FINAL ASSESSMENT Flashcards
Difficult intubation
External anatomic features
• ↓ Head/neck movement (atlanto-occipitaljoint)
• Jaw movement (temporo-mandibular joint), mouth opening, and subluxation of the mandible
• Receding mandible
• Protruding maxillary incisors
• Obesity
Other Predictors
Thyromental distance • Sternomental distance • Visualization of the oropharyngeal structures • Anterior tilt of the larynx • Radiographic assessment
Mouth opening predictors of difficult intubation
A mouth opening (distance between incisors) limited to 3.5 cm or less will contribute to difficult intubation
Other predictors of difficult intubation incision
Protruding maxillary incisors can interfere with
laryngoscope placement and ETT passage
BAG mask ventilation MOANS
Mask seal Obese Age No teeth Snores or stiff
LEMON Laryngoscopy and intubation
L: Look externally ➢ E: Evaluate 3-3 (3 fingers between teeth, 3 fingers chin-neck to thyroid notch) ➢ M: Mallampati class ➢ O: Obstruction ➢ N: Neck mobility
Predictors of a Difficult Airway
➢ High Mallampati Classification ➢ Small mouth opening ➢ Prominent Incisors ➢ Thyromental Distance <6 cm ➢ Decreased neck extension ➢ Neck Circumference
Predictors of Difficult Face Mask Ventilation
➢ Age >55 y.o. ➢ BMI >26-30 kg/m2 ➢ Beard ➢ Snoring ➢ Lack of teeth ➢ Mallampati III or IV ➢ Limited mandibular protrusion
What is the Single most important predictor for both Difficult mask ventilation and difficult intubation
Limited mandibular protrusion
Predictors of Impossible Face Mask Ventilation
MBONM
➢ Male ➢ Beard ➢ Obstructive Sleep Apnea ➢ Mallampatie III or IV ➢ Neck radiation changes
Awake fiberoptic intubation can be performed
without atlanto-occipital extension
What can be left in place with awake fiberoptic intubation
Any head and neck stabilizing device can be left in place to prevent movement of c-spine
Awake intubation should be the technique of choice when?
if there is any reason to believe that maintaining a patent airway after induction of anesthesia may be difficult
Tracheal intubation in patients with an
unstable neck should be done with extreme caution.
Avoid movement that can
cause spinal cord compression and damage
Most conservative approach when difficult airway is
known or suspected
➢ Be careful
Awake intubation
➢ Must explain to the patient and coach through the
procedure
–> with sedatives
Topical anesthesia is the
KEY to successful awake intubation
During awake intubation, important to use
Important to use glycopyrrolate to dry mucous
membranes prior to topical LA (at least 20 min before)
To numb airway
➢ Nebulized LA, LA swish and swallow, LA spray
(hurricane spray), bilateral lingual nerve block, superior
laryngeal nerve block, transtracheal LA injection
Awake vs sleep intubation
Consider presence of at least 3 factors predictive of difficult or impossible to mask ventilate
COPD can lead to
Possible right-sided failure, cor pulmonale
• Peripheral edema
• Increased hepatojugular reflux
Can lead to cor pulmonale
COPD
Chronic Instrinsic pulmonary disorder In late stages, signs
signs of right ventricular failure/cor pulmonale
Treat cor pulmonale
– diuretics, dig, oxygen
Interpreting pulmonary funcitons: CLASS
FEV/FVC = <0.8 (80%)
Restrictive FEV/FVC
Both reduced, ratio is normal or high
Obstructive FEV/FVC
Low ratio , less than 70%
FEF25–75%:
forced expiratory flow over the middle one-half of the
FVC
FEF 25-75% is the
Average flow from the point at which 25% of the FVC has been exhaled to the point at which 75% of the FVC has been exhale
VC, TLC, RV in restrictive
Decreased
Signs of EARLY asthma attack
Alteration of expiratory plateau on capnography
Adventitious lung sounds
Crackles (rales)
■ Wheezes
■ Friction rubs
■ Rhonchi
What is crackles
– Late = pneumonia, CHF, atelectasis
Series of individual clinking or popping noises in an area
May sound like hairs rubbing together, Velcro, or a
crumpling piece of cellophane
Crackles
Sounds are caused by opening of small airways or alveoli that have been collapsed or decreased in volume during expiration because of fluid, inflammatory exudate
Crackles
Heard in both phases of resp
Crackles
Chronic bronchitis and crackles.
