Monitoring Flashcards
What does the picture (Fig.6.1) above depict?
The picture above shows a normal capnography.
In the picture above, what do points A and D denote?
Point A denotes the beginning of exhalation and D denotes the end-tidal CO2 level and the start of inhalation of CO2 free gas.
Differentiate between capnometry, capnogram, and capnography
○ Capnometry is the measurement and numeric representation of the CO2 concentration during inspiration and expiration.
○ A capnogram is a continuous concentration- time display as a waveform, of the CO2 sampled at a patient’s airway during ventilation (Fig.6.2).
○ Capnography is the continuous monitoring of the patient’s capnogram. Capnograph is the machine that generates a waveform and the capnogram is the actual waveform.
Explain the phases of capnography
The capnogram is divided into four distinct phases (Fig.6.3).
Phase I: Exhalation of CO2 free gas from dead space A–B
Phase II: Combination of dead space and alveolar gas B–C
Phase III: Exhalation of mostly alveolar gas C–D Phase
IV: Inhalation of CO2 free gas D–E
How do capnographs work?
○ Capnographs usually work on the principle that CO2 absorbs infrared radiation.
○ A beam of infrared light is passed across the gas sample to fall on a sensor.
○ The presence of CO2 in the gas leads to reduction in the amount of light falling on the sensor changing the voltage in a circuit
What are the types of capnometers?
Types of capnometers:
(a) Mainstream: A cuvette containing the CO2 sensor which is heated to 40°C is placed between the ET tube and the breathing circuit. Response time is fast.
(b)Sidestream: The CO2 sensor is in the main unit away from the patient and expiratory gas is sampled by means of a long capillary tube which is connected to a T-piece placed between the ET tube and the breathing circuit. The rate of gas sampling is usually between 50 and 500mL/min. If the sampling rate is more than the expired gas flow, then contamination from fresh gas occurs. Due to the sampling, there is a certain delay in detection. Advantages include ability to monitor in non-intubated, spontaneously breathing patients and also in prone positions.
Name some uses of capnography?
Capnography is used in the following areas:
○ Expiratory downstroke Phase 1
°Expiration It is essential in determining the appropriate placement of endotracheal tubes and is part of ASA standard in monitoring.
○ As a clue to valve/ CO2 absorber dysfunction/exhaustion.
○ To monitor adequacy of ventilation and cardiac compression during resuscitation.
○ Detection of adverse respiratory events such as hypoventilation, esophageal intubation, endotracheal dislodgement, and circuit disconnection [1, 2].
○ During procedures done under sedation, capnography provides useful information, e.g., on the frequency and regularity of ventilation, than pulse oximetry.
○ Monitoring during postoperative patient-controlled analgesia can improve patient safety and reduce adverse events by early detection of respiratory depression [3, 4].
What are the factors that affect ETCO2?
The factors that affect ETCO2 are:
(a) The factors that increase ET CO2 are:
• Hyperthermia including malignant hyperthermia
• Hyperthyroidism including “thyroid storm”
• Rebreathing (baseline elevation)
• Hypoventilation
• Release of cross-clamp/tourniquet
(b) The factors that decrease ETCO2 are:
• Hypothyroidism
• Pulmonary/air Embolism
• Hyperventilation
• Low cardiac output
What is the principle of calorimetric CO2 detector?
Calorimetric CO2 detector (Fig.6.4) acts as a “detector” and not a monitor.
○ The detector uses chemically treated paper that changes color when exposed to CO2.
○ A typical device has three color ranges based on the amount of CO2 detected, and it requires six breaths for detection.
°Purple—EtCO2 is less than 0.5%
°Tan—EtCO2 is 0.5–2%
°Yellow—EtCO2 is greater than 2% ○ Normal ETCO2 is greater than 4% hence the device has to turn yellow in people with intact circulation.
○ It may change color due to acidic contaminants like stomach acid, lidocaine, or epinephrine.
(ii) The late emptying of alveoli with lower ventilation/perfusion (V/Q) ratios and, therefore, relatively higher PC02.
If all the alveoli had the same PC02, then irrespective of the emptying patterns, phase III would be nearly horizontal. However, this ideal situation does not occur, even in normal lungs which have a wide range of V/Q ratios. Some alveoli have a higher V/Q ratio (over ventilated) than ideal alveoli and hence they have a relatively lower PC02. Others have a lower V/Q ratio than ideal alveoli (under ventilated) resulting in a relatively higher PC02. The delayed emptying of these alveoli with low V/Q (high PC02) contributes to the rising slope of phase III. The mechanisms producing this effect are:-3,4
What do the above waveforms A to D depict?
A.Normal capnograph (Fig.7.1A) A–B: baseline B–C: expiratory upstroke C–D: expiratory plateau D: ETCO2 value D–E: inspiration begins
B.The baseline of the capnogram does not return to zero, e.g., rebreathing (Fig.7.1B)
• An exhausted co2 absorber [1]
• Channeling of the gas within the co2 absorber
• An incompetent unidirectional inspiratory or expiratory valve [1]
• Accidental administration of co2
• Inadequate fresh gas flow
C.Obstruction in airway or breathing circuit (Fig.7.1C)
• Partially kinked or occluded artificial airway
• Obstruction in expiratory limb of breathing circuit [2]
• Bronchospasm
• Presence of foreign body in the airway.
D.Increased end-tidal CO2 (Fig.7.1D)
• Hypoventilation [2]
• Increased metabolic rate
• Hyperthermia
What do the above waveforms E to J depict?
E.Curare cleft (Fig.7.1E)
• Inspiratory efforts of patient
• Hiccups
• Inadequate muscle relaxation
F.Endotracheal cuff leak (Fig.7.1F)
• Leak around the endotracheal tube
• Leakage of the sampling line
G.Cardiac oscillations
• Movement of the heart produces small tidal volumes
• Capnograph can be affected by perfusion and cardiac function
H.ROSC (return of spontaneous circulation) during cardiac arrest
• HA: hypoperfusion, marked hypotension.
• HB: Correction of ET tube obstruction.Increase in pulmonary circulation brings more CO2 into the lungs for elimination.
I.Esophageal intubation
• Endotracheal tube in the esophagus • Little or no CO2 present
J.Flat ETCO2 trace
• Ventilator disconnection
• Airway misplaced extubation, oesophageal intubation
• Cardiac arrest
- Interpret Figs. 15.1 and 15.2
The figures represent electrocardiograms (ECGs) for patients presenting with
chest pain. Figure 15.1 illustrates changes suggestive of myocardial ischemia (ST-segment depression in the anterolateral leads I, aVL, and V2–V6). The ECG shown in Fig. 15.2 depicts changes suggestive of myocardial injury (ST-segment elevation in the lateral leads I and aVL).
- What are the electrocardiographic findings in myocardial ischemia and
infarction?
○ ECG is considered to be an essential tool in the evaluation for myocardial ischemia or infarction.
○ Changes to indicate myocardial ischemia or infarction include peaked or inverted T waves, ST-segment elevation or depression, and changes in the QRS complex.
○ ST-segment elevations present on the ECG accompanied by symptoms or signs concerning of myocardial infarction (including chest pain, dyspnea, or hemodynamic instability) are an emergency that require immediate attention.
