Cardiac Arrest and Monitoring
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1
What is the primary problem in medical cardiac arrest?
A cardiac electrical or pump failure\
2
What is the primary problem in traumatic cardiac arrest?
Hemorrhage, hypovolemia, or obstructed cardiac filling\
3
Why might CPR alone be ineffective in traumatic cardiac arrest?
Compressions cannot correct severe blood loss or obstructed cardiac filling\
4
What does ROSC stand for?
Return of Spontaneous Circulation\
5
What happens to the myocardium following ROSC?
Reperfusion may cause myocardial stunning and hypotension\
6
What happens to pulmonary vascular resistance after a newborn's first breaths?
It decreases\
7
What is the first major resuscitation intervention for a newborn with inadequate breathing?
Positive-pressure ventilation\
8
What are the two shockable cardiac arrest rhythms?
Ventricular fibrillation and pulseless ventricular tachycardia\
9
What does VF look like on an ECG?
Chaotic electrical activity without identifiable QRS complexes\
10
What defines ventricular tachycardia?
At least three consecutive wide QRS complexes at a rate greater than 100 bpm\
11
What QRS duration indicates a wide-complex rhythm?
Greater than 120 milliseconds\
12
What is monomorphic ventricular tachycardia?
VT with a consistent QRS morphology\
13
What is polymorphic ventricular tachycardia?
VT with changing QRS morphology\
14
What type of ventricular tachycardia is torsades de pointes?
Polymorphic VT\
15
What must be confirmed before defibrillating ventricular tachycardia under the cardiac arrest directive?
Pulselessness\
16
What should you check when fine VF resembles asystole?
Lead connections, gain, and another ECG lead\
17
Why must rhythm interpretation occur without compression artifact?
Artifact can mimic or obscure cardiac rhythms\
18
What must a PCP have before using manual defibrillation?
Certification and servicease hospital authorization\
19
What is the first manual defibrillation dose for a child aged 24 hours to under 8 years?
2 J/kg\
20
What is the subsequent manual defibrillation dose for a child aged 24 hours to under 8 years?
4 J/kg\
21
How frequently can manual defibrillation be repeated?
Every 2 minutes\
22
What is the maximum number of manual defibrillation doses listed?
No maximum\
23
What determines manual defibrillation energy for patients aged 8 years or older?
RBHP/manufacturer recommendations\
24
What is the typical Zoll defibrillation energy escalation?
120 J, 150 J, then 200 J\
25
What is the typical LIFEPAK 15 energy escalation?
200 J, 300 J, then 360 J\
26
Do fire service defibrillation shocks count toward energy escalation?
Yes\
27
What happens to automatic energy escalation when joules are manually changed?
Automatic escalation is cancelled\
28
How can pediatric weight be estimated up to age 10?
$(\text\times2)+10$ kg\
29
What is the estimated weight of a 4-year-old using the age-based formula?
18 kg\
30
What is the first shock dose for an 18 kg child?
36 J\
31
What is the subsequent shock dose for an 18 kg child?
72 J\
32
Should pediatric defibrillation energy always be rounded upward?
No, select the closest available setting\
33
What does DSED stand for?
Double Sequential External Defibrillation\
34
What does VCD stand for?
Vector Change Defibrillation\
35
What is refractory VF/pulseless VT under the DSED/VCD pathway?
A shockable rhythm persisting through three consecutive standard shocks\
36
What is the minimum age for DSED or VCD?
18 years\
37
What type of arrest qualifies for DSED/VCD?
Non-traumatic VF/pulseless VT of presumed cardiac origin\
38
How many consecutive standard shocks are required before DSED/VCD?
Three\
39
Do fire service shocks count toward DSED/VCD eligibility?
Yes\
40
Do public access defibrillator shocks count toward DSED/VCD eligibility?
No\
41
What is vector change defibrillation?
Changing the defibrillation pad orientation to anterior-posterior\
42
What is DSED?
Two defibrillators delivering rapid sequential shocks through different pad vectors\
43
When is VCD used instead of DSED?
When a second authorized defibrillator is unavailable\
44
Can a public access defibrillator be used as the second DSED device?
