Monitoring Flashcards

Question

7. What is stroke volume variation?

Answer 1

> 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

Answer 2

> 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

Answer 3

○ 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.

Answer 4

○ 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.

Answer 5

○ Lone atrial fibrillation °An outdated term also known as idiopathic atrial fibrillation.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.

Answer 6

○ 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.

Answer 7

> 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

Answer 8

○ 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.

Answer 9

○ 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

Answer 10

○ 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

Answer 11

8. > 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

Answer 12

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.

Answer 13

If the EKG leads are attached and accurate, this is cardiac arrest presenting as pulseless fine ventricular fibrillation

Answer 14

○ 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

Answer 15

> 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.

Answer 16

○ 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.

Answer 17

○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.

Answer 18

6. 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

Answer 19

7. 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

Answer 20

8. ○ 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

Answer 21

○ 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

Answer 22

○ 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).

Answer 23

2. ○ Ventricular rate can help determine the site of block in conduction system. ○ Junctional rhythm tends to have a ventricular rate between 40 and 60 beats per minutes (bpm), while ventricular escape rhythm will have rates of 40 beats per minute or less, and they are often unstable, requiring immediate cardiology intervention [1]. ○ In most cases, the atrial rate will be faster than the ventricular escape rate, and as a general rule, the more distal the level of block in AV conduction and His-Purkinje system, the slower the ventricular rate will be. ○ If EKG shows: (a) Narrow QRS complex with junctional or AV nodal rhythm, then the AV block has occurred within the AV node or at the level of the bundle of His. (b) Wide QRS complex with subjunctional escape rhythm, then the AV block is distal to the His conduction system

Answer 24

○ 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

Answer 25

Major causes of CHB can be divided into two categories: (a) Pathologic causes: • Myocardial ischemia involving the conduction system • Cardiomyopathy • Fibrosis and sclerosis of conduction system (e.g., amyloidosis, sarcoidosis) • Myocarditis (e.g., Lyme disease) • Congenital heart disease • Endocarditis with abscess formation • Hyperkalemia • Increased vagal tone (b) Iatrogenic causes: • AV nodal blocking medications (e.g., digitalis, calcium channel blockers, amiodarone, adenosine) • Post-cardiac surgery • Post-catheter ablation • Transcatheter aortic valve implantation • Transcatheter ablation of ventricular septal defect (VSD) • Alcohol septal ablation of hypertrophic obstructive cardiomyopathy (HOCM)

Answer 26

5. ○ After excluding all reversible causes of CHB, if surgery is not urgent, then an intracardiac His bundle study can be done in order to determine the need for permanent pacemaker placement (PPP). ○ If HV interval (the interval from the His bundle to the right ventricle) is greater than 100 ms, then PPP is required prior to surgery, but if HV interval is normal or 60–100 ms, then PPP may not be needed; however, central venous access (internal jugular) is recommended before proceeding to surgery for transvenous pacing if needed.

Answer 27

6. ○ A temporary transvenous pacemaker or transcutaneous pacemaker should be placed and checked before proceeding with urgent surgery. ○ All drugs and equipment, necessary for cardiopulmonary resuscitation, should be readily available in the operating room. ○ It is also recommended that defibrillator pads are applied to the patient.

Answer 28

○ In addition to standard ASA monitors, an arterial line will be helpful in a patient with poor ventricular function. ○ The EKG monitor should be set to diagnostic mode. ○ In order to minimize interference from electrocautery, if patient has permanent pacemaker in situ, then the grounding plate should be placed as far from the pacemaker generator as possible. Bipolar cautery should be used, limiting its power output in those cases.

Answer 29

○ 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.

Answer 30

1. 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.

Answer 31

○ The definition of pacemaker dependency varies in the literature. It can be defined as the absence of an intrinsic (or escape) rhythm for 30s during temporary pacing at 30 beats per minute with the pacemaker switched off. ○ To determine if the patient is pacemaker dependent, it is essential to identify the indication for the pacemaker implantation (complete heart block and syncope, for instance, would infer dependency). ○ In addition, pacemaker interrogation in pacemaker-dependent patients would reveal pacing 100% of the time.