○ The threshold values for significant ST-segment elevation vary based on the gender and age of the individual. °For men 40 years of age or older, 2 mm elevation in leads V2 and V3 and 1 mm elevation in all other leads is considered to be significant.
°For men younger than 40 years old, a significant ST-segment elevation is 2.5 mm in leads V2 and V3.
°For women of all ages, ST-segment elevation of 1.5 mm in V2 or V3 and 1 mm in all other leads is considered to be significant.
- How are myocardial ischemia and infarction different?
○ Myocardial ischemia results from an imbalance between myocardial oxygen demand and supply.
°Myocardial oxygen demand is determined by the heart rate,
myocardial contractility, preload (end-diastolic pressure or volume), afterload (arterial impedance), and muscle mass.
°Determinants of myocardial oxygen supply include coronary blood flow and arterial oxygen content.
○ Myocardial infarction (myocardial cell death) occurs if myocardial ischemia is prolonged (as little as 20 min or less).
°Myocardial infarction is characterized by myocyte necrosis as detected by elevated cardiac biomarkers (troponin-T, troponin-I (preferably), or CKMB) along with ischemia symptoms and ECG changes (as described above).
- What is the management of perioperative myocardial ischemia and infarction?
○ Perioperative management of patients with myocardial ischemia and infarction starts from early detection.
○ Myocardial ischemia or infarction can be detected intraoperatively by ECG changes, ventricular arrhythmias, and hemodynamic
instability.
○ If myocardial ischemia or infarction is suspected, a 12-lead unfiltered ECG should be obtained promptly, and cardiac biomarkers should be sent.
°In addition, a transesophageal echocardiogram can be done (if readily available) to detect the ejection fraction and any new myocardial wall motion abnormalities.
○ The surgeon should be informed to make a decision on completing versus aborting the surgery.
○ If tachycardia along with normo or hypertension is present, a beta-blocker (intravenous esmolol or metoprolol) or a non-dihydropyridine calcium channel blocker if left ventricular ejection is normal
(intravenous diltiazem) should be administered. Tachycardia along with hypotension is challenging.
○ Evaluate and treat potential causes (e.g., hypovolemia or anemia).
○ Vasopressors should be added to maintain mean adequate perfusion pressure (mean arterial blood pressure 65 mmHg or more).
○ In cases of tachyarrhythmias
(atrial flutter or fibrillation), direct current cardioversion may be necessary.
○ If ST-segment elevations are present, an emergent cardiology consultation should be obtained to consider coronary angiography and revascularization.
○The management of patient with suspected myocardial infarction or ischemia in the postoperative period is as challenging given the limitations for the use of anticoagulants
and antiplatelet agents. If based on symptoms, acute coronary syndrome is suspected, an ECG should be promptly obtained to assess for changes suggestive of ischemia or infarction.
○ Oxygen should be administered if oxygen saturation is below 90%.
○ Short-acting nitroglycerin (sublingual tablets or oral spray) should be administered to alleviate angina (avoid in hypotension).
○ If there are no contraindications for antiplatelet agents, administer aspirin 162–324 mg oral.
○ Cardiology consult should be sought to direct further management.
○ If changes suggestive of acute ST-segment myocardial infarction are present, cardiology should be contacted emergently. The decision to proceed with invasive coronary angiography should be decided based on the risk-benefit ratio analysis in any given patient
weighing the risk of bleeding and the risk of ongoing myocardial ischemia.
- What is the prognosis of patients with myocardial ischemia or infarction following noncardiac surgery?
○ Patients experiencing a myocardial infarction following noncardiac surgery (whether symptomatic or asymptomatic) are at increased risk for in-hospital and short-term mortality.
○ Nonfatal myocardial infarction is associated with increased in-hospital mortality reaching 25% in some cohorts.
> A 30-day mortality in this subset of patients was estimated to be approaching 12% .
○Patients who experience cardiac arrest perioperatively are at the highest risk for cardiac mortality occurring in up to 65% of the cases.
○ Although silent myocardial infarction is associated with increased adverse outcomes, routine postoperative screening with serum troponin levels is not recommended.
> The usefulness of screening with troponin levels in patients at high risk for myocardial infarction is uncertain especially in the absence of a well-defined management strategy.
- Describe the role of preoperative cardiac evaluation in patient undergoing non-cardiac surgery.
○ Studies have shown that patients undergoing noncardiac surgery are at risk of periprocedural myocardial infarction and increased mortality (up to 2% in some cohorts).
○ The risk of major cardiovascular and cerebral events increases in patients with prior history of diabetes mellitus, hypertension, coronary artery disease, congestive heart failure, stroke, peripheral artery disease, chronic kidney disease, and advanced age.
○ The risk of adverse outcomes
decreases as the length of time following an MI increases.
○ Given those reasons, the need for preoperative evaluation rises especially in patients older than
55 years, with history of coronary artery disease or stroke, or patients with symptoms to suggest myocardial ischemia (angina).
○ One of the best tools to risk stratify patients is using the algorithm and risk calculators available in the 2014 ACC/AHA Perioperative Clinical Practice Guidelines.
○ Based on those guidelines, patients undergoing emergent surgery need to proceed with surgery without delay. Patients with acute coronary syndrome require to be treated prior to the planned surgery based on the practice guidelines. In patients with low calculated risk (<1%) and also in those with high risk but with good functional capacity (four metabolic equivalents (METs) or greater), one may proceed with
surgery without further testing. The subset of patients with high risk and poor functional capacity may require noninvasive functional study (stress test) if it would alter perioperative management. Routine coronary angiography and revascularization are not recommended prior to noncardiac surgery.
During major abdominal surgery, urine output in a 90 kg patient decreases to 20 mL
per hour over the prior 2 h. Noninvasive cardiac output is being monitored in this
patient with a FloTrac system, and the parameters are depicted in Fig. 16.1. which
changes to what is depicted in Fig. 16.2 after a single maneuver by the
anesthesiologist.
1. What do the figures show?
○ The figures above represent the moment before and after a fluid challenge on a patient with low urine output.
○ Notice that the cardiac output/cardiac index increased, while the SVV decreased from 19% to 6%.
○ The patient’s urine output responded accordingly, representing improved kidney perfusion with the fluid challenge
- What is the importance of monitoring cardiac output?
○ Monitoring cardiac output is a common practice in anesthesia and critical care as it provides important information about cardiac function, tissue perfusion, and oxygen delivery.
○ It is utilized as a marker of oxygen delivery to tissues based on the equation below: DO2=CO×(1.39×[Hb]×SaO2+(0.003×PaO2))
DO2: Rate of oxygen delivery
CO: Cardiac output Hb: Hemoglobin concentration
SaO2: Hemoglobin oxygen saturation expressed as a fraction
PaO2: Partial pressure of oxygen in the blood Its measurement can identify patients at risk for morbidity and/or mortality.
○ In addition, monitoring cardiac output can be used to guide treatment with both fluid resuscitation and/or vasoactive/inotropic drugs.
- What are the advantages of the FloTrac/EV1000 system?