– Early inspiratory/expiratory crackles =
Fine vs. coarse
Fine Crackles =
–
brief, discontinuous, popping lung sounds that
are high-pitched
– Wood burning in a fireplace
Fine crackles
Coarse Crackles =
discontinuous, brief, popping lung sounds
Compared to fine crackles , coarse =
louder, lower in pitch, last longer
Bubbling sound, rolling strands of hair between fingers near ears?
Fine crackles
Can be inspiratory or expiratory
Wheezes
■ High-pitched continuous sounds that are generated by airflow through narrowed airways
Wheezes
Caused by airflow obstruction from edema, smooth muscle constriction, secretions
Wheezes
Low-pitched wheezes
– Continuous in both phases
– Snoring, gurgling, rattle-like quality
■ Occur in bronchi!
Rhonchu
■ Most commonly used to describe sounds generated by secretions in airways, usually clear after coughing
Rhonchi
Can also be used to describe coarse crackles from airway secretions
Rhonchi
Sound generated by inflamed or roughened pleural surfaces rubbing against each other during respiration (both phases)
Pleural rub
■ Series of creaky or rasping sounds heard during inspiration & expiration
Pleural rub
– Sounds like cat purring, walking on fresh snow
Pleural rub
Caused by inflammatory disease: pneumonia or pulmonary infarction
Pleural rub
– Not cleared by coughing
Pleural rub
– Localized, may be transient
Pleural rub
Pleural rub stops when_______if it continues.
holding breath, if it continues, it might be a pericardial friction rub (pericarditis!)
Stridor mostly
Inspiratory
Stridor associated with
Epiglottis
Foreign body
Laryngeal edema and croup
Lung Sounds (B, V, BV) – Vesicular
– inspiration/expiratory ratio of 3 to 1 or I:E of 3:1
■ Over most of both lungs (V, B, BV)
Vesicular
■ Inspiratory sounds last longer then expiratory (V, B, BV)
Vesicular
■ NORMAL Soft sound with relatively low pitch (B, V, BV)
Vesicular
Mixture of the pitch of the bronchial breath sounds
heard near the trachea and the alveoli with the vesicular
sound (B, V, BV)
Bronchovesicular
Inspiratory & expiratory almost equal (V, B, BV)
Bronchovesicular
– Medium intensity(B, V, BV)
– Medium pitch
Bronchovesicular
– Heard between scapula & in 1st & 2nd interspaces
anteriorly (B, V, BV)
Bronchovesicular
Abnormal in the lung periphery and may indicate an
early infiltrate or partial atelectasis (B, V, BV)
Bronchovesicular
– Hollow, tubular(B, V, BV)
Bronchial
– Expiratory sounds last longer than inspiratory (1:3)(B, V, BV)
Bronchial
Loud intensity (B, V, BV) – High pitch
Bronchial
Normal over trachea (B, V, BV)
Bronchial
Bronchial breath sounds other than close to the trachea may indicate (B, V, BV)
pneumonia, atelectasis, pleural effusions
Distinct pause between I/E (B, V, BV)
Bronchial
Vital Capacity in obstructive
Normal or decreased
TLC in obstructive
Normal or increased
RV in obstructive
Increase
FEV/FVC
Decreased
Maximum midexpiratory flow rate
Decreased
Maximum breathing capacity
Decreased
Primary Survey
A – Airway with C-spine B – Breathing C – circulation with hemorrhage control D – disability E – Exposure / Environment
Secondary Survery
A – allergies M – medications P – past medical history L – last meal E – events/environment related to injury
Even in smokers with no chronic lung
disease
smoking increases carboxyhemoglobin levels, decreases
ciliary function, increases sputum production, stimulates CV system
Smoke-free interval of
12-18 hours shows significant declines in carboxyhgb & normalization of oxygen-HGB dissociation curve
CO Hb < 15-20
Headache, dizzins and occasional confusion
CO Hb 20-40
N/V, disorientation and visual impairment
CO Hb 40-60
Agitation, combativeness, hallucinations, coma, and shock
CO Hb > 60
Death
Early complications
Carbon monoxide poisoning Airway obstruction Pulmonary edema 1-5 days post-injury ARDS
Late complications
Pneumonia
Atelectasis
Pulmonary emboli
Tension pneumothorax
Immediate threats to life=>Tension pneumothorax
Pneumo and CXR
No time for CXR!