Answer 32

○ This is nomenclature describing the pacemaker therapy modes. ○ Permanent pacemaker nomenclature is based on recommendations by the North American Society of Pacing and Electrophysiology (NASPE) and by the British Pacing and Electrophysiology Group (BPEG). ○ AAI pacemaker is useful for sinus bradycardia if the AV node function is normal. ○ VVI pacemaker is useful in atrial fibrillation with slow ventricular response. ○ DDD is useful if there is complete AV block with a normal sinus node. ○ Pacing modes with AV synchrony are AAI, DVI, DDI, and DDD. ○ Pacing modes that sense atrial activity and trigger ventricular activity are VAT, VDD, and DDD. °They are used during slow ventricular rates or AV nodal block. °These modes are synchronous modes. ○ Asynchronous modes AOO, VOO, and DOO are not inhibited by the electrical activity of the heart or other exogenous electrical activities (cautery) in contrast to synchronous modes like DDD or VVI which are inhibited. Asynchronous mode is used in emergency situations like in the operating rooms by converting AAI to AOO, VVI to VOO, or DDD to DOO.

Answer 33

○ Rate modulation comes into play when metabolic demands are to be met during conditions such as exercise where physical activity increases. ○ With conventional pacemakers, heart rate functions at a set rate, but pacemakers with rate modulating function adjust the paced rate based on the patient’s activity. ○ This is achieved by using sensors like accelerometer to sense motion or by using sensors to calculate thoracic impedance or minute ventilation.

Answer 34

○ The pacemaker syndrome is an iatrogenic condition that occurs as a sequel of ventricular pacing (e.g., VVI). ○ One postulated mechanism is loss of atrio- ventricular synchrony. ○ Symptoms of this syndrome include lethargy, palpitations, hypotension, and syncope. ○ The symptoms of this syndrome overlap with those encountered with pacemaker malfunction; thus excluding pacemaker malfunction is the first step when this syndrome is suspected. ○ Restoration of atrioventricular synchrony results in remission of the symptoms

Answer 35

○ Biventricular pacemaker is used when the right ventricular and the left ventricular activities are asynchronous. It is achieved by three leads (right atrium, right ventricle, and coronary sinus (to pace the left ventricle)). ○ The indication for Bi-V pacing (cardiac resynchronization therapy) with the highest level of evidence is EF ≤ 35% and sinus rhythm with LBBB and QRS duration 150 ms or more and NYHA II–III or ambulatory IV (class I indication). ○ Other indications with lower level of evidence also exist, but a full discussion of the guidelines is beyond the scope of this chapter. It is not indicated (no benefit) for patients with NYHA I–II symptoms, non-LBBB pattern with QRS duration less than 150 ms

Answer 36

○ Cautery current or other external electrical signals are inappropriately recognized as native cardiac activity, and pacing is inhibited (oversensing). ○ Magnets are placed over pacemaker generator to turn off sensing and hence convert them from synchronous to asynchronous or fixed-rate (usually 70–90/min depending on programming and battery life) mode

Answer 37

○ In unipolar cautery the current flows from the generator to the coagulation or cutting end of the cautery tip to the tissues and then through the body to the cautery plate and back to the generator. ○ In bipolar cautery the current flows from the generator to the tip of the bipolar cautery holding the tissues and back to the generator via the opposite tip. ○ As the distribution of current is limited to the cautery tips and tissue held within, electrical interference is restricted minimizing potential pacemaker malfunction

Answer 38

○ Emergency surgery in the middle of the night does not provide much time or access to the CIED team to interrogate and ascertain pacemaker function or dependency. ○ For the purpose of this emergency laparotomy where the top of the incision will probably extend to within 6 inches of the pacemaker generator, it would be safe to assume pacemaker dependency and proceed with the following plan—an arterial line, a magnet over the generator, communication with the surgeon regarding the need for short bursts with the electrocautery, and having external pacing equipment available nearby

Answer 39

○ 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

Answer 40

○ The common reasons that bring about hyperkalemia are: °Excessive intake: oral or intravenous supplementation, salt substitute, and blood transfusions °Decreased excretion: diabetic nephropathy, renal failure, congestive heart failure, hypoaldosteronism, systemic lupus erythematosis, and medications, e.g., ACE inhibitors, NSAIDs, and diuretics °Shift from intra- to extracellular space: hyper osmolality, rhabdomyolysis, malignant hyperthermia (MH), tumor lysis, succinylcholine administration, insulin deficiency, or acuteacidosis °Pseudohyperkalemia: improper blood collection and lab error

Answer 41

○ Stabilize myocardial membrane with the administration of calcium. ○ Drive extracellular potassium into the cells with insulin and glucose, beta-adrenergic agonists (albuterol), or sodium. ○ Eliminate potassium from the body with loop diuretics or dialysis. °Sodium polystyrene sulfonate (kayexalate) may be used for non-emergent management

Answer 42

○ 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.