Among different minimally invasive cardiac output monitors, the FloTrac/ EV1000 system has the following advantages:
°no central line required, any arterial line location can be used,
°easy to set up, no external calibration required, changes in vascular tone and site of arterial cannulation are corrected by built-in software, correction occurs every 60s, waveform analysis occurs every 20s, extrasystoles and small artifacts are eliminated by built-in algorithm, option for attaching central venous pressure with which SVR/SVRI can be calculated, and option to attach PreSep catheter with which ScvO2 can be continuously monitored. °In addition, this monitor is able to calculate stroke volume variation (SVV) which is an extra tool to assess volume status.
- How does the FloTrac estimate stroke volume?
○ The FloTrac system uses pulse contour analysis with patient demographics and physical characteristics for arterial impedance estimation and ultimately stroke volume (SV) calculation.
○ The basic principle is the linear relation between the pulse pressure and the SV.
○ The SV is estimated using the following equation: SV=SDap×X.The waveform analysis that occurs every 20s results in 2000 data points.
°SDap is the standard deviation of these data points and reflects the pulse pressure.
°The factor X stands for the conversion factor that depends on arterial compliance, mean arterial pressure, and waveform characteristics.
°These variables are adjusted by the built-in software, and this process is repeated every 60s.
○ Once SV is calculated, it is multiplied by the heart rate to result in the cardiac output.
- What are the limitations of the FloTrac?
> The use and accuracy of FloTrac/EV1000, specially for monitoring of SVV, may be compromised in the following scenarios: poor signal, intra-aortic balloon pump, ventricular assist devices, open chest, spontaneous breathing, small tidal volumes, arrhythmia, poor lung compliance, high PEEP, severe obesity (effect of abdominal pressure in lung compliance), and medications (norepinephrine, vasodilators, beta-blockers).
- What other minimally invasive monitors are available?
○ Minimally invasive CO monitors using pulse contour analysis can be divided into uncalibrated (or autocalibrated) and calibrated.
○ FloTrac, PulsioFlex, LiDCOrapid, PRAM, Nexfin, and esCCO monitors are examples of uncalibrated monitors, while PiCCO plus and LiDCOplus are examples of calibrated ones.
○ Three other principles support other types of monitors: pulse Doppler technology, applied Fick principle, and bioimpedance/bioreactance
○ Calibrated: The PiCCO plus monitor uses the pulse contour analysis to estimate CO and utilizes the transpulmonary thermodilution method for intermittent calibration. It involves the administration of a cold injectate in the superior vena cava (central venous catheter required) and its detection by a thermistor in the aorta or a major arterial branch (femoral, axillary, or brachial).
○ Other variables measured by this device are global end-diastolic volume (preload estimate), intrathoracic blood volume, extravascular lung water, and pulmonary vascular permeability index.
○ The LiDCOplus monitor uses lithium dilution technique to intermittently calibrate the system, generate a curve, and use a built-in equation to calculate CO based on pulse power rather than pulse contour analysis. This system uses a pulse pressure algorithm called PulseCO to obtain such analysis.
○ Uncalibrated: PulsioFlex is a monitor that uses a ProAQT sensor that connects to the peripheral arterial catheter and analyzes the arterial waveform 250 times per second. Patient’s characteristics (biometrics) are also inserted into the system. The LiDCOrapid system has the same technology as the LiDCOplus but instead of thermodilution uses nomograms for the calculation of the CO. PRAM (pressure recording analytical method) is based on a mathematical assessment of the pressure signal obtained from an arterial line (pulse contour analysis), without calibration, resulting in estimates of SV and therefore CO.The Nexfin monitor does not require an arterial line catheter. It uses an inflatable cuff around the middle phalanx of the finger that is able to generate a pressure waveform. Through a built-in software, the system is able to construct a brachial artery waveform based on the finger version, which is then used as the basis for calculation of continuous CO.The esCCO monitor uses a technology that derives the CO using the pulse wave transit time (PWTT), which is obtained by the pulse oximetry and the electrocardiogram signals in each cardiac cycle. It is also completely noninvasive, like the Nexfin system.
○ Others: Pulse Doppler technology uses esophageal or transthoracic Doppler probes to estimate CO by multiplying the cross-sectional area of the aorta by blood flow velocity. Applied Fick principle is used in the NICO system, which uses the calculation of carbon dioxide production and elimination every 3min to estimate CO.Electrical bioimpedance uses electric current stimulation to identify thoracic or body impedance variations induced by blood flow changes resulted from each heartbeat. The signal variation is analyzed by built-in algorithms, continuously providing the estimation of the cardiac output. Electrodes can be placed on the skin or endotracheal tubes. Devices that use bioreactance technique need further validation studies
- What is stroke volume variation?
> Stroke volume variation is a functional hemodynamic variable that estimates fluid responsiveness in ventilated patients with low preload and thus also aids in the guidance of fluid resuscitation therapies.
The concept is that cyclic changes in the intrathoracic pressure during positive pressure ventilation induce changes in SV and pulse pressure variation (PPV) secondary to multiple mechanisms.
SVV represents the variability of SV during a respiratory cycle, in which it increases during inspiration and decreases during expiration (the opposite occurs during spontaneous ventilation).
It is calculated by the following equation: SV max–SV min/SV mean.
A result of more than 13% (10–15%) suggests potential preload responsiveness
- Why is the stroke volume higher during the inspiratory phase of the respiratory cycle?
> In a given respiratory cycle, during mechanical ventilation, the initial effects of increased intrathoracic pressure cause a preload increase as blood is expelled from the lungs, an afterload decrease, a direct pressure of the expanded lungs on the heart assisting the pump effect, and an improved left ventricular compliance due to the volume decrease in the right chambers of the heart.
As the cycle progresses in what is called pulmonary transit time, those effects become overtaken by the gradual decrease on venous return, resulting in a decrease in SV.
Such variability is found to be more pronounced in under-resuscitated patients
- What is the relationship of stroke volume variation and the Frank-Starling curve?
○ In the zone of the ascending limb of the Frank-Starling curve, SVV is pronounced indicating low preload (fluid responsiveness).
○ In the shallow part of the curve, SVV is small, indicating no fluid responsiveness.
A 76-year-old female patient is in the postanesthesia care unit after an ORIF of an acetabular fracture. She underwent general anesthesia with an uneventful surgical procedure. You have been called to evaluate the rhythm above (Fig. 17.1).
Pulse 136, BP 110/50, and SpO2 97% on 2 L O2 via nasal cannula NKDA
Medical history: hypertension (takes amlodipine for it).
Preoperative vital signs SpO2 98%, blood pressure 140/90, HR 96, temp 36.4, EKG normal sinus rhythm, normal transthoracic echocardiogram.
1. How would you describe this rhythm?
○ This rhythm is atrial fibrillation (AF) with a rapid ventricular response.
○ The pattern is irregularly irregular.
○ The rhythm strip has no distinct p wave but instead many f waves (also known as fibrillary waves) followed intermittently by narrow QRS complexes.
- Name and define different types (based on occurrence and duration) of the arrhythmia shown above.
○ Lone atrial fibrillation
°An outdated term also known as idiopathic atrial fibrillation.
°It originally meant atrial fibrillation that occurs in a person 40 years or younger without intrinsic cardiac disease.