Tension PNeumo Treatment:
14 gauge angiocatheter at 2nd intercostal midclavicular line or 4th intercostal midaxillary line
Anesthesia Considerations for Burns
No easy way to induce – slow & steady
Hypovolemia and/or depleted catecholamines
lead to hypotension with all agents
Burns and succ
No succinylcholine after 1st 24 hrs, and for up to 2
yrs
Burn pts and NDNMB
are resistant to nondepolarizers
Up to 5X normal dose!
Opioid requirements and BURNS
increased
Regional and
is an option unless electric burn
Cardiac Tamponade
Beck’s triad
Electrical alternans
May need to drain under local before general
induction
Beck’s Triad
JVD, Hypotension, Muffled heart sounds
C-collar
Manual in-line stabilization – 2 people
No traction
2nd person will stabilize both shoulders
Remove anterior C-collar
C-Collar 1 person
1 person stabilizes and aligns head in neutral position
WITHOUT cephalad traction
Greater than 1 MAC
increase CBF , • Ketamine, > 1 MAC volatiles
Normal ICP =
5-15 mm Hg
ICP waveform Lundberg A wave
“plateau waves”
Worst
ICP waveform Lundberg B wave
Sharp, brief
ICP wavefrom C wave
Benign
o CBF and CBV
1mm Hg increase = 2ml /100g/min increase in CBF
o PaO2 below 50 =
vasodilation = increase in CBF
Increase ICP Meds:
mannitol, Lasix, corticosteroids, acetazolamide,
Central neurogenic hyperventilation –
spontaneous and severe, PaCO2 may decrease to less than 20 mm Hg
Related to
cerebral thrombosis, embolism, or closed head injury
Ataxic breathing (Biot’s breathing)
completely random pattern of tidal volumes related to disruption of medullary neural pathways by trauma, hemorrhage, or compression by tumors
Apenustic breathing –
prolonged end-inspiratory pauses maintained for as long as 30 seconds, related to lesions in the pons or basilar artery infarct
Cheyne-Stokes –
breaths of progressively increasing and then decreasing tidal volume (crescendo-decrescendo pattern), followed by periods of apnea lasting 15-20 seconds related to basal ganglia or cerebral hemispheres brain injury
Central neurogenic hyperventilation –
spontaneous and severe, PaCO2 may decrease to less than 20 mm Hg Related to cerebral thrombosis, embolism, or closed head injury
Post hyperventilation apnea –
awake apnea following moderate PaCO2 decreases related to frontal lobe injury
Brain compression and its signs and symptoms
(pupils, movement, posturing, etc)
• Patients with diffuse brain dysfunction
above the level of the diencephalon will react with purposeful or semi purposeful movements toward the painful stimulus
• Decorticate responses to pain includes
flexion of elbows, adduction of the shoulder, and extension of the knee and ankle = diencephalic dysfunction
• Decerebrate responses include
extension of the elbow, internal rotation of the forearm, and leg extension = more severe brain dysfunction
• No response =
pontine or medullary lesions
Chiari malformation =
displacement of the cerebellum
s/s = HA extending to shoulders/arms, pain w/ coughing/ head movement, syringomyelia
Chiari Class 4 –
cerebellar hypoplasia, no displacement of posterior fossa content
Chiari Class 2 –
displacement of cerebellar vermis
Chiari Class 1 –
displacement of cerebellar tonsil down over cervical spinal cord
Chiari Class 3 –
displacement of cerebellum into occipital encephalocele
Forces that affect cerebral blood flow
CMRO2 ICP Drugs CPP PaCO2-Pao2 tension Intracranial anomalies CO SNS and PNS Cerebral autoregulation
Brain herniation 3 =
tonsillar herniation
Brain herniation 2 =
transtentorial (uncal) herniation
Brain herniation 4 =
bad day = transcalvarial
Valve lesions and their corresponding murmurs
MS –Apex, holodiastolic decrescdeno with opening snap , tx – maintain preload, avoid tachy and acidosis
MR –
pansystolic murmur
AS –
systolic crescendo decrescendo
AR –
early diastolic decresncdo murmur
PS –
crescendo decrescendo, increases with deep inspiration
PR –
decrescendo diastolic murmur
TR –
pansystolic highpitched increases with inspiration
TS –
diastolic
Accentuated S1
Mild mitral stenosis
- Shortened PR interval
* Leaflets have less time to drift back together; forced shut from wide distance