Answer 43

Left bundle branch block (LBBB)

Answer 44

Atrial fibrillation

Answer 45

Normal sinus rhythm. Normal ECG.

Answer 46

○ Mobitz type II second-degree AV block. ○ PR intervals constant. ○ P waves blocked intermittently, PR intervals normal.

Answer 47

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)

Answer 48

Mobitz type I second-degree AV block. ○ PR intervals progressively prolonged until P wave is blocked.

Answer 49

7. 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

Answer 50

Complete heart block. ○ P-P intervals constant, R-R intervals constant but no relationship.

Answer 51

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.

Answer 52

○ 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.

Answer 53

12. 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).

Answer 54

ST and T wave changes secondary to hyperkalemia.

Answer 55

○ 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.

Answer 56

2. ○Neuromuscular function is monitored intraoperatively by evaluating the muscular response to supramaximal stimulation of a peripheral motor nerve. ○There are two kinds of stimulation: electrical and magnetic. °Electrical nerve stimulation is used most commonly clinically. °Magnetic stimulation has a theoretical advantage of not being painful and not requiring body contact. °However, the bulk of the equipment and difficulty monitoring the train-of-four responses to stimulation preclude its practical use in the operating room.

Answer 57

○ The reaction of a single muscle fiber to an electrical stimulus is an all-or-none occurrence. ○ The response of the muscle will decrease depending on the number of muscle fibers blocked in response to a neuromuscular blocking agent. ○ The electrical stimulus applied should be 20% to 25% above that necessary for a maximal response to obtain a consistent response. This supramaximal stimulation, although painful, is possible during anesthesia. ○ A current of uniform amplitude (20–60 mA) at a short duration (0.1–0.2 ms) is applied to a peripheral nerve and the motor response is observed. ○ Common sites include facial nerve (facial twitch) and ulnar nerve (thumb abduction). ○ A current of greater than 0.5 ms will cause direct muscle stimulation which is not optimal. ○ Assessment is most commonly by tactile or visual method of elicited muscle twitches. While this is the most practical method, it is subjective and not accurate. ○ Objective methods including electromyography, acceleromyography, and mechanomyography will give a more accurate assessment compared to tactile responses. ○ The peripheral nerve stimulator should be able to generate 60 to 70 mA, be battery operated, and alarm if the current is not being delivered. ○ The stimulator should be able to deliver single-twitch stimulation, TOF, and double-burst, tetanic stimulation and have a time constant to facilitate a posttetanic count.

