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NSER 7210 > Module 2 > Flashcards

Module 2 Flashcards

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1
Q

What is distributive shock?

A

Massive dilation of blood vessels.
Pipe issue. Can have enough fluid but not in the right space.

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2
Q

Name two shock presentations of distributive shock.

A

Septic shock
Anaphylactic shock

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3
Q

What are three hemodynamic consequences of sinus tachycardia?

A
  1. Increased HR = decreased ventricular filling = decreased CO
  2. Decreased coronary artery perfusion
  3. Increased myocardial oxygen demand.
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4
Q

What is AWS?

A

Alcohol withdrawal syndrome
Symptoms of autonomic hyperactivity (agitation, tremors, irritability, anxiety, hyperreflexia, confusion, HTN, tachycardia, diaphoresis.

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5
Q

When may the first signs of AWS be noted?

A

AWS may develop 6-24 hours after abrupt discontinuation or decrease in ETOH consumption.

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6
Q

What percent of adults experience AWD in the ED?

A

20%

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7
Q

Why does AWS occur (patho)?

A

ETOH produces CNS depression due to enhanced GABAergic neurotransmission and reduced glutamatergic activity.
Chronic use produces adaptive changes to NTM systems to restore neurochemical equilibrium. Abrupt reduction/cessation of ETOH produces acute imbalances.

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8
Q

Why does ETOH tolerance happen?

A

Chronic use produces adaptive changes to NTM systems (GABA, glutamate, norepi pathways) to compensate for ETOH-induced destabilization and restore neurochemical equilibrium.

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9
Q

How do EDs screen for AWS?

A
  1. Consider as possible differential diagnosis in pts with symptoms.
  2. Ask about drinking habits, typical onset of symptoms, and past hx with AWS.
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10
Q

List first degree AWS symptoms

A

Mild w/d: tremors, diaphoresis, NV, HTN, tachycardia, hyperthermia, tachypnea.
6-12 hours after last drink.

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11
Q

List second degree AWS symptoms

A

ETOH hallucinations: dysperception (visual, auditory, and tactile).
12-24 hours after last drink.

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12
Q

List third degree AWS

A

ETOH withdrawal seizures: generalized tonic-clinic (with short/no postictal period).

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13
Q

List fourth degree AWS

A

DT: delirium tremens - psychosis, hallucinations, hyperthermia, malignant HTN, seizures, coma.

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14
Q

What significant changes are seen in co-morbid patients taking BBs?

A

VS changes: BP, HR may be masked as normal.

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15
Q

What is DT?

A

Characterized by rapid fluctuation of consciousness and change in cognition occurring over a short period of time, severe autonomic symptoms (sweating, N, palpitations, tremor) and psychological symptoms (anxiety).
Typical: agitation, hallucination, disorientation.
Onset 24-72 hours - 10 days later.

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16
Q

What do the CIWA score numbers indicate?

A

<8 mild withdrawal
8-15 moderate withdrawal (marked autonomic arousal)
>15 severe withdrawal, predictive of the development of seizures and delirium.

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17
Q

What scale is used to assess the risk for severe AWS?

A

LARS
(Luebeck Alcohol withdrawal Risk Scale)

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18
Q

What are routine examinations for AWS?

A

Blood/breath ETOH concentrations, CBC, renal function tests, lytes, glucose, liver enzymes, urinalysis, urine toxicology

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19
Q

What are supportive care interventions for AWS?

A

Correcting fluid depletion (iv fluids), treat hypoglycemia and lyte disturbances, supplementations (thiamine and B complex).

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20
Q

What is WE?

A

Wernicke’s Encephalopathy

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21
Q

What medication is the gold standard treatment for AWS?

A

BZD - Benzodiazepines
Monitor for reduced liver function (elderly/advanced illness) for over sedation/respiratory depression.

Risk for excessive sedation, motor, memory deficits, respiratory depression and liver/kidney impairment.

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22
Q

What medication is recommended for AWS and elderly/advanced illness?

A

Oxazepam and lorazepam, due to absence of oxidative metabolism and active metabolites.

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23
Q

T/F, AWD can start with DT?

A

T, especially in patients with previous DT history or hx of repeated AWS

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24
Q

What is sepsis?