No\
45
How must DSED shocks be delivered?
Sequentially, not simultaneously\
46
Why must DSED shock buttons not be pressed simultaneously?
They may damage the defibrillators\
47
What is the target interval between DSED shocks?
Less than one second\
48
Which defibrillator should shock first when using a fire service AED for DSED?
The fire AED\
49
Why should the fire AED shock before the paramedic monitor?
The AED may detect the first shock and dump its charge\
50
Where is the posterior pad positioned for DSED/VCD?
Left back between the scapula and spine\
51
How many consecutive shocks are delivered before transport in the on-scene refractory VF/pVT pathway?
Six, consisting of three standard and three DSED/VCD shocks\
52
When should crews begin preparing for transport during DSED/VCD?
After the fifth shock\
53
Does a conversion to a non-shockable rhythm justify another DSED shock?
No\
54
What is the DSED/VCD approach for patients under 18?
Continue standard defibrillation\
55
What was the name of the 2022 Ontario trial investigating DSED?
DOSE VF\
56
How many adults were included in the DOSE VF trial?
405\
57
What was survival to hospital discharge with DSED in the DOSE VF trial?
30.4%\
58
What was survival to hospital discharge with VCD in the DOSE VF trial?
21.7%\
59
What was survival to hospital discharge with standard defibrillation in the DOSE VF trial?
13.3%\
60
What is the first action for a witnessed cardiac arrest occurring en route?
Stop in a safe location and perform at least one rhythm analysis\
61
How many total shocks are used for refractory VF/pVT during an en-route arrest before resuming transport?
Four\
62
What should happen if an en-route arrest converts to PEA or asystole?
Stop further shocks and initiate transport\
63
Can authorized manual defibrillation be performed in a moving ambulance?
Yes, when safe and rhythm interpretation is reliable\
64
Can SAED/AED rhythm analysis be performed while the ambulance is moving?
No, the ambulance must be stopped\
65
What is the maximum suggested on-scene resuscitation period under the SWORBHP non-TOR directive?
Up to 20 minutes\
66
What is the minimum number of analyses in the SWORBHP non-TOR extended resuscitation approach?
Four\
67
What does TOR stand for?
Termination of Resuscitation\
68
Does defibrillation prevent eligibility for Medical TOR?
Yes\
69
Does a public access defibrillator shock affect Medical TOR eligibility?
Yes, it is a contraindication\
70
What are the reversible causes of cardiac arrest commonly called?
The H's and T's\
71
Which electrolyte abnormalities can cause cardiac arrest?
Hyperkalemia and hypokalemia\
72
Which acid-base disturbance is a reversible cause of cardiac arrest?
Acidosis\
73
Which obstructive thoracic condition can cause cardiac arrest?
Tension pneumothorax\
74
Which cardiac compression condition can cause arrest?
Cardiac tamponade\
75
Which two types of thrombosis can cause cardiac arrest?
Pulmonary and coronary thrombosis\
76
What is the PCP indication for EPINEPHrine during medical cardiac arrest?
Suspected anaphylaxis causing the arrest\
77
What is the PCP cardiac arrest EPINEPHrine concentration?
1 mg/mL (1:1,000)\
78
What is the PCP EPINEPHrine dose for suspected anaphylactic arrest?
0.01 mg/kg IM\
79
What is the maximum PCP IM EPINEPHrine dose in anaphylactic arrest?
0.5 mg\
80
How should the PCP anaphylactic arrest EPINEPHrine dose be rounded?
To the nearest 0.05 mg\
81
How many IM EPINEPHrine doses are permitted for PCP anaphylactic arrest?
One\
82
What is the onset of IM EPINEPHrine?
3–10 minutes\
83
What is the peak effect of IM EPINEPHrine?
Approximately 20 minutes\
84
What is the duration of IM EPINEPHrine?
20–30 minutes\
85
Which adrenergic receptors does EPINEPHrine stimulate?
Alpha-1, beta-1, and beta-2\
86
What does EPINEPHrine-induced vasoconstriction improve during CPR?