Answer 58

There are five patterns of stimulation: (a) Single-twitch stimulation: • A single supramaximal electric current is applied at a frequency ranging from 1.0 Hz (one every second) to 0.1 Hz (one every 10 s). (b) Train-of-four stimulation: • Four stimuli at 2 Hz are applied (four stimuli in 2 s) that are repeated every 10 to 12 s if needed. • The ratio of the fourth response to the first response (T4/T1 ratio) is used to assess the presence of neuromuscular blockade and its degree. • In the absence of neuromuscular block, the ratio is 1. • During a nondepolarizing block, the ratio decreases in proportion to the degree of the block. • A depolarizing block, on the other hand, decreases all the four responses equally with TOF ratio of 1. ° A decrease in the TOF ratio after the administration of succinylcholine is indicative of phase II block. •TOF value of 0.70 is associated with impaired respiratory muscle function, hypoxia, and aspiration in the immediate postoperative phase. ° Neostigmine is given only when the TOF count has returned spontaneously to three and preferably four responses. • The availability of sugammadex as a reversal agent does not obviate the need for monitoring. ° The appropriate dose of sugammadex is adjusted according to the TOF and posttetanic stimulation responses. (c) Tetanic stimulation: • A stimulus of 30, 50, 100, or 200 Hz is applied for 5 s and the response of the muscle is recorded. • The response of the muscle to this stimulus is sustained both in normal neuromuscular transmission and in a depolarizing block. • The response however is not sustained in a nondepolarizing block and a phase II depolarizing block. • The decrease in the response is called fade and is caused by depletion of acetylcholine stores over time and is directly proportional to the degree of neuromuscular blockade. • Posttetanic facilitation is caused by an increase in the muscle response when stimulated right after tetanic stimulation. ° This is caused by mobilization and synthesis of acetylcholine to give a stronger response. • The degree of posttetanic potentiation is also dependent on the degree of neuromuscular block. • The major disadvantage of tetanic stimulation is that is it painful and only applicable in an anesthetized patient (Fig. 24.1C and D). (d) Posttetanic count stimulation: • When response to TOF and single-twitch stimulation is absent due to high degree of neuromuscular block, posttetanic count stimulation can be used to determine the degree of blockade. • A tetanic stimulation (50 Hz for 5 s) is applied, and the posttetanic response to single-twitch stimulation given at 1 Hz starting 3 s after the end of tetanic stimulation is observed. • During very intense blockade, there is no response to either tetanic or posttetanic stimulation. • The first response to posttetanic twitch stimulation occurs as the block begins to dissipate. •The time until the return of the first response to TOF stimulation is related to the number of posttetanic twitch responses present at a given time (the posttetanic count). (e) Double-burst stimulation: ○ DBS consists of two short bursts of 50-Hz tetanic stimulation separated by 750 ms. ° The duration of each square wave impulse in the burst is 0.2 ms. ○ The most commonly used is DBS with three impulses in each of the two tetanic bursts. • In the absence of neuromuscular blockade, the response to DBS is two short muscle contractions of equal strength. ○ In nondepolarizing block, the second response is weaker than the first. • DBS allows for detection of small amounts of residual blockade during emergence and in the postoperative period. ○ The DBS response is more easily felt than TOF making it a superior option. ○ As with all modalities of testing, the frequency and duration should be kept constant for the entire operative time (Fig. 24.1E).

Answer 59

○ The ulnar and fascial nerves are the most common sites used for peripheral nerve stimulation. ○ Other sites include common peroneal and posterior tibial nerves. ○ In the case of ulnar nerve, the electrodes are placed on the volar surface of the wrist with the negative electrode 1 cm proximal to the wrist on the ulnar nerve and the positive electrode 2–5 cm proximal to it, and the response to adductor pollicis is recorded. ○ In the case of fascial nerve, the negative electrode is placed directly over the fascial nerve and the positive electrode is placed over the forehead and response of orbicularis oris and corrugator supercilii muscles is recorded.

Answer 60

○ The diaphragm is the most resistant muscle to neuromuscular blockade; however, it recovers the fastest compared to the hand muscles. ○ The most sensitive muscles include the abdominals, the muscles of the extremities, and upper airway. ○ The response to facial nerve stimulation mimics the response of laryngeal muscles; however, an adequate response might not be an indicator for extubation as the peripheral muscles might still be blocked. ○ Reliance on facial muscles is associated with an increased incidence of postoperative residual neuromuscular block in the PACU. ○ A normal response from the ulnar nerve would ensure that the muscles of the diaphragm and larynx have completely recovered. ○ On the other hand, an absent response during intubation may not ensure appropriate intubating conditions.

Answer 61

7. ○ The tactile and visual responses are subject to human error especially when the TOF ratio is greater than 0.4. ○ Quantitative monitoring techniques give a more precise assessment of neuromuscular blockade especially during emergence, before, and after neostigmine administration. ○ There is good emerging evidence that objective monitoring performed perioperatively ensures both a TOF greater than 0.9 and a subsequent decrease in the incidence of postoperative residual paralysis. ○ The techniques include mechanomyography (MMG), electromyography (EMG), acceleromyography (AMG), and phonomyography (PMG). > AMG measures the isotonic acceleration of the stimulated muscle. ° It uses a small piezoelectric transducer, which is attached to the stimulated muscle. > The movement of muscle generates voltage in the piezoelectric crystal, which is proportionate to the acceleration of that muscle. ° The signals are analyzed and recorded. ° The monitors are small, portable, and easy to use. ○ PMG measures low-frequency sounds that are generated by the contraction of skeletal muscles, and MMG measures force of the contraction to indicate the degree of neuromuscular blockade. ○ While all these techniques give you quantitative measures, they cannot be reliably compared to each other.

