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SRNA3AnesthesiaMgt > Clinical Related Complications > Flashcards

Clinical Related Complications Flashcards

1
Q

Laryngospasm causes (4)

A
  1. Foreign (secretions) substances
  2. visceral pain reflex
  3. Extubation during light anesthesia (Stage II)
  4. insertion of oral airway
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2
Q

Signs and Symptoms of Laryngospasms

A
  • partial = crowing sound, stridorous breath sounds

* total= no sound d/t no air movement.

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3
Q

Tx of Laryngospasm

A

Goal: Support ventilation

  1. head tilt/jaw thrust (call for an assistant) with 100% Fi02 + gentle airway pressure
  2. Give 1.5 mgs/kg Lidocaine IV
  3. Give 0.15-0.30 mg/kg Anectine IV ; SL/IM 5mg/kg
  4. Reintubate (+ ETCO2 and improving sats)
  5. Sedate patient and SIMV or AV
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4
Q

Complications of Laryngospasm

CXR, breaths

A

Cx:** pink frothy sputum = Negative Pressure Pulmonary Edema
** Coarse breath sounds

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5
Q

TX of complications of Laryngospasm :

A 
Increase Fi02
CPAP/PEEP
NO fluid restrictions
NO diuretics
= will self correct within 24 hrs
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6
Q

Laryngeal Edema Tx

A

***laryngeal edema
TX: nebulized racemic epinephrine
IV corticosteroids

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7
Q

Bronchospasm=

A

is bronchoconstriction

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8
Q

Causes of Bronchospasm

A

 mechanical obstruction
 foreign bodies
 ET is irritating carina
 Light anesthesia

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9
Q

S/SX of Bronchospasm

A

 intraoperative wheezing (r/o mechanical or physical obstruction, pulmonary edema or pneumothorax)
 ETC02 waveform = upstroke rises slowly

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10
Q 
Tx of Bronchospasm 
R/O 
2. Administer 100% 
3.  anesthesia
4. Give
A
  1. R/O obstruction d/t migration of ETT, secretions, and kinking *most definitive is through fiberoptic
  2. Administer 100% Fi02 and manually
    ventilate with sufficient expiratory time.
  3. Deepen anesthesia
  4. Give Beta adrenergic agonist (Albuterol)
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11
Q

Most definitive Dx of Bronchospasm is through

A

Fiberoptic

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12
Q

Tx of Bronchospasm (5-7)
Give IV
6. IV or IM
7.

A
  1. Give IV Aminophylline, SQ Terbutaline, or IV/nebulized lidocaine
  2. Ketamine IV or IM
  3. Extubation = very controversial; ETT contributory factor.
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13
Q

Intraoperative Aspiration

Mortality is ____

A

Aspiration = is the active (vomiting) or passive (regurgitation) passage of material from the stomach, esophagus, pharynx, mouth, or nose to the trachea.
 Mortality is 5%

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14
Q

Recurization

A

Paralyzed again after extubation

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15
Q

Reintubation in the PACU

A

Affect reimbursement

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16
Q

Intraoperative aspiration AVERAGE HOSPITAL STAY IS

A

21 DAYS WITH ICU

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17
Q

Complications of Intraoperative aspirations:BPA

A 
Bronchospasm
Pneumonia
ARDS
lung abscess 
empyema.
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18
Q

Signs you can reverse

A

Sustained head lift

Tetany for 5 seconds w/o fade

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19
Q

Intraoperative aspiration causes

A

 Food or any foreign body

 Fluids (blood, saliva, GI contents = pH <2.5 and content >25 mls)

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20
Q

S/sx: Acidic Aspirates

A

-> alveolar-capillary breakdown -> interstitial edema , intraalveolar hemorrhage, increased airway resistance ->
hypoxia.