○ Paroxysmal atrial fibrillation
°AF that occurs spontaneously, lasts less than a week, and occurs at variable frequency.
○ Persistent atrial fibrillation
°Atrial fibrillation that lasts longer than 7 days.
°It may go away on its own or resolve with treatment.
○ Long-standing persistent atrial fibrillation
°AF lasting longer than 12 months.
°Permanent atrial fibrillation—more of a therapeutic decision between the patient and clinician to stop attempting to treat AF for conversion to sinus rhythm.
- What is the incidence of AF in the general population? What is the incidence after cardiothoracic surgery and after non-cardiac surgery?
○ Atrial fibrillation is the most common heart arrhythmia.
○ It affects an estimated 2.7–6.1 million people in the United States. About 2% of people over the age of 45 have atrial fibrillation, while 9% of people greater than age 65 have it. It is more likely after cardiac surgery and can affect from 10% to 65% of patients after cardiac surgery. ○ AF is rare after non-cardiac surgery and can affect about 1–3% of the patients. Patients who develop postoperative atrial fibrillation have higher morbidity and mortality rates and have higher costs of care.
A 76-year-old female patient is in the postanesthesia care unit after an ORIF of an
acetabular fracture. She underwent general anesthesia with an uneventful surgical
procedure. You have been called to evaluate the rhythm above (Fig. 17.1).
Pulse 136, BP 110/50, and SpO2 97% on 2 L O2 via nasal cannula NKDA
Medical history: hypertension (takes amlodipine for it).
Preoperative vital signs SpO2 98%, blood pressure 140/90, HR 96, temp 36.4, EKG normal sinus rhythm, normal transthoracic echocardiogram.
4. How would you treat this patient?
> Complete discussion of the treatment of atrial fibrillation is extensive, but some basic tenets can be kept for this patient’s new-onset AF.
(a) Correct manageable causes
(b) Rate and/or rhythm control
(c) Anticoagulation if CHADS2 and CHA2DS2-VASc (see description below)
scores indicate a benefit
○ Acute treatment of atrial fibrillation focuses on keeping the patient hemodynamically stable.
°Rate and rhythm control are of paramount importance.
°Symptomatic and unstable patients with mental status changes, chest pain, congestive heart failure, or hypotension should be treated with electrical cardioversion if rate control cannot be accomplished with intravenous medications.
○ A history and physical exam should be conducted.
°Special attention should be paid to cardiac and pulmonary comorbidities.
° Electrolytes, complete blood count, cardiac enzymes (troponin), thyroid studies (TSH and free T4), renal function, and chest radiograph should be obtained.
°A transthoracic echocardiogram should be performed to assess for causes of AF and to rule out a thrombus in the left atrial appendage.
°Consultation of a cardiologist may be necessary
°Rate control could be achieved using intravenous medications such as beta-blockers (BBs) like esmolol, metoprolol, or propranolol and nondihydropyridine calcium channel antagonists (CCAs) such as diltiazem and verapamil.
○ The effect of these medications is slowing of AV node conduction.
°Digoxin is not typically used for acute rate control and is more often reserved for chronic AF caused by heart failure (do not use beta-blockers in decompensated heart failure) or in patients
who do not respond to BBs or CCAs.
°Amiodarone may be used for patients whose atrial fibrillation is unresponsive to beta-blockers or the calcium antagonists.
○ Rhythm control strategies use electrical and chemical cardioversion.
○ Medications include amiodarone, flecainide, dofetilide, propafenone, ibutilide, and others.
○ Additionally, anticoagulation may be warranted in several different situations.
Some of these include
(1) when the patient remains in AF even after pharmacologic or electrical cardioversion attempts,
(2) if there are plans of cardioversion and the AF had an onset of >48 h, and
(3) to decrease the risk of stroke by providing antithrombotics 4 weeks after cardioversion
- What concerns are there whenever a patient with persistent AF is cardioverted?
○ There is a concern that a thrombus could be located in the left atrial appendage which could embolize to the brain and cause a stroke.
○ A transthoracic echocardiogram or transesophageal echocardiogram is usually performed to rule out the existence of a thrombus.
What are precipitants of postoperative atrial fibrillation?
○ Congestive heart failure
○ Dilated chambers on the left side of the heart
○ Ischemic heart disease
○ Age >65
○ Hypomagnesemia
○ Hyperkalemia
○ Hypokalemia
○ Anemia
○ Hypovolemia
○ Hypervolemia
○ Hypertension
○ Obesity
○ European ancestry
○ Diabetes
○ Hyperthyroidism
○ Chronic kidney disease
○ ETOH use
What are the CHADS2 and CHA2DS2-VASc scores?
○ The CHADS2 and CHA2DS2-VASc scores are (Fig. 17.2) clinical tools used to assess the risk of stroke in patients with or without atrial fibrillation.
○ Ultimately, the scores help determine the need for anticoagulation to prevent stroke.
○ The CHADS2 score is an acronym tool that assigns one or two points for each stroke risk factor (congestive heart failure, hypertension, age >75 years, diabetes, stroke/transient ischemic attack/thromboembolism).
○ The CHA2DS2-VASc is an updated version of the CHADS2 score.
°It gives two points for a patient >75 years of age and adds other risk factors such as vascular
disease (such as previous myocardial infarction, age 65–75, or female sex).
°CHA2DS2-VASc also includes heart failure with or without preserved ejection fraction under the C listing
- Is there any relation between neuraxial anesthesia and atrial fibrillation?
- > There are case reports that have documented the onset of atrial fibrillation with the placement of an epidural.
This is a rare occurrence and does not necessarily mean that the patient has underlying heart pathology. However, it would be prudent to perform a cardiac workup if atrial fibrillation is encountered in these patients.
A meta-analysis showed no clear benefit of reducing supraventricular tachyarrhythmias after placement of thoracic epidurals for cardiac surgery
- How does the treatment for Wolff-Parkinson-White syndrome with preexcitation AF differ from atrial fibrillation alone?
9.
○ Treatment with amiodarone, adenosine, digoxin, or nondihydropyridine calcium channel antagonists (diltiazem, verapamil) in patients with Wolff-Parkinson White syndrome who have preexcitement AF can cause an accelerated ventricular rate that leads to ventricular fibrillation.
○ Because of this danger, treatment with electrical cardioversion is usually a better choice for rate and rhythm control.
You are on the obstetrics ward. You are answering an “Anesthesia Stat” call to the
operating room. As you walk into the operating theater, this is the rhythm that is present on the vitals monitor:
A parturient, gravida 7 para 6 at 38 weeks gestation, was placed under general
anesthesia for an emergent C-section secondary to fetal bradycardia (Category III fetal heart rate tracings)
The anesthesiologist who performed the induction briefs you that a rapid
sequence induction included cricoid pressure, 100 μg of fentanyl, 120 mg of propofol, and 100 mg of succinylcholine administered intravenously. A grade I view of the airway was obtained with laryngoscopy and a #7 oral endotracheal tube placed without difficulty. Initially, ETCO2 was positive and auscultation of the lungs revealed bilateral breath sounds.
Preinduction vital signs were SpO2 100%, pulse 88, BP 110/56, temp 36.6, and
weight 55 kg.