A

A life threatening organ dysfunction caused by a dysregulated host response to an infection

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25
What is SIRS?
Systemic Inflammatory Response Syndrome An innate exaggerated response to a foreign invader (infection, trauma, sx, inflammation, ischemia, malignancy) that causes a cascade of responses.
26
What factors are influencing the rise of sepsis and septic shock?
Aging population Increased number of Immune compromised patients with chronic illnesses/malnourished Increased surgeries Increased use of broad spectrum antibiotics causing proliferation and resistant organisms
27
List the SIRS cascade responses.
Causes uncontrolled coagulation, widespread vasodilation/leakage, poor distribution of circulating volume, and an imbalance of o2 supply and o2 demand.
28
What else can cause SIRS other than an infection?
Surgery, trauma/burns, pancreatitis
29
List the 4 SIRS criteria
HR > 90 bpm RR > 20/min T > 38 and < 36 Altered mental status Must have two.
30
List 5 more risk factors contributing to sepsis (according to the sepsis algorithm):
Looking unwell Age > 65 Recent surgery Immunocompromised (AIDS, chemo, neutropenia, asplenia, transplant, chronic steroids) Chronic illness (DM, Renal Failure, Liver failiure, Ca, ETOH, IVDU)
31
How is septic shock different than hypovolemia?
Hypovolemia: cool, pale extremeties Septic Shock: inflammatory response causes massive vasodilation causing warm, flushed skin. Total fluid volume may be normal but circulating volume is low (leaky vessels, vasodilation). Coagulation system malfunctions earlier than hypovolemic shock, depleting clotting factors, causing bleeding and potential hemorrhage.
32
Is there a distinction between the types of sepsis?
No. Patients are categorized as having sepsis or progressing to septic shock (circulatory, cellular, and metabolic abnormalities lead to greater risk of mortality)
33
How is septic shock clinically idenified?
By vasopressor requirement to maintain SBP > 90 and/or MAP > 65, serum lactate >2 mmol/L despite adequate fluid management.
34
What is qSOFA?
Must have 2/3 Altered mental status, RR of > 22/min, SBP < 100.
35
What does a positive qSOFA mean?
Suspected multi-organ dysfunction
36
What is the three hour bundle?
1. Blood cultures before administration of antibiotics 2. Serum lactate measurement 3. Infusion of broad-spectrum abx.
37
What is the one hour bundle?
1. Measure lactate level. Re-measure if initial level is >2. 2. Obtain blood cultures prior to abx. 3. Adminiser broad-spectrum abx. 4. Begin rapid administration of 30ml/kg of crystalloid for hypotension or a lactate > = 4. 5. Apply vasopressors of pt hypotensive during/after fluid administration to maintain MAP of 65. Vasopressors - norepi (alpha -no HR/BP change) , vasopressin (alpha - contractility), dobutamine beta1/2 increase hr, conductivity), or epi (alpha, beta 1/2 Increase hr, bp, svr, co)
38
Why is the lactate level drawn?
Elevated levels indicate tissue hypoperfusion/tissue hypoxia (accelerated aerobic glycolysis.
39
What are the initial goals of sepsis management?
1. Early recognition and detection 2. Early blood pressure control, vasopressors, and antibiotics
40
List some indicators of organ dysfunction that nurses can QUICKLY use to potentially identify sepsis?
Altered mental status Hypotension Poor capillary refill Tachypnea Tachycardia
41
How does sepsis negatively impact CO?
Decreases preload due to impaired vascular tone (dilation) and leaky capillaries, causing fluid shifts. Reduces circulating volume, decreases venous return, and preload. Afterload is decreased (does not negatively alter CO as it allows heart to eject fluid more effectively). The body increases HR and contractility in an attempt to compensate for the reduced preload.
42
What happens if the HR is too high?
Decreased coronary perfusion, decreased ventricular filling, and increased myocardial demand.
43
How does sepsis decrease a patients O2 supply?
Decreased diffusion causing impaired alveolar gas exchange and deceased preload causing decreased CO
44
What does sepsis look like on the oxyhemoglobin curve?
A shift to the right (release). Caused by increased Temp and acidosis resulting in poor perfusion. A shift to the right means hemoglobin has a decreased affinity to O2 resulting in decreased oxygen carrying capacity.
45
What increases the patients O2 demand in sepsis?
Fever, pain, and stress
46
How is oxygen transported to tissues and cells?
1. Dissolved in plasma - small portion of oxygen transported in cells 2. Bound with hemoglobin - does majority of the work, 99%, of transporting oxygen to cells
47
What does PaO2 mean?
Oxygen dissolved in plasma, represented as a partial pressure. P = plasma Small amount of O2 carrying capacity but can be life-saving mode of transport.
48
What does SaO2 mean?
O2 saturation levels indicated by the % of hgb molecules that are fully saturated with O2. S = saturation
49
What does a high affinity for O2 mean?
Shift to the left Hgb picks up O2 easily from the lungs but does not release it as easily to the tissues. Poor tissue oxygenation and poor end-organ perfusion
50
What does a low affinity for O2 mean?