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21
Q

S/sx: Non-Acidic Aspirates PATHO

A
  • > destroys surfactant, alveolar collapse and atelectasis

- -> hypoxia

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22
Q

Particulate/food matter

A

–> physical obstruction and later inflammatory response ->

alternating areas of atelectasis and hyperexpansion ->hypoxia, hypercapnia

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23
Q

S/sx of Intraoperative Aspiration

A

 Fever (90%)
 Tachypnea
 Rales in 70% of cases
 Cough, cyanosis & wheezing (30-40%)

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24
Q

Tx of intraoperative Aspiration

ABCC

A

A. Prevention. Recognize risks in preop. (Coexisting, fasting times, preop meds).
B. Induction. RSI. However, ETT does not guarantee that no aspiration will occur.
C. After the fact: Supportive care remains mainstay. a. Suction asap.
C. Fi02 x 100% PEEP < CPAP (severe insult, atelectasis, or respiratory failure)

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25
Q

Negative pressure Pulmonary Edema

A

PInk frothy sputum

Need POSITIVE PRESSURE

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26
Q 
Tx of Intraoperative Aspiration
Monitor
Pulmonary 
\_\_\_\_\_
Controversial?
not shown to be helpful
A

d. Monitor fluid and cardiovascular status
e. Pulmonary lavage with obstruction (not
with aspiration).
f. Rigid Bronchoscopy = only when removing
solid particles
g. Antibiotics and corticosteroids still
controversial
h. Lavage trachea with sodium bicarbonate =
not shown to be helpful.

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27
Q

Pneumothorax Causes

A

Causes:

  1. Positive pressure ventilation
  2. Central venous access placement
  3. Bronchoscopy procedure
  4. Surgical and invasive procedures near the proximity of the lungs.
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28
Q

Laryngospasm FULL

A

MASK VENTILATE DIFFICULT
More propofol
Muscle relaxants
BAG

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29
Q

5 hallmarks of tension Pneumothorax:

A 
 1. hypotension
 2. hypoxemia
 3. tachycardia
 4. increased CVP
 5. increase PIP
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30
Q 
Pneumothorax
breath sounds
 ventilatory pressures (PIP, MA)
 chest 
 progressive 
 lungs
  changes
 Displacement of 
 percussion
 02 saturation 
 Extreme
A 
unilateral decreased in breath sounds
 increased ventilatory pressures (PIP, MA)
 Asymmetric chest 
 progressive tracheal deviation
 wheezing
 cardiovascular changes
 Displacement of cardiac impulse
 Hyperresonance topercussion
 02 desaturation d/t V/Q mismatch
 Extreme anxiety
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31
Q

IF tube too deep by carina

A

You may have spasm

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32
Q

Patient is bucking

A

Take off vent
Manual vent
Give more propofol

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33
Q

Pneumothorax  Tx: definitive

A

***** Chest decompression

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34
Q

Chest decompression for pneumothorax done by
_______where ?
What do you leave?

A

large bore needle through chest wall
 2nd intercostal space mid clavicular line
 = leave needle in place until chest tube is placed or thoracotomy is performed

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35
Q

PE Causes:

A
  1. DVT from non mobility (hospital or activity related).
  2. FAT EMBOLISM from Total Joint Replacement
    (long bones, pelvis, ribs)
  3. Bone Cement Embolism
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36
Q

Fat Embolism when does it occur

A

may occur 12-40 hours after trauma or surgery.

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37
Q 
FAT embolism Early S/Sx:
Neuro
Urine
Skin
CNS
Lungs
A 
Hypoxia
Altered mental state,
Fat globules in urine/sputum, 
Petechiae (chest, axilla, upper extremities, conjunctiva), CNS depression
Pulmonary edema
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38
Q

FAT EMBOLISM Minor s/sx:

HR, temp, ESR, urine, Platelet /hematocrit

A

↑HR, ↑temp, ↑ESR, fat emboli(retinal), urinary and/or sputum fat, ↓platelet or hematocrit.

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39
Q

FAT embolism TRIAD

A

Hypoxemia, Confusion, Petechiae

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40
Q

Type I DM

A

Always Full Stomach

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41
Q 
PE Signs and Symptoms
acute/sudden onset of 
 lungs
 skin symptoms
 BP
HR
 Psychological
 O2 sats
 HTN
 bronchioles, PIP
 ETC02
NEURO
A 
acute/sudden onset of dyspnea (80-85%).
 wheezing
 diaphoresis
 increasing hypotension
tachycardia
 sense of impending doom
 Hypoxemia unresponsive to 02 treatment)
 Pulmonary hypertension
 Bronchospasm ↑PIP
 Decreased ETC02
 Altered mental State
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42
Q

PE Treatment

A 
Tx:
 Give supplemental 02
 reintubate PRN
 Support CV function = be aggressive with
hypotension.
 give Heparin IV
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43
Q

Cause of Airway Fire

A
  • most common is laser surgery of the airway
  • another cause is cautery with pooled skin prep;
  • Remember your
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44
Q

Airway Fire triad

A

Triad: 02, heat, fuel

s/sx: duh

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45
Q

Airway Fire: Ventilation Techniques

A

Ventilation Techniques with Laser Surgery

Jet Ventilation

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46
Q

Jet Ventilation and Risks

A

through operating laryngoscope attached wall 02 (entrains air/02 mixture thru Venturi effect)
 aim at trachea.
Risks: barotraumas, pneumothorax  mediastinal or SQ air.