1. How would you describe this arrhythmia?
If the EKG leads are attached and accurate, this is cardiac arrest presenting as pulseless fine ventricular fibrillation
- In general, what are the potential causes of this arrhythmia in parturients?
○ In 2015, the American Heart Association released its first statement regarding maternal cardiac arrest. In that statement they listed common etiologies of maternal arrest and mortality.
○ This list is a mnemonic of the letters A through H, most of which are listed below.
°Anesthetic complications - (neura xial, hypoxia, hypotension) and accidents/trauma (trauma and suicide)
°Bleeding—coagulopathy, placental causes, uterine atony and/or rupture, surgical causes
°Cardiovascular causes—myocardial infarction, cardiomyopathy, pulmonary hypertension, valvular disease, aortic dissection
°Drugs—oxytocin, magnesium, drug error (local anesthetic), illicit drugs, opioids, insulin, and anaphylaxis
*Note that many anesthetic drugs may cause prolonging of the QT interval (volatile anesthetic agents, ondansetron, antibiotics such as ciprofloxacin, erythromycin, etc.) which may result in ventricular fibrillation.
°Embolic causes—pulmonary embolism, amniotic fluid embolism, cerebro-vascular event
°Fever—sepsis and infections
°General—Hs and Ts (hypoxemia, hypovolemia, hypo-/hyperkalemia, hydrogen ion (acidosis), hypothermia, tension PTX, tamponade—cardiac, toxins, thrombosis—coronary, thrombosis, pulmonary)
°Hypertension—preeclampsia, eclampsia, HELLP syndrome, intracranial bleed
- What are the common causes and prevalence of maternal cardiac arrest?
> According to Suresh and colleagues, the major causes of maternal cardiac arrest are:
- Pulmonary embolism 29%
- Hemorrhage 17%
- Sepsis 13%
- Peripartum cardiomyopathy 8%
- Stroke 5%
- Preeclampsia-eclampsia 2.8%
Anesthesia complications (failed intubation, LAST, aspiration) 2% [1]
Mhyre et al. reported different findings for the Nationwide Inpatient Sample (NIS) from 1998 to 2011:
- Postpartum hemorrhage 27.9%.
- Antepartum hemorrhage 16.8%.
- Heart failure 13.3%.
- Amniotic fluid embolism 13.3%.
- Sepsis 11.2%.
- Anesthesia complications 7.8%.
Maternal cardiac arrest occurs in 1 in 12,000 hospitalizations for delivery.
- What are your next steps in managing this case? Maternal cardiac arrest
○ Help should be summoned by announcing maternal code blue.
○ In this cardiac arrest scenario, it is vital to start immediate cardiopulmonary resuscitation (chest compressions of 100–120 per minute, 2 inches in depth with full recoil, and the person doing compressions should switch every 2 min). ○ For a parturient with a uterus located at or above the umbilicus, a left uterine tilt of 15° should be instituted, or if enough help is available, a manual lateral tilt might provide better resuscitation results.
○ Maintaining the airway and avoiding hyperventilation is paramount.
*ACLS guidelines should be followed.
○ An AED or defibrillator should be obtained as quickly as possible, pads placed, and the patient defibrillated with the manufacturer recommended joules, 360 J if it is monophasic or the maximum amount of energy if the recommended energy is unknown.
○ Internal fetal monitors should be removed before defibrillation to reduce chances of team member electrocution.
○ Anesthetic gases should be discontinued and 100% oxygen administered. For the anesthesiologist, it is imperative to verify that the endotracheal tube is secured despite an easily placed airway.
○ Effective chest compressions should show EtCO2 of >10 mmHg.
○ A backboard may not be necessary on a minimally cushioned OR table but should be considered.
○ A person should be assigned to document the event.
○ Epinephrine 1 mg IV should be given after the second defibrillation and repeated every 3–5 min.
○ Amiodarone 300 mg IV may be administered for ventricular fibrillation resistant to defibrillation (after three shocks).
○ Intravenous access should be present above the diaphragm.
○ A crisis checklist should be used if available and team members are trained in using one.
You are on the obstetrics ward. You are answering an “Anesthesia Stat” call to the operating room. As you walk into the operating theater, this is the rhythm that is present on the vitals monitor:
A parturient, gravida 7 para 6 at 38 weeks gestation, was placed under general anesthesia for an emergent C-section secondary to fetal bradycardia (Category III fetal heart rate tracings).
The anesthesiologist who performed the induction briefs you that a rapid
sequence induction included cricoid pressure, 100 μg of fentanyl, 120 mg of propofol, and 100 mg of succinylcholine administered intravenously. A grade I view of the airway was obtained with laryngoscopy and a #7 oral endotracheal tube placed without difficulty. Initially, ETCO2 was positive and auscultation of the lungs revealed bilateral breath sounds.
Preinduction vital signs were SpO2 100%, pulse 88, BP 110/56, temp 36.6, and weight 55 kg.
5. What laboratory tests would you order to help in your management?
○If time permits an arterial blood gas or venous blood gas will permit quick assessment of electrolyte abnormalities, blood status, oxygenation, and ventilation status.
○ A transthoracic echocardiogram or transesophageal echocardiogram will allow quick assessment of the cardiac function.
○ A chest X-ray may help with assessment of the thorax.
- When should perimortem C-section start?
- Perimortem C-section should start at 4 min and the baby delivered by 5 min.
However, the obstetric team should prepare for Cesarean section before this time
An OR team member identifies an empty 250 mL bag of 0.25% ropivacaine and 2 μg of fentanyl per mL. With more investigation, the team realizes that this bag was accidentally brought into the OR and administered as “antibiotics.”
7. Knowing this information how would you manage the case?
- Local anesthetic toxicity treatment requires Intralipid 20% administered in an initial dose of 1.5 mL/kg infused intravenously with simultaneous high-quality CPR maintained.
○ A continuous infusion of 0.25–0.5 mL/kg/min is recommended.
○ Dosages of epinephrine should be decreased to 1 μg/kg.
○ Notify appropriate personnel for cardiac bypass
- Which medications would you avoid in treating this disorder? LAST
- ○ Medications to avoid in local anesthetic toxicity would be lidocaine (once a treatment for ventricular tachycardia or PVCs), calcium channel blockers, vasopressin, and beta-blockers.
○ Propofol should not be substituted for Intralipid
- Is there an upper limit to the amount of medicine/treatment that you would give in this situation? LAST
○ ASRA recommends an upper level of 12 mL/kg of lipid emulsion infused over 30 min.
○ Infusion longer than this may indicate other causes of cardiac collapse
A 71-year-old male with no known past medical history was admitted to the hospital
with a chief complaint of dyspnea on exertion, swollen legs, and frequent falls since
the last 3 weeks. On admission the patient had leukocytosis, bradycardia, and
hyponatremia, and an EKG showed second-degree AV block with 2:1 AV conduc-
tion. An EKG taken a few hours later is shown below.1. How will you interpret this EKG? (Fig. 19.1)
○ This EKG shows atrial (P waves) and ventricular (QRS complexes) activity which are independent of each other, and there is no association between P waves and QRS complexes.
○ That confirms that our patient has sinus rhythm with complete heart block (CHB).