Coronary and cerebral perfusion pressure\
87
What is a potential cardiac adverse effect of EPINEPHrine?
Tachycardia or arrhythmias\
88
Is EPINEPHrine routinely administered by PCPs for every cardiac arrest?
No\
89
What is the priority in asthmatic cardiac arrest?
Effective ventilation and oxygenation\
90
How is uncomplicated electrocution-related arrest managed?
Under the Medical Cardiac Arrest directive\
91
When does electrocution-related arrest require the Trauma directive?
When significant trauma is also present
92
What type of trauma activates the Trauma Cardiac Arrest directive?
Severe blunt or penetrating trauma causing cardiac arrest\
93
What directive applies when cardiac arrest has no obvious significant trauma?
Medical Cardiac Arrest\
94
What rhythm is required for Trauma TOR?
Asystole\
95
Can Trauma TOR be considered after defibrillation?
No\
96
What authorization is required before applying Trauma TOR?
Base Hospital Physician authorization\
97
What are the immediate reversible causes to address in traumatic arrest?
Hemorrhage, hypovolemia, hypoxia, and obstructive causes\
98
What intervention controls external hemorrhage during traumatic arrest?
Direct hemorrhage control\
99
Why might pelvic stabilization be important in traumatic arrest?
It can reduce hemorrhage from an unstable pelvic fracture\
100
Should IV fluid administration delay transport in traumatic arrest?
No\
101
What is the priority for airway management in traumatic arrest?
Effective basic airway management and ventilation\
102
When should an advanced airway be used in traumatic arrest?
Only when needed\
103
What is the priority when Trauma TOR criteria are not met?
Transport to the closest appropriate receiving facility after the first analysis or defibrillation\
104
What three initial questions determine whether a newborn needs routine care?
Term gestation, good muscle tone, and breathing or crying\
105
What care does a vigorous term newborn usually require?
Warmth, drying, airway support, and routine care\
106
How frequently is newborn heart rate reassessed during resuscitation?
Every 30 seconds\
107
What is the preferred method of monitoring newborn heart rate?
ECG monitoring\
108
Where should preductal SpO₂ be measured in a newborn?
Right hand\
109
Why is newborn SpO₂ initially lower than adult SpO₂?
Pulmonary circulation and oxygenation are transitioning after birth\
110
What is the primary resuscitation treatment for a newborn with inadequate breathing?
Positive-pressure ventilation\
111
What oxygen concentration is initially used for newborn PPV in the lecture?
Room air (21%)\
112
When are newborn chest compressions indicated?
HR below 60 bpm after 30 seconds of effective PPV\
113
What oxygen concentration is used once newborn chest compressions begin?
100%\
114
What does MR SOPA stand for?
Mask seal, Reposition, Suction, Open mouth, Pressure increase, Alternate airway\
115
What complication can excessive newborn PPV pressure cause?
Pneumothorax\
116
What complication can an ineffective newborn mask seal cause?
Inadequate ventilation\
117
What is the newborn PPV treatment goal?
HR at least 100 bpm with effective spontaneous breathing\
118
What is the recommended action for uncertain newborn gestational age?
Initiate resuscitation and transport\
119
Below what gestational age may newborn resuscitation be considered futile in the lecture?
20 weeks\
120
When does the ROSC directive begin?
Immediately after a pulse returns\
121
What oxygen saturation target is specified in the ROSC directive lecture?
94–98%\
122
What EtCO₂ target is specified in the ROSC directive lecture?
30–40 mmHg\
123
Why should hyperventilation be avoided after ROSC?
It can reduce cerebral blood flow\
124
What ECG should be acquired after ROSC?
12-lead ECG\
125
Why is a 12-lead ECG important after ROSC?
It may identify STEMI and influence destination decisions\
126
What is the minimum age for the PCP post-ROSC fluid bolus?
2 years\
127
What conditions must be present before giving post-ROSC saline?
Hypotension and clear chest auscultation\
128
What is the post-ROSC normal saline bolus dose?
10 mL/kg IV\
129
What is the maximum post-ROSC saline bolus volume?
1,000 mL\
130
How often is saline reassessed in patients aged 2 to under 12 years?