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47
Q

Spontaneous Ventilation and RISKS=

A

inhalation agents
thru laryngoscope attachment.
Risks: hypoventilation, hypercarbia and aspiration.

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48
Q

Airway and ventilation techniques ETT =

A

PVC (least flammable), red rubber,

silicone ET, ETs wrapped with metallic tape.

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49
Q

Airway Fire Interventions

A

An ounce of prevention:
Reduce flammability of airway by decreasing 02
concentration (Fi02 23%) and use of wet lap sponges.

50
Q

AIRWAY FIRE PROTOCOL

  1. stop
  2. disconnect
  3. remove
  4. surgical field
  5. Fi02
  6. perform ___And _____ to ______
  7. full monitors
  8. use
  9. continue____and _______ as needed.
A
  1. stop ventilation
  2. disconnect 02 source
  3. remove ETT
  4. flood surgical field with saline
  5. mask ventilate with 100% Fi02 then reintubate
  6. perform rigid laryngoscopy and bronchoscopy to assess damage and remove
    debris
  7. full monitors x 24 hours
  8. use short term steroids
  9. continue ventilatory support and antibiotics as needed.
51
Q

FACTS of ATYPICAL PSEUDOCHOLINESTERASES

 Typical = normal

A

Anectine, mivacurium, local anesthetics and trimethaphan = affect Dibucaine Test

52
Q

Primary route of elimination for Anectine?

A

PseudoChE.

53
Q

Secondary route of elimination for Anectine?

A

Kidneys = longer!

54
Q

The longer the case

A

The more risk for PE

55
Q

Dibucaine is an

A

amide local anesthetic

56
Q

Dibucaine number =

A

reflects the effectiveness and quality of the enzyme; not

the quantity or concentration of the enzyme in plasma

57
Q

DIBUCAINE TST: Hence, even in homozygote type,

A

the concentration of the enzyme is normal. The

quality of both enzyme is abnormal.

58
Q

Dibucaine Test Procedure is a_______ procedure

A

blood test

59
Q

Airway fire LASER CASES

A

Armored tube
Foil wrap tubes
wrap ETT tube with wet gauze

60
Q

Dibucaine test Result Classification:

1. Normal test result =

A

test will decrease pseudoChE by 80.

61
Q

DIBUCAINE 1 normal and 1 abnormal (Heterozygotes) =

test will decrease pseudoChE by

A

30-70 , Anectine will be slightly prolonged.

62
Q

Abnormal (Homozygotes) = test will

decrease peudoChE by

A

16-25  Anectine will be prolonged (6-8 hrs).

63
Q 
Treatment Goal of Atypical 
Ensure 
 a pure phase II block is reversible with \_\_\_\_\_
 if a block is mixed (phase I and 2),giving an anti
cholinesterase will \_\_\_\_\_\_\_the block 
most practitioners: 
 Giving blood is 
 Allergy: 
 Testing for
A

Ensure an adequate airway and gas exchange
 a pure phaseII block is reversible with anticholinesterase
 if a block is mixed (phase I and 2),giving an anti
cholinesterase will prolong the block
most practitioners: ventilatory support until muscle strength returns
 Giving blood is more risky than beneficial.
 Allergy: Sux!
 Testing for Dibucaine Number

64
Q

MH first sign

A

MASSETER SPASM

65
Q

Recurarizaton

A

= immediately apparent in the PACU d/t declining 02 sats and respiratory effort.