Does this patient require any urgent intervention?
○ Our patient has ventricular rate of 46 beats per minute with narrow QRS complexes which indicate that blockade is around AV node or at the His bundle.
○ Even though our patient has frequent falls, currently he is hemodynamically stable.
○ This patient needs to be admitted to a telemetry bed for continuous EKG monitoring along with serial 12-lead EKG.
○ Cardiology consultation should take place as early as possible to determine the need for pacemaker placement, although an
immediate intervention may be needed if ventricular rate stays less than 40 bpm along with any of the following signs/symptoms:
(a) Hypotension
(b) Altered mental status
(c) Signs of shock
(d) Ischemic chest discomfort
(e) Acute heart failure
A 65-year-old female presents for emergency laparotomy in the middle of the night.
Her ECG is presented below.
What is shown in the above image?
○ The image shows a 12-lead ECG with pacing spikes before P waves (a spike) and QRS complexes (v spike), at a rate of 60/min indicating a dual chamber pacemaker.
What is shown in the above image?
- The image shows a 12-lead ECG with pacing spikes before P waves (a spike) and QRS complexes (v spike), at a rate of 60/min indicating a dual chamber pacemaker.
A 68-year-old man with hypertension and diabetes on an ACE inhibitor and insulin
presents for an AV fistula placement. He appears lethargic and complaints of nau-
sea. His ECG shows the following rhythm
1. What is concerning about this ECG?
○ The clinical scenario and presentation along with the ECG suggests hyperkalemia.
○ Hyperkalemia is defined as a potassium level >5.5 mEq/L.
°Moderate hyperkalemia is a serum potassium >6.0 mEq/L, and
°severe hyperkaliemia is a serum potassium >7.0 mE/L.
○ Easily distinguished ECG signs of hyperkalemia are:
□ Serum potassium >5.5 mEq/L [1]
°Peaked T waves
□ Serum potassium >6.0 mEq/L
°P wave widening and disappearance
°Prolongation of the PR interval
°QT interval shortening
□ Serum potassium >7.0 mEq/L
°ST changes (which may mimic myocardial infarction)
°Conduction block
°Wide QRS, which may progress to a sine wave pattern and asystole
What are the risks of anesthetizing a patient with this ECG?
○ Hyperkalemia alters cardiac conduction, increasing automaticity and enhancing repolarization.
○ The use of succinylcholine can dangerously aggravate hyperkalemia.
○ As the effects of hyperkalemia are aggravated by hypoventilation and acidosis, potassium must be lowered preoperatively; otherwise, the patients are at risk of developing ventricular premature contractions, ventricular tachycardia, fibrillation, and cardiac arrest.
- A 68-year-old male with type II diabetes mellitus being evaluated for inguinal
hernia surgery.
what is the diagnosis/abnormality?
Left bundle branch block (LBBB)
- A 65-year-old asymptomatic male with hypertension and COPD awaiting total
knee replacement.
Atrial fibrillation
- A 45-year-old asymptomatic female awaiting cholecystectomy.
Normal sinus rhythm. Normal ECG.
- A 68-year-old male with ischemic heart disease and diabetes mellitus type II
and presents with syncope.
○ Mobitz type II second-degree AV block.
○ PR intervals constant.
○ P waves blocked intermittently, PR intervals normal.
A 55-year-old asymptomatic male with chronic obstructive pulmonary disease
Right bundle branch block (RBBB).
○ QRS duration > 120ms
○ RSR’ pattern in V1-3 (“M-shaped” QRS complex)
○ Wide, slurred S wave in lateral leads (I, aVL, V5-6)
- A 40-year-old asymptomatic male with hypertension being treated with
beta-blockers.
Mobitz type I second-degree AV block.
○ PR intervals progressively prolonged until P wave is blocked.
A 24-year-old female with palpitations.
- Narrow complex tachycardia (SVT) at a rate of about 150 per minute.
○ Management:
° If the patient is stable, then vagal maneuvers followed (if unsuccessful) by adenosine 6 and 12 mg IV push (repeated twice if needed) followed by beta-blocker and an expert consult.
° Unstable (chest pain, hypotension, altered mental status) patients require synchronized cardioversion
- A 78-year-old male with type II diabetes mellitus and hypertension admitted
with facial trauma and complains of extreme fatigue and dizziness.
Complete heart block.
○ P-P intervals constant, R-R intervals constant but no relationship.
- A 60-year-old male with heart failure and reduced systolic function (EF 30%)
and history of syncope.
Wide complex tachycardia.
○Rate 188 per minute. Is it VT or SVT with aberrancy?
°Chapters have been written and there are algorithms for differentiating the two.
○ Generally, VT occurs in people over 35 years of age with heart disease or a family history of sudden cardiac death.
°VT is generally regular (maybe polymorphic Torsades) and demonstrates AV dissociation with occasional P waves showing
capture (SA node “captures” the ventricles producing a normal QRS) or fusion beats (sinus and a ventricular complex fuse to produce a hybrid complex) [4].
Brugada’s sign: Onset of QRS to the nadir of the S wave >100 ms.
Ultrasimple Brugada criterion: Onset of QRS to S nadir or peak R if
greater than 50 ms in lead II favors VT.
Management: If the patient is stable, then expert help can be sought or
amiodarone 150 mg over 10 min.
An unstable patient requires synchronized cardioversion.
○ Dextrocardia
- Occurs in 1:12,000 people.
- QRS negative in leads I and II (is it northwest axis?).
- aVR and aVL are reversed meaning the complexes are positive in aVR and negative in aVL.
- In the chest leads the R waves regress from V1 to V6.
○ The differential diagnosis is reversed arm leads which would show similar features, but the chest leads show normal R wave progression.
- A 45-year-old male awaiting ventral hernia repair. He was recently prescribed azithromycin for acute bronchitis.
- Normal sinus rhythm, prolonged QT.
○ Normal QT interval is 350–430 ms; prolonged QT is usually >440 ms.
○ QT interval varies with heart rate and several formulae exist for determining corrected QT (QTc).
°Bazett’s formula is the most widely used QTc=QT/ RRinterval.
○ QT prolongation can be inherited as in Romano-Ward or Jervell and Lange-Nielsen syndromes or acquired in a variety of clinical settings including electrolyte abnormalities, medications, acute intracranial event, or hypothermia.
○ Prolonged QT is a risk factor for developing polymorphic ventricular
tachycardia (Torsades de pointes).
- A 60-year-old female with end-stage renal disease on dialysis awaiting AV fis-
tula repair.
ST and T wave changes secondary to hyperkalemia.
- What does the above figure depict?
○ Figure 24.1 illustrates the different patterns of stimulation obtained when monitoring peripheral neuromuscular function.
○ The responses recorded serve as a guide during critical periods including intubation and recovery from a general anesthetic.
○ Neuromuscular monitoring should be always used as an adjunct to other clinical signs of muscle recovery, including grip strength, sustained head lift maneuver, and respiratory mechanics.
- The above sequence of waveforms was encountered during a line placement in a patient. Describe what you see.
○ When inserted, the PA catheter is first advanced through the sheath and at approximately 15–20 cm, the balloon is inflated.