Every 100 mL\
131
How often is saline reassessed in patients aged 12 years or older?
Every 250 mL\
132
What type of fluid is 0.9% sodium chloride?
Isotonic crystalloid\
133
How does normal saline improve blood pressure?
It increases intravascular volume and preload\
134
What pulmonary finding contraindicates a post-ROSC fluid bolus?
Pulmonary edema\
135
What should be reassessed before and after a post-ROSC fluid bolus?
Chest auscultation\
136
What should you do if a patient re-arrests after ROSC?
Return to the appropriate cardiac arrest directive\
137
What information should be included in a cardiac arrest patch?
Arrest history, rhythm, treatments, response, and the specific request\
138
What must be done after receiving an order from the Base Hospital Physician?
Read the order back
139
What does capnography measure?
Exhaled carbon dioxide\
140
What does EtCO₂ stand for?
End-tidal carbon dioxide\
141
What does pulse oximetry measure?
Peripheral oxygen saturation\
142
What is the difference between ventilation and oxygenation?
Ventilation removes CO₂; oxygenation transfers O₂ into blood\
143
What is the normal EtCO₂ range?
35–45 mmHg\
144
How much lower is EtCO₂ normally than PaCO₂?
Approximately 2–5 mmHg\
145
What does PaCO₂ represent?
Partial pressure of carbon dioxide in arterial blood\
146
What does PvCO₂ represent?
Partial pressure of carbon dioxide in venous blood\
147
What is the approximate normal arterial PaCO₂?
40 mmHg\
148
What is the approximate normal venous PvCO₂?
46 mmHg\
149
What is the approximate inspired PO₂ on humidified room air at sea level?
150 mmHg\
150
What is the approximate normal alveolar PAO₂?
100 mmHg\
151
What is the normal arterial PaO₂ range?
80–100 mmHg\
152
What does an increased PaCO₂–EtCO₂ gradient suggest?
Increased dead space or reduced pulmonary perfusion\
153
What are the three physiological factors determining EtCO₂?
Metabolism, perfusion, and ventilation\
154
How does metabolism influence EtCO₂?
Cellular metabolism produces CO₂\
155
How does perfusion influence EtCO₂?
Blood flow transports CO₂ to the lungs\
156
How does ventilation influence EtCO₂?
Alveolar ventilation removes CO₂\
157
Why does EtCO₂ decrease during poor cardiac output?
Less CO₂ reaches the alveoli\
158
Why can EtCO₂ increase during fever?
Increased metabolism produces more CO₂\
159
How does hyperventilation affect EtCO₂?
It decreases\
160
How does hypoventilation affect EtCO₂?
It increases\
161
Why can supplemental oxygen conceal respiratory depression on pulse oximetry?
SpO₂ may remain normal despite inadequate ventilation\
162
Which monitor usually detects hypoventilation first in a patient receiving oxygen?
Capnography\
163
What are the five components of P-Q-R-S-T capnogram interpretation?
Presence, Quantity, Rate, Shape, and Trend\
164
What does P represent in capnogram interpretation?
Presence of a waveform\
165
What does Q represent in capnogram interpretation?
Quantity of exhaled CO₂\
166
What does R represent in capnogram interpretation?
Respiratory rate\
167
What does S represent in capnogram interpretation?
Waveform shape\
168
What does T represent in capnogram interpretation?
Trend over time\
169
What does Phase I of a normal capnogram represent?
Exhalation of CO₂-poor dead-space gas\
170
What does Phase II of a normal capnogram represent?
Rapid mixing of alveolar and dead-space gas\
171
What does Phase III of a normal capnogram represent?
Alveolar plateau\
172
What does Phase 0 of a normal capnogram represent?
Inspiration\
173
Where is EtCO₂ measured on the capnogram?
At the end of the alveolar plateau\
174
What is the typical shape of a normal capnogram?
Rectangular with a nearly flat plateau\
175
What does a shark-fin capnogram suggest?
Bronchospasm or lower airway obstruction\
176
What causes the slanted upstroke in bronchospasm?
Slow, obstructed exhalation\
177
Which conditions commonly produce shark-fin waveforms?