66
Q

Recurarizaiton S/Sx

A 
s/sx:
02 sats
 unresponsive patient
 appears “floppy” or uncoordinated
 ineffective abdominal and intercostal
activity
S/sx:
• sometimes can verbalize: suffocating feeling
• unable to sustain head lift or hand grasp
67
Q

Dandrolene intiial dose

A

2.5mg/kg up to 10 mg

68
Q

Recurarization worst case Signs and symptoms

A

pharyngeal collapse and respiratory obstruction

69
Q

Ryanodex

A

Each vial of RYANODEX® contains 250 mg of dantrolene sodium and requires reconstitution with only 5 mL

70
Q

Recurarization Treatment goal

A

Treatment Goal: Treat urgently and aggressively
 Re-sedate the patient
 Give additional reversalagents in divided doses
(Neostigmine 0.05 mg/kg IV = longer duration of
action. Careful with bradycardia).

71
Q

MMA embolism first sign

A

HYPOTENSION

72
Q

ACUTE DISSEMINATED INTRAVASCULAR COAGULATION

(DIC) Causes:

A

 shock
 ischemia
 infection
 OB (abruption, amniotic fluid embolism)

73
Q

S/sx of DIC

A 
 bleeding with oozing
  platelet (thrombocytopenia)
 prolonged PT/thrombin time
  Factors: I,IIa, V, VIII, XIII.
 increased fibrin degradation products.
74
Q

DIC Classification:

 Type 1 (Secondary Fibrinolysis) =

A

90% –> generation of thrombin and activation of

plasmin.

75
Q

DIC Classificaiton :Type 2

A

(consumptive) –> plasminogen is exhausted and uncontrolled clotting occurs.

76
Q

 Type 3

A

(Primary)  exclusive activation of

plasmin alone.

77
Q

DIC Treatment:

A

 removal of underlying cause

 give platelets, FFP, and cryoprecipitate

78
Q

What is MH?
What is increased?
Not able to

A

defect is in the Sarcoplasmic Reticulum of skeletal muscle; SR fails to sequester Ca++ leading to hypercalcemia
→sustained contraction and ↑BMR
Hypothalamus is not able to regulate heat
during this event.

79
Q

Trigger agents of MH

A

Trigger Agents: Anectine, Vapors, dTubocurarine

80
Q 
Signs and Symptoms of MH
What happens to metabolism? HR, RR? O2? BP?
ECG, K, CA, H+
Early sign
Temp
CPK
A 
Increase metabolism --> SNS activation 
Increase HR and RR
Cyanosis
Unstable BP
dysrhythmias
Increase K+, Ca++, H+; Decrease  02 
Masseter muscle spasm (early sign)
Temperature Increase  1-2C every 5mins.
CPK >20,000
81
Q

Most sensitive and earliest sign.

A

ETC02 (>100 mmHg with pH<7.0)

most sensitive and earliest sign.

82
Q

Decrease SPO2 means

A

?hypotension

83
Q

Interventions for a KNOWN MH

A
  1. Epidural without dantrolene pre treatment.
  2. Room Preparation
     preop meds are ok
     disposable circuit
     change soda lime
     drain/empty/disconnect vaporizers
     flush machine for several hours at 3-5 L/min02
84
Q
  1. GETA with dantrolene pre treatment
A

 non depolarizers can be used except dTubocurarine

 preop meds are ok

85
Q

Intraoperative Considerations of MH

A

 use non triggering agents
 vigilance with 2 parameters: ETC02 and temperature
Continued Postoperative  VIGILANCE

86
Q

Drugs of choice of MH

A

Dandrolene

87
Q

Dandrolene act on

A

the Ryanodine receptor on the skeletal muscle cell

88
Q

Main action is to

A

↓ CA release from SR

89
Q

Dose of dandrolene

A

2.5mg/kg max 20mg/kg

90
Q

Therapeutic levels

A

2.5mg/ml

91
Q

Acute interventions for acute MH

A

Cool patient
gastric lavage stop at 38C not ESOPHAGEAL
]temperature

92
Q

MH: Lidocaine treatment for PVC

A

15m/kg IV

93
Q

Diagnosis made on CPK>

A

20000

94
Q

Another diagnostic test

A

Halothane Caffeine Contracture test

95
Q

MH: Sodium Bicarbonate

A

1-2 moles/kg

96
Q

Treatment for Hyperkalemia: MH

A

Immediate direct reversal of cardiotoxicity with administration of CaCl
Quickly assist with K shift from ECF to cells
Hyperventilation
Beta adrenergic stimulation
sodium bicarbonate
Insulin and glucose