Answer 62

○ 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

Answer 63

○ 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:

Answer 64

○ PA catheter data may be unreliable due to intrathoracic pressure variations. ○ Balloon inflation will not occlude capillaries unless it is placed in West lung zone III (arterial pressure exceeds venous, which exceeds alveolar pressure), wherethe capillaries can remain open. ○ Placement in zone I or II can obstruct blood flow rendering the readings inaccurate, reflecting alveolar rather the pulmonary occlu-sion pressures. ○ Thus, it is important to remember that intravascular volume depletion or PEEP, for example, may convert a lung zone III to a zone II (alveolar pressure exceeds arterial pressure), thereby affecting the readings. ○ This may also occur during any ventilation management in which there is insufficient expiratory time (air trapping or inverse ratio ventilation). ○ Pressures are evaluated at end expiration to minimize the effect of pleural pressures on intracardiac pressures.

Answer 65

○ 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.

Answer 66

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.

Answer 67

○ 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.

Answer 68

Indications for PAC use include the following: • Cardiac conditions—valvular disease, myocardial ischemia management, evidence of heart failure • Fluid management for shock, sepsis, acute burns • Pulmonary artery hypertension management • Obstetric conditions—placental abruption ○ Contraindications include left bundle branch block (insertion when this is present will trigger complete heart block) and certain arrhythmias such as WPW or • Epstein’s anomaly due to the possibility of inducing tachyarrhythmias. ○ Evidence, Outcome: UK National Health Service PAC-Man (PAC in patient management in ICU)—no difference in hospital mortality in groups managed with and without a PAC. ESCAPE (Evaluation Study of Congestive Heart Failure and PAC Effectiveness) trial—no difference in hospital mortality and length of hospital stay in groups using clinical judgment and PAC compared with clinical judgment alone. ○ Complications: Incidence of complications was 10% in the PAC-Man and 5% in the ESCAPE studies. Any prolonged use, over 48h, has been associated with complications that range from arrhythmias (particularly on insertion), clot development, or infections to serious ones rarely, such as pulmonary artery rupture. Concluding comments: ○ Judicious data interpretation should be used when evaluating the PA catheter information. Aside from the potential errors mentioned above, there are a few pitfalls associated with hemodynamic indices’ interpretation worth mentioning: 1. Adjusting SVR to body weight or using RAP in certain calculation (e.g., septic shock where large beds of capillaries are removed increase arteriolar resistance but not tone). 2. Careful evaluation of contractility indices (left and right ventricular stroke work indices) needs to be performed to avoid underestimation of contractility (when PAOP is different from LVEDP).

Answer 69

1. 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.

Answer 70

○ 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.

Answer 71

Clinical Scenarios: ○ Cardiac Surgery • Multiple clinical outcome studies support the concept that CO may allow clinicians to use the brain as an index organ that points to the adequacy of tissue perfusion and oxygenation of other vital organs. • Data from the Society of Thoracic Surgeons (STS) National Database strongly suggest that the intraoperative use of CO in cardiac surgery patients frequently (23%) served as a “first alert” indicator of an intraoperative dynamic that could lead to potential adverse Clinical outcomes in both adult and pediatric patients. • The cerebral frontal cortex is a vulnerable watershed tissue that is sensitive to small decreases in oxygen saturation and therefore can provide an “early warning” about compromised oxygen delivery to the rest of the brain and other major organs. ○ Patients whose saturations fell below 75% of preoperative levels and who were treated spent less time in the ICU and had less morbidity/mortality than the untreated group. • Cerebral oximetry has been shown to predict the lower limits of autoregulation during cardiopulmonary bypass. • Real-time monitoring of rSO2 provided more accurate information than routine blood pressure monitoring in identifying the lower limit of autoregulation. ○ Cerebral Vascular Surgery, Geriatric Surgery, and Thoracic Surgery Cerebral oximetry preinduction value and/or an intraoperative decrease in rSO2 value can guide in advance decisions regarding blood pressure manipulation or elective shunting for carotid endarterectomy. ○ For cerebral vascular disease, a cutoff value of 25% or 20% below baseline for prolonged hypoperfusion is used to opt for shunting . ○ Aggressively treating values that fall below 75% of baseline rSO2 in general surgery and geriatric patients improved or maintained scores on the Mini-Mental State Examination at postoperative day 7 and reduced the length of stay in the postanesthesia care unit. ○ Early cognitive dysfunction after thoracic surgery with single lung ventilation was found to be directly related to intraoperative decline of rSO2. ○ Trauma NIRS cerebral oximetry has been found to correlate with cerebral blood flow in trauma patients with brain injuries . • This monitor has found a use in trauma patients on the scene and en route to the hospital providing valuable information. • Cerebral oximetry may be a useful technique for predicting mortality and/or adequacy of CPR from cardiac arrest. ○ Heart Failure and ECMO • In heart failure patients, rSO2 may be a potential important biomarker and useful monitor of target organ perfusion. • When ECMO must be used for a pro-longed period of time, brain perfusion in the setting of normal vital signs is undetermined. Sensors measuring rSO2 can be placed on the forehead and lower extremities to monitor perfusion. • When rSO2 values drop to below 40 or greater than 25% of baseline, interventions such as fluid administration, increase in ECMO flow, vasopressors, or replacement of a functioning distal perfusion catheter can be initiated to reduce the incidence of stroke or limb ischemia . ○ Beach Chair Position • This is an emerging area of cerebral oxygen saturation monitoring. • Cerebral malperfusion may be unappreciated in this setting. Blood pressure monitoring may not be optimal, head position may impede cerebral venous drainage thereby decreasing CBF, and positive pressure ventilation impedes an already compromised decreased venous return to the heart because of beach chair positioning.

