campaign?
Performance improvement program that includes sepsis screening for acutely ill/high risk pts SOP (protocol) for treatment
67
**Possible interventions for septic shock
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
**Prevention of septic shock
Good hand hygiene Monitor temp, WBC Standard precautions Keep pt clean Oral & airway care Catheter and wound care *ID high risk patients
69
Examples of pts at high risk for sepsis
Basically anyone in CC unit, but: > 65 yrs Compromised immunity Co-morbidities
70
*Desired outcomes for pts with septic shock
CVP 8-12 mmHg MAP 65 mmHg *if on vasopressor UOP > or equal to 0.5 mL/kg/hr SvO2 65%
71
Possible interventions for Initial Resuscitation of septic shock
*Medical emergency Begin treatment/resuscitation immediately *At least 30mL/kg crystalloid for hypotension in first 3 hrs (more if Bp is worse)
72
Suggested guidelines for initial resuscitation of septic shock
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
Hemodynamic management of septic shock
- *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
Recommendation for ventilation for pts with septic shock
*HFNC If ARDS, follow current guidelines for ARDS
75
When should a pt with septic shock be fed and how?
Start enteral feeding if tolerated within 72 hours
76
Long-term outcomes/goals for pts with septic shock
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
VAP bundle for prevention of sepsis
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
5 moments for hand hygiene to prevent sepsis
Before pt contact Before aseptic task After body fluid exposure After pt contact After contact with pt surroundings
79
In general, what are the problems for all types of shock?
Decreased tissue perfusion related to decreased circulating blood volume, decreased myocardial contractility, and widespread vasodilation
80
Baseline measurements that should be obtained for all types of shock
RAP PAOP/PCWP
81
When monitoring fluid volume in a patient with shock, which patient responses should be monitored?
PA pressures (PA catheter to judge fluid replacement) Vital signs Urine output *Body weight (would be best measurement, but rarely accurate) *LOC
82
Guidelines for treating shock with crystalloids
LR or NS 3:1 rule (replace with 3 mL for every mL of blood loss)
83
Colloids for treatment of shock
Hypertonic fluids that pull fluid from 3rd space into vascular space to increase BP No evidence that colloids are a good treatment
84
Positioning for pts with shock
*Avoid trendelenburg position (tricks the baroreceptors!) HOB 20-30 degrees FOB elevated Pt should be turned frequently
85
Types of mechanical interventions for cardiogenic shock
Intra-aortic balloon pump Ventricular assist device
86
Benefits of intra-aortic balloon pump
Inflated diastole, deflated systole: Increased coronary artery perfusion Decreased afterload
87
Potential complications of intra-aortic balloon pump
Thromboembolism Decreased perfusion to extremities
88
Nursing interventions for ventricular assist device
Maximize O2 delivery & reduce O2 consumption (limit activity) Positioning Maintenance of body temp Nutritional support Maintenance of skin integrity Psychological support
89
Potential complications for a ventricular assist device
Cerebral edema DIC Leukopenia ARDS Acute renal failure Decreased liver function MODS

Critical Care (35 decks)

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