Accentuated S1 which stenosis
Mild mitral stenosis
Accentuated S1 and blood flow
• Impeded flow → prolonged diastolic pressure gradient → keeps leaflets farther apart during late diastole → loudly forced shut from far apart during systole
- High CO states or tachycardia
* Shortened diastole, less time to drift back together
Accentuated S1
• Diminished S1
• Lengthened PR interval
• More time to float back together before systole • Mitral regurgitation
Diminished S1
Leaflets do not fully come together when they close •
Diminished S1
Severe mitral stenosis
Diminished S1
• Higher than normal ventricular pressure at end of diastole → leaflets drift together more rapidly → close from a smaller than normal distance during systole
Diminished S1
• Leaflets are nearly fixed in position • Stiff left ventricle
Diminished S1
Abnormalities in S2
Intensity =
velocity of blood flow toward valves with sudden arrest by closing valves
Diminished S2
Severe AS or pulmonic stenosis → valve nearly fixed in position = Dim S2
Accentuated S2
Systemic HTN/Pulmonary artery HTN → greater diastolic pressure → increased velocity of blood flow
Abnormal splitting patterns of S2: A2 and P2
widened, fixed, paradoxical • Widened
Increased time interval between A2 and P2; noticeable even during expiration and becomes wider on inspiration
Abnormal splitting patterns of S2
Delayed closure of pulmonic valve (RBBB)
Occur shortly after S1 and coincide with opening of aortic/pulmonic valves
Ejection clicks
Presence of aortic/pulmonic valve stenosis or dilatation of pulmonary artery or aorta Sharp, high-pitched
Ejection clicks
Mid/late extra systolic heart sounds
Usually from systolic prolapse of mitral or tricuspid valves
Ejection Click: Leaflets bulge abnormally from
ventricular side of the AV junction into the atrium during ventricular contraction
Commonly associated with valvular regurgitation
Extra diastolic heart sounds: opening snap (OS), third heart sound (S3), fourth heart sound (S4), pericardial knock
Commonly associated with valvular regurgitation
Extra diastolic heart sounds: opening snap (OS), third heart sound (S3), fourth heart sound (S4), pericardial knock
early diastole following opening of AV valves during ventricular filling due to tensing of chordae tendineae during rapid filling/expansion of ventricle
S3 (ventricular gallop
Normal in children and young adults, Suggests dilated ventricle (heart failure) or advanced mitral/tricuspid regurgitation in middle- aged/older
S3
occurs late in diastole coinciding with contraction of the atria and flow of blood into a stiffened ventricle (CAD)
S4 (atrial gallop)=
S4, S1, S2, S3 Tachycardia →
shortened duration of diastole, S3 and S4 coalesce = summation gallop
Pericardial knock
Seen in severe constrictive pericarditis
Appears early in diastole after S2
High-pitched
Quadruple rhythm/summation gallop
S4 (atrial gallop)=
Eye opening response
4 = spontaneous 3 = to verbal command,speech shout 2 = to pain (not applied to face) 1 = NO eye openin g
Verbal response
5= Oriented
4= Confused converstation, but able to answer questions
3= Inappropriate responses, words discernable
2= Incomprehensive sounds or speech
1=NO verbal response
3 areas Glasgow Coma scale measure
Eye opening
Verbal response
Motor response
Motor Response
6=obeys commands for movement
5= purposeful movement to painful stimulus
4=Withdraws from pain
3= Abnormal flexion, decorticate posture2=
2= Extensor rigid response, decerebrate posture
1= NO motor response
Trunk burn %
9%
Back burn %
9%
Legs each burn %
9%
Arms each back and front burn %
4%
Head front and back burn %
4 1/2%
Penis or genital burn %
1%
Right axis Deviation RALeftPO
Right axis deviation
Acute R heart strain
Left Posterior Fascicular Block
Left Axis Deviation
Inferior wall MI
Left anterior fascicular Block
Left axis deviation
Ataxic Biot breathing location
MEdulla
Pattern of ataxic
Unpredictable sequence of breaths varying in rate and tidal volume
Apneustic breathing location
Pons
Pattern of Apneustic
Gasps and prolonged pauses at full inspiration