Answer 72

○ 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

Answer 73

○ The guiding principle in the treatment of cerebral desaturation (Fig. 10.2) is to increase oxygen delivery to the brain and/or decrease cerebral metabolic rate of oxygen utilization. ○ Ways to augment CBF include: (a) Increasing cerebral perfusion pressure if it is below the lower limit of cere-bral autoregulation and autoregulation is intact (b) Increasing cerebral perfusion pressure irrespective of the lower limit if auto-regulation is impaired (c) Augmenting cardiac output (d) Avoiding hyperventilation and hypocapnia, maintaining PaCO2 greater than or equal to 40 mmHg (e) Administering a cerebral vasodilator (f) Using inhalational anesthetic agents based on their intrinsic cerebral vasodilating properties at less than 1 MAC (g) Checking head position to assure optimal cerebral venous outflow (h) Augmenting cerebral venous drainage with 30 degree reverse Trendelenburg position. > Additionally, interventions capable of improving arterial blood oxygen content such as increased inspired oxygen fraction and red blood cell transfusion should be considered to boost oxygen delivery to the brain. > On the consumption side, deepening anesthesia causes a progressive decline in cerebral metabolic rate of oxygen until EEG becomes isoelectric. > Too deep of an anesthetic though causes hypotension and abolishes autoregulation which would be counterproductive. > Interventions depending on the clinical scenario but would include: Cardiac Surgery: correction of patient or cannula positioning, increasing blood pressure, increasing cardiac output or CPB flow to greater than 2.5 L/m2/min, increasing FI02, increasing PaC02 to >40 mmHg by decreasing minute ventilation or decreasing oxygenator fresh gas sweep flows during CPB, administering anesthesia and/or muscle relaxants as indicated, and administering a red blood cell transfusion if the hematocrit is <20%. > Carotid Endarterectomy: all of the above maneuvers aside from those related to CPB would be appropriate. Additionally, if rSO2 values are particularly low on the one side or the other, elective shunting would be indicated for the proce-dure rather than just clamping the vessel.

Answer 74

> Essentially any pharmacologic or anatomic abnormality which might involve blood flow, hemoglobin abnormalities affecting light absorption in the same spectra as NIRS, or distance between the near and far-field photodetection. > Variations in oximeter design, use of systemic vasoconstrictors, and underlying skin pigmentation may affect the accuracy of cerebral oximetry readings. > Deeper anatomical structures such as the skull and frontal sinus may also play a role. Hyperostosis frontalis interna with the resultant shallow frontal sinus may cause unreliable rSO2 readings. > With skull thickness causing low readings, moving the oximeter probes to a more lateral or more cephalad positions where the skull is not as thick or the sinus as superficial might improve readings. > Bilirubin dampens the spectrophotometry determined cerebral saturation at 733 and 809 nm. Normal absorption spectra for this technology are 700 to 1000 nm. A bilirubin level of 370 mmol/L, tissue pigment deposits, or both may render cerebral oxygen saturation impossible

Answer 75

7. Current devices approved by the FDA for CO monitoring include: INVOS (Somanetics Corporation, Troy, MI, recently COVIDIEN, Boulder, CO) FORE-SIGHT (CAS Medical Systems, Inc., Branford, CT) EQUANOX (NONIN Medical, Inc., Minneapolis, Minn.)