Asthma and COPD\
178
What does a capnogram baseline that does not return to zero suggest?
CO₂ rebreathing\
179
What does a curare cleft indicate?
Spontaneous respiratory effort during assisted ventilation\
180
What can cause sudden disappearance of a capnography waveform?
Apnea, disconnection, airway obstruction, dislodgement, or circulatory arrest\
181
What waveform pattern suggests hyperventilation?
Fast waves with low EtCO₂ and normal shape\
182
What waveform pattern suggests hypoventilation?
Slow waves with elevated EtCO₂\
183
What EtCO₂ finding is common in opioid respiratory depression?
Elevated EtCO₂, often above 50 mmHg\
184
Why can EtCO₂ be falsely low during extremely shallow breathing?
Insufficient tidal volume reaches the sampling device\
185
What is the adult assisted ventilation rate with a pulse?
One breath every 6 seconds\
186
What is the pediatric assisted ventilation rate with a pulse?
One breath every 2–3 seconds\
187
What is the adult ventilation rate during CPR with an advanced airway?
10 breaths/min\
188
What is the pediatric ventilation rate during CPR with an advanced airway?
20–30 breaths/min\
189
Why is excessive ventilation harmful during CPR?
It increases intrathoracic pressure and reduces venous return\
190
What ventilation strategy is used in obstructive lung disease?
Slower breaths with prolonged exhalation\
191
What is permissive hypercapnia?
Accepting elevated CO₂ to avoid harmful excessive ventilation\
192
What does sidestream capnography use to sample CO₂?
A sampling line or nasal cannula\
193
Where is an in-line capnography adapter placed?
Between the BVM and mask or advanced airway\
194
What is the primary method of confirming SGA placement?
Continuous waveform capnography\
195
What does a colorimetric CO₂ detector measure?
Exhaled CO₂ using a colour change\
196
What colour indicates less than 4 mmHg on a colorimetric CO₂ detector?
Purple\
197
What colour indicates approximately 4–15 mmHg?
Tan\
198
What colour indicates approximately 15–38 mmHg or higher?
Yellow\
199
Why can a colorimetric detector remain purple during cardiac arrest?
Insufficient pulmonary blood flow delivers CO₂\
200
What can cause a falsely yellow colorimetric CO₂ detector?
Gastric acid or medication contamination\
201
What equipment problems can distort capnography readings?
Water, secretions, kinks, leaks, or disconnections\
202
What EtCO₂ value during CPR suggests poor perfusion or CPR quality?
Below 10 mmHg\
203
What CPR factors should be reassessed when EtCO₂ is below 10 mmHg?
Compression depth, rate, recoil, and ventilation\
204
What compression rate should be maintained during CPR?
100–120 compressions/min\
205
What sudden EtCO₂ change suggests ROSC?
An abrupt sustained rise, often to 35–40 mmHg or higher\
206
When should a suspected ROSC be confirmed by pulse check?
At the next rhythm analysis\
207
Can persistently low EtCO₂ alone justify termination of resuscitation?
No\
208
What can cause a temporary EtCO₂ decrease after EPINEPHrine?
Changes in pulmonary perfusion\
209
What can cause a transient EtCO₂ increase after sodium bicarbonate?
Additional CO₂ production\
210
What happens to EtCO₂ during a massive pulmonary embolism?
It decreases\
211
Why does pulmonary embolism lower EtCO₂?
Reduced pulmonary perfusion increases dead space\
212
What EtCO₂ finding may support diabetic ketoacidosis?
Low EtCO₂, often below 25 mmHg\
213
Why does DKA cause low EtCO₂?
Kussmaul respirations compensate for metabolic acidosis\
214
What EtCO₂ value is a warning sign in suspected sepsis?
25 mmHg or lower\
215
Why can sepsis lower EtCO₂?
Metabolic acidosis and reduced perfusion\
216
What is the usual EtCO₂ target in traumatic brain injury?
35–45 mmHg\
217
Why is hypocapnia harmful in traumatic brain injury?
It causes cerebral vasoconstriction\
218
Why is hypercapnia harmful in traumatic brain injury?