Shift to the right. Hgb picks up O2 less readily from the lungs but releases it easily to the tissues. Poor tissue oxygenation and poor end-organ perfusion
51
What is the relevance of the Oxyhemoglobin Dissociation curve?
1.Helps to explain the relationship between oxygen saturation and partial pressure of oxygen. SaO2 can maintain O2 better than PaO2. (preoxygenation for RSI). 2. Considerations of all factors which might affect tissue oxygenation are required for potentially compromised patients 3. Caring for critically ill and ventilated patients requires a broad knowledge of ventilation, perfusion, and oxygenation. .
52
What is innate or non-specific immunity?
Natural resistance that people are born with. ie SIRS
53
What is acquired or specific immunity?
Protection gained through prior exposure to antigens (foreign substances) or through transfer for protective antibodies (vaccination). Antibodies/immunoglobulins are generated in response to antigens.
54
What is the patho cascade in an allergy response?
Immunoglobulin E (IgE) triggers release of histamine and vasoactive substances from mast cells/basophil cell, causing vasodilation and fluid/protein to leak out of the vascular space into the surrounding tissues.
55
What is an allergic reaction?
Hypersensitivity to a foreign protein/antigen. Anaphylaxis is a profound reaction.
56
Definition of anaphylaxis?
Continuum of acute symptoms affecting multiple systems in the body after exposure to an allergen. 1. presence of skin signs, respiratory involvement, 2+ body symptoms, organ dysfunction, and/or hypotension.
57
List some triggers of anaphylaxis
Nuts, bug bites/stings, radiocontrast dye, ethonal, opioids, food, latex, drugs, exercise
58
List some symptoms of anaphylaxis
Angioedema - tongue, lips, oropharynx Urticaria Flushing Tachycardia, hypotension Narrowing or airway (wheeze, stridor, bronchospasm, dyspnea, voice changes) Altered LOC, syncope, dizzy NVD
59
Differential dx to anaphylaxis
Hypoperfusion states - hypovolemia, endotoxic, hemorrhagic, cardiogenic, vasovagal MI, arrhythmia PE, inhaled foreign substance, asthma, obstructive lung disease Anxiety CVA, seizure ACEI, hereditary angioedema, pheochromocytoma
60
Why may ACEI cause angioedema?
May precipitate mast cell mediated responses and stop allergic mechanisms by increasing levels of bradykinin (vasodilator).
61
What are the treatment interventions of anaphylaxis?
Rapid assessment and VS trending Supplemental O2/intubation Large bore IV (2 if hypotension) Heart monitor Reassessment Rapid infusion of bolus crystalloid's Medications
62
What medications are used for anaphylaxis?
Epinephrine (IM) - IM lateral aspect of thigh (seconds) Glucocorticoids for bronchospasm - B agonist like albuterol (bronchodilating) (seconds) Antihistamines H1/H2 - prevent/reduce histamine release - ranitidine/diphenhydramine (30-45 minutes) Corticosteroids to decrease inflammation (4-6 hours)
63
Anticipated labs for anaphylaxis?
Not to be used to dx. Provide first line tx. Tryptase - 90 min peak for up to 3 hours Histamines - 10 minute peak for up to 1 hour.
64
What type of shock is anaphylaxis?
Distributive shock - histamine is strong vasodilator. Increases blood flow and leakage of proteins/fluids
65
What symptoms should trigger you to suspect anaphylaxis
hypotension, NV, SOB, syncope, urticara
66
What is HIV/AIDS?
Human Immunodeficiency Virus Acquired Immunodeficiency Virus
67
What is the definition of AIDS?
Severe stage of immunodeficiency with a wide range of features/symptoms + r/f opportunistic infections
68
What is the definition of HIV?
Virus that attacks the bodies natural immune system (Helper T cells aka CD4 cells). Destroys CD4 by attaching to cell wall and releasing RNA. Once dead, HIV RNA is replicated in the blood and infects more CD4 cells.
69
What are the 3 days stages of HIV/AIDS?
Acute stage - a few weeks after exposure, the person experiences flu-like symptoms. Latency stage - viral replication stabilizes, immune system decreases viral load and increases CD4 = asymptomatic/minimally symptomatic. Final state - viral load increases, CD4 decreases and makes it difficult to combat other illnesses. AIDS develops
70
Questions to ask in the ED pertaining to HIV/AIDS
CD4 count Known illnesses Viral load Dx of AIDS Any difficulties with heart, liver, kidneys while on HARRT? Take medications as prescribed?
71
What is the normal/abnormal CD4 count?
N - 500-1500 mm3 AIDS - HIV+ with <200mm3 (acutely compromised)
72
What symptoms can be noted in an HIV + patient?
Pneumonia, skin rashes, peripheral neuropathy, mental status changes
73
What is ART?
Antiretroviral Therapy - increased life from 9 months to 70 years
74
List some categories that would indicate an immunocompromised person
Health hx- diseases that attack immune system (HIV), Health concerns impact immune system (asplenia, Ca), Connective tissue diseases (RA, lupus) Medications- immunosuppressive, active chemo, antirejection drugs Special populations- NB < 2 months
75
Name 6 infection control considerations for the immunocompromised
Close proximity to ill/infectious Variety of illnesses in ED Multiple interactions with health care staff Nontraditional care spaces Infection control overlooked when treating life threatening issues

NSER 7210 (1 decks)

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