Cheynes stokes breathing
Cyclic crescendo-decrescendo tidal volume pattern interrupted by apnea
Cheynes stokes breathing pattern
Cerebral hemispheres
Cheynes stokes breathing what conditions
CHF
Central neurogenic hyperventilation Pattern
Marked hyperventilation
Site of lesion/conditions with neurogenic hyperventilation pattern
Cerebral thrombolism
Embolism
Post hyperventilation apnea breathing
Awake apnea following moderate decreases in PaCo2
Location of post hyperventilation apnea
Frontal lobes
Region of compression : Diencephalon
pupillary examination
Small pupils ;reactive to light
Region of compression : Diencephalon
response to oculocephalic or cold caloric testing
normal
Region of compression : Diencephalon
Gross motor findings
Purposeful semi-purposeful or DECORTICATE (flexor ) posturing
Region of compression : Midbrain
Pupillary examination
Midsize pupils; UNREACTIVE To light
Region of compression :Midbrain
response to oculocephalic or cold caloric testing
May be impaired
Region of compression : midbrain
Gross motor findings
Decerebrate (extensor) posturing
Region of compression : PONS or MEDULLA OBLONGATA
Pupillary examination
Midsize pupils: UNREACTIVE TO LIGHT
Region of compression : PONS or MEDULLA OBLONGATA
response to oculocephalic or cold caloric testing
Absent
Region of compression : PONS or MEDULLA OBLONGATA
Gross motor findings
No response
Systolic ejection murmurs associated with
Aortic stenosis
Pulmonic Stenosis
Aortic stenosis murmur characteristics
Radiates to the neck
Pansystolic mumur is associated with
MR and TR
Mitral Regurgitation murmur characteristics
Location at apex and radiates to Axilla
Tricuspid Regurgiation murmur characteristics
Left Lower sternal border–> R Lower sternal border
Late systolic associated with
MVP
MVP murmur at
Apex radiates to Axilla
Early diastolic murmur are
Aortic Regurgitation
Pulmonic Regurgitation
Mid to late systolic
Mitral stenosis
Mitral stenosis heard at
Apex
CVA risk factors : Systemic Hypoperfusion
Hypotension
Hemorrhage
Cardiac arrest
CVA risk factors : Embolism and Thromboembolism
MIS PDW
Male gender Ischemic heart disease Smoking Peripheral vascular disease Diabetes Mellitus White race
CVA risk factors : Subarachnoid hemorrhage and Intracerebral hemorrhage
Often none HTN Coagulopathy Drugs Trauma
‘OFTEN NONE” risk factors
SAH
Early phase of burn CV System
Increase HR,Increase PVR and SVR
Decrease CI
Decrease SV
Decrease contractility
LATE phase of burn CV System
Increase HR, Increase CI Normal or Increase SV Decrease SV Decrease contractility Decreased SO2
Early Phase of burn: Blood
Increase hematocrit
Late Phase of burn: Blood
Decrease Hematocrit
Early Phase of burn: Lungs
Pulmonary Edmea
Bronchospasm
Bronchorrhea
Late Phase of burn: Lungs
Pneumonia
ARDS
Atelectasis
Early Phase of burn: Kidneys
Myoglobinuria
Oliguria
Fena <1%
Late Phase of burn: Kidneys
Increase GFR
Decrease Tubular Function
Both Early and LATE Phase of burn: Brain
Possible Cerebral Edema
Increase Pain response
Altered mental status
Early Phase of Burn : Endocrine and metabolic function
Increase aldosterone and Cortisol
Late Phase of Burn : Endocrine and metabolic function
Increase insulin resistance
Increase O2 consumption and Co2 production
Muscle catabolism
Left axis deviation is
< -30 degrees
Moderate left axis deviation
30-45 degrees
Marked degrees
-45 - (-90 degrees)
Broached Notched R or slurred R waves in lead
LBBI, aVl, V5 and V6
Occasional rS pattern in V5 and V6 or V1
Right Axis deviation
>
- 90
Right axis deviation moderate
90-120 degrees
Right axis Marked
120-180 degrees
Rhythm common under anesthesia
Junctinal escape rhythm
V3, V4
Anterior LAD
V1, V2
Septal LAD
II, III, aVF
Inferior RCA
I, aVL, V5, V6
Lateral Circumflex only V6 is just lateral
Axis when Lead I and AvF upright
normal axis
Axis when lead I up and avF down
Left axis
Axis when lead I Down, and AvF up
Right Axis
Predictors of difficult video laryngoscopy
- Scarring
- Radiation
- Masses
- Large neck circumference
- TMD < 6 cm
- Limited neck mobility
- Operator experience
Brain Herniation 1
Subfalcine (cingulate) herniation