It can increase intracranial pressure\
219
What EtCO₂ range may be used briefly for signs of brain herniation under applicable standards?
30–35 mmHg\
220
What does rising EtCO₂ in a tiring asthmatic suggest?
Impending ventilatory failure\
221
What does improvement from a shark-fin to a square waveform suggest?
Reduced bronchospasm\
222
What does falling EtCO₂ with unchanged ventilation suggest?
Reduced perfusion
223
What does SpO₂ stand for?
Peripheral oxygen saturation\
224
What does SaO₂ represent?
Arterial oxygen saturation measured directly\
225
What does PaO₂ represent?
Partial pressure of oxygen dissolved in arterial plasma\
226
What two wavelengths are used in pulse oximetry?
660 nm red and 940 nm infrared\
227
Which hemoglobin absorbs more red light?
Deoxygenated hemoglobin\
228
Which hemoglobin absorbs more infrared light?
Oxygenated hemoglobin\
229
Why does pulse oximetry require a pulsatile signal?
To distinguish arterial blood from surrounding tissues\
230
What is the typical pulse oximeter accuracy between 70% and 100% saturation?
Approximately ±2–3%\
231
Why are SpO₂ readings below 70–80% less reliable?
Limited calibration data\
232
What is the maximum number of oxygen molecules carried by one hemoglobin molecule?
Four\
233
Approximately how much oxygen can 1 gram of hemoglobin carry?
1.34 mL\
234
What percentage of blood oxygen is normally hemoglobin-bound?
Approximately 98%\
235
What is the arterial oxygen content equation?
$CaO_2=1.34\times Hb\times SaO_2+0.003\times PaO_2$\
236
What is the oxygen delivery equation?
$DO_2=CO\times CaO_2$\
237
What three factors determine tissue oxygen delivery?
Oxygen saturation, hemoglobin concentration, and cardiac output\
238
Why can a severely anemic patient have SpO₂ of 98% but inadequate oxygen delivery?
Too little hemoglobin is available to carry oxygen\
239
Why can shock cause tissue hypoxia despite normal SpO₂?
Cardiac output is inadequate\
240
What is the oxyhemoglobin dissociation curve?
The relationship between PaO₂ and hemoglobin oxygen saturation\
241
What PaO₂ approximately corresponds to SpO₂ of 90%?
60 mmHg\
242
Why is SpO₂ below 90% particularly concerning?
Small PaO₂ decreases can cause rapid desaturation\
243
What does a right shift of the oxyhemoglobin dissociation curve mean?
Hemoglobin releases oxygen more easily\
244
What does a left shift of the oxyhemoglobin dissociation curve mean?
Hemoglobin holds oxygen more tightly\
245
What does CADET stand for in the right-shift mnemonic?
CO₂, Acid, 2,3-DPG, Exercise, Temperature\
246
How does increased temperature affect the oxyhemoglobin dissociation curve?
Shifts it right\
247
How does acidosis affect the oxyhemoglobin dissociation curve?
Shifts it right\
248
How does hypothermia affect the oxyhemoglobin dissociation curve?
Shifts it left\
249
How does carbon monoxide affect the oxyhemoglobin dissociation curve?
Shifts it left\
250
What is the Bohr effect?
Changes in hemoglobin oxygen affinity caused by CO₂ and pH\
251
What is the Haldane effect?
Deoxygenated hemoglobin carries more CO₂\
252
What is a plethysmograph?
A waveform representing pulsatile changes in tissue light absorption\
253
What does a reliable pleth waveform look like?
Regular, consistent waves matching the perfused pulse\
254
What ECG feature should correspond with each normal pleth wave?
A QRS complex\
255
What is a dicrotic notch on a pleth waveform?
A small notch on the descending portion of the pulse wave\
256
Can a pleth waveform directly measure blood pressure?
No\
257
Can pleth waveform height reliably measure stroke volume?
No\
258
What does Perfusion Index indicate?
Relative strength of the pulsatile signal\
259
What causes motion artifact on a pleth?
Patient movement, shivering, seizures, or transport vibration\
260
What does a tiny noisy pleth waveform suggest?