○ Along this path the catheter will pass through the
(1) right atrium,
(2) the right ventricle, and
(3) the pulmonary artery, at which point, with slight advancement into a small arterial branch, it can obtain
(4) the pulmonary artery occlusion pressure.
○ The right atrial pressures (values 0–5 mmHg) will be similar to a central
venous tracing that varies with respiration.
○ A sudden systolic pressure increase (values 15–30 mmHg) confirms
entrance into the right ventricle.
○ Advancement into the pulmonary artery will result in a sudden increase in diastolic pressures (values 8–15 mmHg) confirming entrance into the pulmonary artery.
○ The pulmonary capillary wedge pressure (values 8–12 mmHg) will rapidly fall once the balloon is inflated and reveal a left atrial pressure waveform with a, c, and v waves, just like a central venous tracing except the waves appear later
- What information does the PA catheter provide?
○ The PA catheter provides a more precise left ventricular diastolic pressure estimation.
○ The right ventricular pressures do not correlate with pulmonary artery pressures distal to the occlusion point.
○ However, this is not true for the relationship PAOP, LAP, and LVEDP which correlate.
○ Theoretically at least, at end diastole no pressure gradient should occur, making end diastole the best time for pressures correlation.
○ The values obtained from the PA catheter are as follows [2]:
(a)Cardiac output (CO)—the only value measured (all the rest are calculated values).
• The cardiac output measurements are obtained by the thermodilution method, the basic principle being that the difference in temperature between the cold injectate and body temperature is inversely proportional to the pulmonary blood flow (cardiac output).
• Accuracy of measurements is directly dependent on the speed of injection and precise quantification of injectate volume and temperature.
• Once the average value of three measurements is obtained, calculations can provide the rest of the data derived from the PA catheter.
(b)Cardiac index(CO/BSA) where CO represents cardiac output and BSA is body surface area
(c)Systemic and pulmonary vascular resistance:
When is the pulmonary artery occlusion pressure (PAOP), also referred to as pulmonary capillary wedge pressure (PCWP), different from the left ventricular end-diastolic pressure (LVEDP)?
○ There are conditions when PAOP overestimates or underestimates the LVEDP.
Overestimation:
(a) Tachycardia (shortened diastolic filling time).
° At rates greater than 115/min, the pulmonary artery end-diastolic pressure (PAEDP) is greater than the PAOP.
(b) Increase in pulmonary vascular resistance (sepsis, pulmonary disease, obstruction to venous drainage).
(c) Mitral stenosis, atrial myxoma.
(d) Increased intrathoracic pressures (mediastinal tumors).
(e) Conditions associated with large PA v waves (large v waves may obscure catheter wedging with pulmonary artery rupture being a real danger).
> The normal PA waveform has an arterial waveform with an upward slope, a downward slope, and a dicrotic notch associated with the pulmonic valve closure.
> While the peak systolic wave on the PA tracing corresponds to the
electrographic T wave, by contrast, the large v waves occur after the electrocardiographic T wave.
> Large v waves on the PAC are seen in mitral regurgitation, VSD, and CHF.
Underestimation:
(a) Aortic regurgitation.
(b) Non-compliant left ventricle—transmyocardial filling pressure and LVEDP have a curvilinear relationship, therefore changes in left ventricular end-diastolic volume (LVEDV) will result in changes in the LVEDP based on the location on the curve.
° Of note, ventricular compliance is affected by vasoactive drugs, and beta-blockers.
(c) Pulmonary embolism.
(d) Right bundle branch block (delay in right ventricular systole).
(e) Pulmonary edema.
What do large v waves on the PA catheter tracing mean?
Large v waves are seen in
(1) myocardial ischemia,
(2) mitral regurgitation,
(3) decreased atrial compliance,
(4) or increased SVR.
The diastolic PAOP offers the best approximation for the LVEDP when large v waves are present.
How can you accurately interpret mixed venous oxygen saturation?
○ Fiber-optic PACs can be used to measure mixed venous oxygen saturation (SvO2).
○Mixed venous oxygen saturation is the percentage of oxygen bound to the hemoglobin returning to the right side of the heart.
○ It reflects the “leftover” oxygen after tissues have removed their needed oxygen (oxygen extraction).
○ Normal SvO2 values are 60–80% with a 10% change considered significant.
○ Low mixed venous oxygen saturation (SvO2) is caused by the following:
• Decreased oxygen delivery
– Low cardiac output
– Decrease in arterial oxygenation (SaO2)
– Decrease in hemoglobin concentration
• Increased oxygen consumption
– Hyperthermia
– Neuromuscular blocker re-dosing needed during anesthesia
○ High SvO2 is caused by the following:
• Increased O2 delivery (high FiO2, hyperoxia)
• Decreased O2 demand (hypothermia, neuromuscular blockade)
• High flow states (sepsis, liver disease)
○ Changes in SvO2 come early before changes in hemodynamics manifest.
○ A surrogate of SvO2 measurement the SvcO2 (normally being over 70%) is obtained from the internal jugular vein or subclavian vein and used to identify changes in a patient’s oxygen extraction.
○ An increase in extraction is the way tissue oxygen needs are met
when the amount of oxygen reaching tissues is decreased.
○ It is important to note, however, that a normal SvO2 value does not always reflect adequate oxygenation.
○ In situations such as carbon monoxide poisoning and sepsis,
○ SvO2 levels may be normal or high despite end-organ hypoxia.
○ The accuracy of the SvO2 values is affected by the optical intensity of the reflected light at the end of the catheter.
° This may be affected by physical factors such as migration of the catheter, its kinking, occlusion, or clot at the end.
° Signal quality indicator is displayed continuously on the monitor which should be used to evaluate the accuracy of the measurement.
- What is cerebral oximetry?
- Cerebral oximetry (CO) has been available to clinicians for more than two decades.
○ Currently this monitor can be used as a “first alert” of impending organ dysfunction.
○ The cerebral cortex is an area of the brain that is particularly susceptible to changes in the demand and supply of oxygen and has a limited oxygen reserve.
○ CO estimates the oxygenation of regional tissue by transcutaneous measurement thru the cerebral cortex.
- How does cerebral oximetry work? Is it similar to pulse oximetry?
○ Cerebral oximeters consist of adhesive sensors applied over the frontal lobes which both emit and capture reflected light based on near-infrared spectroscopy (NIRS).
○ CO depends on the ability of light to penetrate the skull to determine hemoglobin oxygenation from the underlying brain tissue according to the amount of light absorbed by hemoglobin.
○ NIRS uses two photodetectors with each light source.
○ Selective sampling of tissue beyond a specified depth beneath the skin is measured by the technology.
○ Near-field photodetection can be subtracted from far-field photodetection to provide selective measurements of tissue oxygenation.
○ Tissue sampling is mainly from venous (70–75%) rather than arterial (25%) blood (Fig. 10.1).
○ It is independent of pulsatile blood flow.
○ As opposed to pulse oximetry, which monitors arterial blood hemoglobin saturation (SpO2), cerebral oximetry monitors hemoglobin saturation in mixed arterial, venous, and capillary blood in cerebral tissue (SctO2). As a result SctO2 is determined by two physiologic considerations.