97
Q

Removal of K+ from the body (definitive

treatment)

A

 diuretics
 Kayexalate
 Dialysis

98
Q

Treatment for dysrhythmias = starts with

A

PVCs→ Vtach →V fib (d/t hyperkalemia: same treatment as above withhyperkalemia)

99
Q

(MMA)

A

METHYLMETHACRYLATE EMBOLISM

100
Q

Methylmethacrylate =

A

is the usual bone cement used to stabilize implant with the bone in orthopedic surgeries (usually knees and hips)

101
Q

MMA heat from cement

A

expands intramedullary gas, raises intramedullary pressure and forces fat and air into venous circulation

102
Q

IN MMA intense heat causes

A

reflex bradycardia or cardiac arrest

103
Q

In MMA intrapulmonary MMA

A

intrapulmonary MMA activation of the clotting
cascade  pro inflammatory substance
production.

104
Q

Prophylaxis pre-cementing:

A 
 Increase Fi02
 D/C N20
 maintain euvolemia
 create vent holes in the distal femur
 high pressure lavage of femoral shaft to remove
debris
 using uncemented femoral component
105
Q

MMA Embolism s/sx:

A

 Sudden hypotension (30-60 secs. Post
cementing).
 Hypotension (10 mins post cementing).

106
Q

MMA Embolism s/sx:

A

 Sudden hypotension (30-60 secs. Post
cementing).
 Hypotension (10 mins post cementing).

107
Q

BONE CEMENT IMPLANTATION

SYNDROME (BCIS)

A

 closely resembles Fat Embolism syndrome

 survivors develop subacute form of FES over 24-48 hours.

108
Q

BONE CEMENT IMPLANTATION SYNDROME (BCIS)

A

 closely resembles Fat Embolism syndrome

109
Q

BCIS survivors develop

A

subacute form of FES over 24-48 hours.

110
Q

Risk factors of BCIS

A

 elderly and debilitated pts
 preexisting cardiopulmonary disease
 CAD
 Pulmonary hypertension

111
Q

BCIS signs and symptoms

O2 sats, BP, ECG, pulm, CO

A
  1. Acute pulmonary hypertension
  2. Hypoxemia
  3. Hypotension with (hypoxia, dysrhythmia, pulmonary HTN), decreased cardiac output
  4. Right ventricular failure
  5. Circulatory collapse
112
Q
  1. Provide
  2. Support
  3. Augment
  4. Consider
A

Provide 100% 02 and controlled ventilation
 Support aortic pressure and Right ventricular
contractility with vasopressors
 Augment right ventricular preload with CVP with or
without PAC guidance
 Consider future treatment of pulmonary hypertensive crisis with inhaled Nitric Oxide or prostacyclin

113
Q

VAE Cause:

A

operative field is elevated 5 cm

or more above the heart’s right atrium

114
Q

VAE Incidence:

A

40-45% operated on sitting position

115
Q

VAE: Most Sensitive → least sensitive

monitors

A

TEE > Precordial Doppler > PAC> Capnography (ETC02) > Mass spectrometry (ETN2)

116
Q

VAE Interventions

A
  1. Notify surgeon immediately
  2. Surgical field flooded with saline and packed
  3. Bone edges are waxed
  4. Turn off N20 (if being used); give Fi02 100%
  5. Neck veins are compressed as means of ↑Jugular venous pressure
117
Q

VAE aspiration
Aspiration of air from the ______atrial catheter (tip should be ____Cm. where? . Doppler over ____should be placed over ____or_____ intercostals space at _____

A

Aspiration of air from the right atrial catheter (tip should be 3 cms. Below the junction of SVC and RA). Doppler over RA should be placed over 3rd to 6th intercostals space at right of sternum.

118
Q

TEE and VAE aspiration

A

TEE is still 5-10x more sensitive.

119
Q

If significant VAE,

A

lower the head to heart level

120
Q

VAE Support pressure if Hypotensive with

A

pressors and rapid volume infusion

121
Q

VAE AVOID:

A

PEEP or valsalva maneuver to further avoid paradoxical VAE thru a patent PFO.

122
Q

VAE : Position horizontal

A

→ failed → left lateral with slight Trendelenburg (head down) →failed→ supine and begin CPR

SRNA3AnesthesiaMgt (13 decks)

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