Poor peripheral perfusion\
261
How can a poor-perfusion SpO₂ reading be improved?
Warm the site or move the probe to the ear or forehead\
262
Why might PVCs cause the pulse oximeter rate to be lower than the ECG rate?
Some PVCs do not produce a perfusing pulse\
263
What can exaggerated respiratory variation in pleth amplitude suggest?
Hypovolemia, severe asthma, tamponade, or tension physiology\
264
Why can a BP cuff interfere with SpO₂ readings?
Cuff inflation temporarily reduces distal blood flow\
265
How long can finger SpO₂ readings lag behind physiological changes?
30 seconds to over one minute\
266
Which pulse oximeter sites may respond faster than a finger probe?
Ear or forehead\
267
How can bright ambient light affect pulse oximetry?
It interferes with the optical signal\
268
How can dark nail polish interfere with SpO₂?
It alters light transmission\
269
Why can carbon monoxide poisoning produce a falsely normal SpO₂?
Carboxyhemoglobin is misread as oxyhemoglobin\
270
What oxygen treatment is indicated for suspected carbon monoxide poisoning?
High-concentration oxygen regardless of SpO₂\
271
Why can cyanide poisoning produce normal SpO₂ despite tissue hypoxia?
Cells cannot utilize oxygen\
272
What SpO₂ reading is commonly associated with methemoglobinemia?
Approximately 85%\
273
What substances may cause methemoglobinemia?
Dapsone, benzocaine, and nitrites\
274
What appearance may be associated with methemoglobinemia?
Chocolate-coloured cyanosis\
275
What medications or dyes can temporarily cause falsely low SpO₂?
Methylene blue, indocyanine green, or isosulfan blue\
276
What is occult hypoxemia?
Low arterial oxygen saturation despite reassuring pulse oximeter readings\
277
How can darker skin pigmentation affect pulse oximeter accuracy?
SpO₂ may overestimate arterial oxygen saturation\
278
What was the occult hypoxemia rate reported for Black patients in the cited 2020 study?
11.7%\
279
What was the occult hypoxemia rate reported for White patients in the cited 2020 study?
3.6%\
280
What is the general adult SpO₂ target under the BLS PCS oxygen standard?
92–96%\
281
What is the specified SpO₂ target for COPD patients with listed clinical features?
88–92%\
282
What is the initial oxygen adjustment for a qualifying COPD patient on home oxygen?
2 L/min above their home flow\
283
How frequently may oxygen flow be increased by 2 L/min for worsening qualifying COPD patients?
Every 2–3 minutes\
284
What oxygen concentration is indicated for cardiac arrest under the BLS PCS?
High concentration\
285
What oxygen concentration is indicated for upper airway burns?
High concentration\
286
What oxygen concentration is indicated for sickle cell crisis?
High concentration\
287
What oxygen concentration is indicated for diving emergencies?
High concentration\
288
What oxygen concentration is indicated when a critically ill patient has no interpretable pleth?
High concentration\
289
What SpO₂ target does the pulse oximetry lecture cite from AHA 2025 after ROSC?
92–98%\
290
What oxygenation threshold should be avoided in traumatic brain injury?
SpO₂ below 90%\
291
Why should routine high-flow oxygen be avoided in non-hypoxic patients?
Hyperoxia may cause vasoconstriction and oxidative injury\
292
What effect can excessive oxygen have in COPD?
Worsened hypercapnia and ventilation-perfusion mismatch\
293
What did the IOTA meta-analysis associate liberal oxygen therapy with?
Increased in-hospital mortality\
294
What did the DETO2X-AMI trial find about routine oxygen in non-hypoxic myocardial infarction?
No demonstrated benefit\
295
What did the SO2S trial find about routine oxygen in non-hypoxic stroke?
No improvement in outcomes\
296
What must be assessed before trusting an SpO₂ reading?
Pleth quality and pulse-rate agreement\
297
What should be documented alongside an SpO₂ measurement?
Oxygen delivery device and flow rate\
298
Why should EtCO₂ and SpO₂ be monitored together?
They assess ventilation and oxygenation separately
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