° The first is the proportional volumes of arterial, venous, and capillary blood in the
brain region illuminated by cerebral oximetry. SctO2 is higher if the sample has an increased ratio of saturated arterial blood to desaturated venous blood and conversely lower if the ratio is decreased. The volume percentage of each blood compartment is not fixed. It varies interindividually and possibly between different brain
regions of the same individual. It may also change with hypoxia, hyper-/hypocap-
nia, neural excitation, and vasoconstrictor administration [5].
° The second consideration is the balance between cerebral oxygen supply and
demand. Cerebral oxygen supply is determined by cerebral blood flow and arterial blood oxygen content. If arterial blood content is stable, an increase in CBF
will expand arterial blood volume and shift the volume ratio toward more arterial
blood.
○ Cerebral oxygen demand is determined by cerebral metabolic rate of oxygen. If cerebral oxygen supply is stable, an increase in cerebral metabolic rate of oxygen will expand venous blood volume ratio toward more venous blood.
○ These physiologic processes alter SctO2 readings.
○ When CMRO2, arterial blood content, and the volume percentage of different blood compartments are all relatively stable, SctO2 can be regarded as a surrogate of cerebral perfusion.
- What are normal values? What are abnormal values?
○ In this technology, near-field photodetection is subtracted from far-field photo-detection to provide selective tissue oxygenation measurement beyond a pre-defined depth.
○ Normal Sr02 baseline values would be 60–80%.
○ Generally speaking, greater than 25% decrease or 20% decrease from baseline or a SrO2 value less than 40% is considered a trigger for intervention
A patient is in pre-op holding with these vital signs.
HR 102 BP 135/88 RR 22 SaO2 89%.
Supplemental O2 6 L/min is administered by face mask with no improvement.
ABG: pH 7.42 PaO2 206 PaCO2 35 SaO2 100%.
The patient is asymptomatic with cyanosis, but an otherwise normal physical exam.
Why is the O2 saturation different between the pulse oximeter and the blood gas?
> There are three distinct methods of determining the oxygen saturation of blood.
The results may be interchangeable in healthy people, but different in
dyshemoglobinemias.
(a) Pulse oximetry utilizes the Beer-Lambert law, which states that light absorbance is proportionate to the concentration (c) of the light attenuating substance.
Oxyhemoglobin (O2Hb) and deoxyhemoglobin (HHb) have differing absorption of light.
Oxyhemoglobin (O2Hb) absorbs more at 940 nm and deoxyhemoglobin (HHb) more at 660 nm, and it is the ratio of absorption of light at 660 nm to 940 nm that determines the saturation, using an algorithm derived from healthy controls.
The SaO2 assumes the presence of only O2Hb and HHb, thus
SaO = cO2Hb/cO2Hb+ cHHb
*cO2HB is content of oxy Hb and cHHb is deoxy Hb.
It will be inaccurate if abnormal hemoglobin’s such as methemoglobin (MetHb) and carboxyhemoglobin (COHb) are present.
MetHb is absorbed at both 660 and 940 nm.
COHb is absorbed at 940 nm, similar to O2Hb
(b) In the arterial blood gas (ABG) analysis, the pH and partial pressure of oxygen in the blood are measured, and the saturation is calculated from the
standard oxygen dissociation curve.
(c) Cooximetry also utilizes the Beer-Lambert law.
Using multiple wavelengths of light, the concentrations of O2Hb and other Hb species are determined by their different absorption at various wavelengths (Fig. 9.1).
This allows the calculation of a fractional SaO2 or percentage of oxyhemoglobin as a percent of total Hb including abnormal species.
Fractional SaO2= O2x100/ O2Hb+HHb+MetHb
Cooximetry results for this patient measured 70% O2Hb, 29% MetHb,
and 1% COHb; thus, the fractional SaO2 would only be 70%. Only 70% of
the Hb is available for O2 transport.
What variants of hemoglobin are detected by the cooximeter?
Cooximeters measure absorbance at more than two wavelengths from a minimum of six to as many as 128.
○ Fractions of HHb, O2Hb, COHb, and MetHb are routinely measured.
○ Arterial or venous blood may be used. It is important to note the difference of O2 saturation versus fractional oxyhemoglobin in the presence of increased COHb or MetHb.
What does Fig. 11.1 represent? Describe the characteristics of various EEG waveforms
○ This is a bilateral, multichannel EEG recording, showing normal (i.e., non-pathologic) waveforms.
○ EEG signals originate from the pyramidal cells of the cerebral cortex. ○ Each EEG electrode can capture the electrical activity of the
underlying 1 in square cerebral cortex.
○ For this reason, multiple electrodes simultaneously recording several channels are required to get an overall representation of the electrical activity of the brain.
○ EEG signals are classified in four frequency bands. These are alpha (8–13 Hz), beta (>13 Hz), theta (4–7 Hz), and delta (<4 Hz) [1].
○ In a nonanesthetized individual, normal EEG can display waveforms that can fall in any one of these categories. However, location of the
recording (e.g., posterior vs frontal), age of the individual, and conscious state are all important factors to determine whether a particular frequency band can be regarded as normal or not.
Identify some of the dominant waveforms seen in Fig. 11.1.
○ There are predominantly beta and alpha frequencies in Fig. 11.1.
○ The solid vertical lines indicate 1 s intervals, which is crucial to determine frequency.
○ In the frontal channels (e.g., Fp1-F7), waveforms have low voltage with a frequency of greater than 13 Hz (i.e., more than 13 small waves between 2 vertical solid lines).
° These are beta waves.
○ On the other hand, posterior channels (e.g., T5-O1) pre-
dominantly display waveforms that have a higher voltage with a frequency in the 8–13 Hz range.
○ The ocular electrodes (last two channels) indicate closed eyes.
This is a normal pattern (i.e., alpha dominance in posterior channels) in healthy adults, who are awake with eyes closed.
○ There is symmetry between corresponding channels on the left and right hemispheres.
○ Therefore, this is a normal EEG.
- What does Fig. 11.2 represent? What is the significance of this EEG pattern for the anesthesia provider?
○ Figure 11.2 shows bursts of EEG activity interrupting an isoelectric waveform, commonly known as burst suppression pattern.
○ It can be observed secondary to high doses of certain anesthetic drugs (i.e., iatrogenic) or as a result of a disease process (i.e., pathologic).
○ Certain inhalation anesthetics (e.g., isoflurane, sevoflurane) can cause burst suppression of the EEG in the higher end of their dose range, typically around 1.3 MAC [2].
○ However, in elderly individuals or patients with severe coexisting severe systemic illness, burst suppression can be observed even around 1 MAC (age adjusted) [3]. Among intravenous anesthetics, barbiturates, propofol, and etomidate can result in burst suppression of the EEG at high plasma concentrations.
○ Short periods of burst suppression can be unintentionally observed during the course of an anesthetic. However, it can be specifically aimed to provide brain protection during procedures in which ischemic brain injury is possible. ○ An example to this is temporary clip application during cerebral aneurysm clipping. This is usually achieved by a continuous infusion of an intravenous agent such as pentobarbital.
○ Burst suppression secondary to underlying pathology is usually an ominous sign and can be seen in critically ill patients with hypoxemia and hypotension [4].