Answer 76

○ A sensor in the form of a probe is generally placed on the finger, toe, or earlobe of the patient. ○ The probe has diodes which emit light of two different wave lengths—660 nm in the visible red light range and 940 nm in the infrared range in a rapid on—off mechanism. ○ The oxygenated hemoglobin allows red light through and absorbs infrared light, while the deoxygenated hemoglobin allows infrared light through and absorbs more red light. ○ The ratio of oxygenated to deoxygen-ated hemoglobin determines the amount of red and infrared light absorbed which is read by a sensor attached to a photodetector. ○ Comparison of their absorption at these wavelengths enables the oximeter to calculate the oxygen saturation which is read during the pulsatile component of the blood. ○ The microprocessor displays SpO2, heart rate, and a plethysmograph on the screen.

Answer 77

○ Pulse oximeters work on the principle of absorption spectrophotometry explained by Beer’s and Lambert’s laws. ○ Beer’s law states that the absorption of radiation by a given thickness of a solution of a given concentration is the same as that of twice the thickness of a solution of half the concentration. ○ Lambert’s law states that each layer of equal thickness absorbs an equal fraction of radiation which passes through

Answer 78

○ Isosbestic points are wavelengths at which both oxyhemoglobin and deoxyhemoglobin absorption is similar which is 808 nm, and the absorbance at this point depends only on the hemoglobin concentration. ○ Earlier pulse oximeter models used a wavelength at an isosbestic point to compensate for hemoglobin concentration but newer models use various wavelengths.

Answer 79

Common sources of error: • Strength of Arterial Pulse: Any factor that reduces arterial pulsations will reduce the ability of the instrument to obtain and analyze the signal, hypothermia, hypotension, and vasopressor use. • Body Movement: Extraneous movements can cause interference—shivering and Parkinsonian tremors. • Carboxyhemoglobin (CoHb): CO binds to heme competitively with 250 times the affinity of oxygen, and COHb has the same absorption pattern of 660 nm light as O2Hg causing artificial high SpO2 readings. • Methemoglobin: Methemoglobin absorbs as much 660 nm red light as it does the 940 nm infrared. Saturation approaches 85% and is falsely low at high SpO2 and falsely high at low SpO2 • Methylene blue, indigo carmine, and indocyanine green cause a drop in SpO2. • Color Interference: Pulse oximetry is not affected by skin color but is affected by artificial or opaque nail finishes that may interfere with transmission of light. • Physical factors like electrocautery and restriction of blood flow during BP cuff inflation. • Venous pulsations secondary to AV fistulas. • Saturations below 80% are inferred and the saturation is overestimated.

Answer 80

Some of the common signs and symptoms of hypoxemia are: • Restlessness • Altered or deteriorating mental status • Increased or decreased pulse rate • Increased or decreased respiratory rate • Decreased oxygen oximetry readings • Cyanosis (late sign)

Answer 81

7. > Additional information received from pulse oximeter include heart rate and perfusion index if the oximeter is designed with this special feature. > Pleth variability index (PVI) is an automatic and continuous monitor of the respiratory variation of the pulse oximeter’s plethysmographic waveform amplitude. > This has been shown to predict fluid responsiveness noninvasively in mechanically ventilated patients.

Answer 82

○ Ratio between the pulsatile and the nonpulsatile blood is used to measure the perfusion index (PI) in the peripheral tissues. ○ Optimum monitoring sites may be chosen based on relatively high PI. ○ Another use would be a spike in PI indicating that epidural anesthesia has initiated peripheral vasodilatation which occurs before the onset of anesthesia.

Answer 83

> 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.

Answer 84

○ Cooximetry may be indicated if cyanosis or hypoxia measured by pulse oximetry fails to improve with O2 administration or if there are discrepancies between O2sat and PaO2 by ABG. ○ It is also indicated for suspected carbon monoxide exposure. ○ The cooximeter measures absorption at multiple wavelengths and can measure the concentration of many different Hb species. ○ Pulse cooximetry applies multiple wave lengths of light to measure dyshemoglobins such as COHb and total hemoglobin concentration. ○ They are not yet as accurate as a lab cooximeter and should be confirmed by the lab.

Answer 85

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.

Answer 86

> In methemoglobinemia the normal ferrous (Fe++) in the hemoglobin (Hb) is oxidized to the ferric (Fe+++) state which cannot bind oxygen and also shifts the oxygen dissociation curve to the left. > Autoxidation of Hb to MetHb occurs spontaneously with a normal level of <2%. > This is balanced by its reduction back to the ferrous state by cytochrome b5 reductase; an alternative is the NADPH generated by G6PD in the RBC, requiring an exogenous electron donor such as methylene blue. > Methemoglobinemia may be hereditary, but it is more commonly acquired. > Substances which may cause methemoglobinemia include: > With high levels of MetHb, the pulse oximeter reading trends toward 85%; the O2 dissociation curve shifts to the left. > The fractional oxyhemoglobin will be lower than the SaO2. When acutely acquired, MetHb levels <20% maybe asymptomatic. > Symptoms include headache, fatigue, dyspnea, and lethargy. > At levels >40%, altered consciousness, seizures, and death may occur. > The diagnosis should be considered if the pulse oximetry is lower than the O2 sat from an ABG. This can be confirmed with cooximetry. > The treatment is to identify and stop the causative agent and administer methylene blue (MB) 1 to 2 mg/kg IV over 5 min. The response is usually rapid, and the MB may be repeated after 1h if MetHb persists. > MB will be ineffective and should be avoided in individuals with G6PD deficiency, more common in those of African or Mediterranean or Southeast Asian descent. > If MB is contraindicated, ascorbic acid may be given 300–1000 mg/day orally. > Supportive care as indicated may include ventilation, high inspired oxygen, and exchange transfusion

Answer 87

> Carbon monoxide poisoning is common and causes include faulty home heaters, inadequate home ventilation, auto exhaust, and house fires. > Exposure may be chronic or acute. > Iatrogenic carbon monoxide poisoning may result from the reaction of halogenated volatile agents, particularly desflurane and isoflurane with desiccated soda lime or baralyme. > This has typically occurred on a Monday morning after O2 was left flowing through the circuit drying out the absorbent canister. > Carbon monoxide has 200 times the affinity for Hb as O2; thus low concentrations can produce significant COHb. COHb is normally 0–2% in non-smokers and up to 9% in smokers. > High levels of COHb reduce oxygen carrying capacity of the blood and will give a falsely high pulse oximetry reading. > CO causes inflammatory response and binds to cytochrome c oxidase at the mito-chondrial level, impairing cellular respiration. There are high rates of early and late neurocognitive and cognitive deficits, as well as cardiovascular dysfunction and acidosis. > Symptoms are nonspecific and range from mild such as headache to severe such as confusion, loss of consciousness, or death. > Treatment is administration of 100% O2 at high flow rates. This hastens the release of CO from the Hb. Hyperbaric oxygen has been demonstrated to decrease late neurologic sequelae and may be indicated if COHb > 25%.

Answer 88

○ 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.

Answer 89

○ EEG electrodes are placed on the scalp at precise locations based on their distance from standard landmarks. ○ Most common method is the International 10–20 system, employing 21 electrodes. ○ Majority of the electrodes are labeled with a letter followed by a number. ° Letters indicate the region of the scalp: frontal (F), parietal (P), frontal polar (Fp), temporal (T), occipital (O), and central (C). Auricular (A) electrodes are commonly used as reference point. ° Odd and even numbers that follow the letters indicate left and right sided placement, respectively. ° The smaller the number, the closer the location of the electrode to the midline. ° Midline electrodes are labeled with a letter “z” instead of a number (e.g., Fz for the “frontal midline” electrode location). ○ Labels of the individual channels indicate the active (recording) electrode followed by the reference electrode. ○ If both of these are active electrodes, then it is a “bipolar” montage (e.g., Fp1-F7). ○ Alternatively, the reference electrode can be a non-cephalic electrode, which makes the montage “referential” (e.g., Fp1-A1). ○ In the top figure, there are 20 bipolar channels that are arranged in the following fashion: 5 left-hemispheric (starting with Fp1-F7), 5 right-hemispheric (starts with Fp2-F8), 4 right-hemispheric (starts with Fp1-F3), 4right-hemispheric (starts with Fp2-F4), and 2 midline (Fz-Cz and Cz-Pz) channels. ○ There is also one EKG lead (to assist with artifact rejection) and two ocular electrodes to document eye opening/clo-sure which is an important factor for analysis.

Answer 90

○ 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.

Answer 91

○ 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].

Monitoring Flashcards

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