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APEX Study Guide > Unit 3: Cardiovascular > Flashcards

Unit 3: Cardiovascular Flashcards

1
Q

Define:

  • Chronotropy
  • Inotropy
  • Dromotropy
  • Lusitropy
A

Chronotropy = Heart Rate

Inotropy = Strength of contraction (Contractility)

Dromotropy = Conduction velocity

Lusitropy = Rate of myocardial relaxation (during diastole)

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2
Q

What is the function of the sodium-potassium pump?

A

Maintains cell’s resting potential – separates the charge across the cell membrane keeping the inside relatively negative and outside relatively positive

  • removes Na+ that enters during depolarization
  • returns K+ that left during repolarization
  • for 3 Na+ ions removed – 2 K+ ions enter
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3
Q

What are the five phases of ventricular action potential? Describe the ionic movement during each phase

A

Phase 0: Depolarization –> Na+ influx
Phase 1: Initial Repolarization –> K+ efflux and Cl- influx
Phase 2: Plateau –> Ca2+ influx
Phase 3: Repolarization –> K+ efflux
Phase 4: Na+/K+ pump restores resting membrane potential

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4
Q

What are the three phases of SA node action potential? Describe the ionic movement during each phase

A

Phase 4: Spontaneous Depolarization –> leaky to Na+ (Ca2+ influx occurs at the very end)
Phase 0: Depolarization –> Ca2+ influx
Phase 3: Repolarization –> K+ efflux

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5
Q

What process determines the intrinsic heart rate? What physiologic factors alter it?

A

The rate of spontaneous phase 4 depolarization in SA node

Can increase HR by manipulating 3 variables:
-rate of spont phase 4 depolarization increases (reaches TP faster)
-TP becomes more negative (shorter distance between RMP and TP)
-RMP becomes less negative (shorter distance between RMP and TP)
*when RMP and TP are close it is easier for the cell to depolarize

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6
Q

What are the two calculations for MAP? What is normal?

A

MAP = (1/3 x SBP) + (2/3 x DBP)

MAP = [(CO x SVR) / 80] +CVP

normal = 70-105

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7
Q

What is the formula for SVR? What is normal?

A

SVR = [(MAP - CVP) / CO] x 80

normal = 800-1500

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8
Q

What is the formula for PVR? What is normal?

A

PVR = [(MPAP - PAOP) / CO] x 80

normal = 150-250

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9
Q

What is the Frank-Starling relationship?

A

Describes the relationship between ventricular volume (preload) and ventricular output (CO)

  • increased preload –> increased myocyte stretch –> increased CO
  • decreased preload –> decreased myocyte stretch –> decreased CO

*increased preload increases CO only up to a point – additional volume overstretches ventricular sarcomeres decreasing # of cross-bridges that can be formed thus reducing CO (contributes to pulm congestion and increases PAOP)

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10
Q

What is on the y-axis and x-axis of the Frank-Starling curve?

A

Y-Axis = Ventricular Output (CO, SV, LVSW, RVSW)

X-Axis = Filling Pressures (CVP, PAD, PAOP, LAP, LVEDP) or End Diastolic Volume (RVEDV, LVEDV)

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11
Q

What factors increase and decrease myocardial contractility?

A

Increased Contractility:

  • SNS stimulation
  • Catecholamines
  • Calcium**
  • Digitalis
  • Phosphodiesterase inhibitors

Decreased Contractility:

  • Myocardial ischemia
  • Severe hypoxia
  • Acidosis
  • Hyperkalemia
  • Hypocalcemia
  • Volatile anesthetics
  • Propofol
  • Beta-blockers
  • Ca2+ channel blockers

*Chemical affect Contractility - particularly Calcium

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12
Q

What are the steps in excitation-contraction coupling in the cardiac myocyte?

A
  1. AP is propagated from adjacent cell
  2. Depolarization of T-tubule opens voltage-gated L-type Ca2+ channel (Ca2+ enters myocyte) – occurs during phase 2 of AP
  3. Influx of Ca2+ activates ryanodine-2 receptor (RyR2)
  4. Ca2+ is released from sarcoplasmic reticulum (Ca2+ induced Ca2+ release)
  5. Ca2+ binds to troponin C – stimulates cross bridge formation and causes myocardial contraction
  6. Ca2+ unbinds from troponin C – myocardial relaxation
  7. Calcium is returned to sarcoplasmic reticulum via SERCA2 pump (when inside binds to calsequestrin)
  8. Some calcium is removed from myocyte by Na/Ca exchange pump
  9. Na/K-ATPase restores resting membrane potential
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13
Q

What is afterload? How is it measured in the clinical setting?

A

Afterload = force the ventricle must overcome to eject its stroke volume

SVR = surrogate for LV afterload

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14
Q

What is the equation for SVR and PVR? What is normal?

A 
SVR = [(MAP - CVP) / CO] x 80 
normal = 800-1500 
PVR = [(MPAP - PAOP) / CO] x 80 
normal = 150-250
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15
Q

What law can be used to describe ventricular afterload?

A

Law of Laplace

-wall stress = (intraventricular pressure x radius) / ventricular thickness

*wall stress is reduced by decreased intraventricular pressure, decreased radius, increased wall thickness

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16
Q

What two conditions set afterload proximal to the systemic circulation?

A

Aortic Stenosis

Coarctation of the aorta

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17
Q

Describe the Wiggers diagram

A

Pay attention to:

  • 6 stages of cardiac cycle
  • 4 pressure waveforms
  • How the pressure waveforms match up to the EKG
  • How the valve position changes match up to the EKG
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18
Q

What are the six stages of the cardiac cycle? How do they relate to the LV pressure-volume loop?

A
  1. Rapid Filling (diastole)
  2. Reduced Filling (diastole)
  3. Atrial Kick (diastole)
  4. Isovolumetric Contraction (systole)
  5. Ejection (systole)
  6. Isovolumetric Relaxation (diastole)
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19
Q

What is ejection fraction? How do you calculate it?

A

Measure of systolic function (contractility) – Percent of blood ejected from heart during systole (SV relative to EDV)

EF = [(EDV - ESV) / EDV] x 100

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20
Q

What are the classifications of ejection fraction dysfunction?

A

Normal = >50%
Mild Dysfunction = 41-49%
Moderate Dysfunction = 26-40%
Severe Dysfunction = <25%

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21
Q

How can you calculate the stroke volume and/or ejection fraction with a pressure volume loop?

A

SV = width of the loop

EDV = right side of the loop at the x-axis

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22
Q

What is the best TEE view for diagnosing myocardial ischemia?

A

Midpapillary muscle level in short axis

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23
Q

What is the equation for coronary perfusion pressure?

A

CPP = Aortic DBP - LVED

*increasing AoDBP or decreasing LVEDP (PAOP) improves CPP

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24
Q

Which region of the heart is most susceptible to myocardial ischemia? Why?

A

LV subendocardium = most susceptible to ischemia

  • it is best perfused during diastole
  • as aortic pressure increases, LV tissue compresses its own blood supply and reduces blood flow
  • high compressive pressure in LV subendocardium coupled with decreased coronary artery blood flow during systole increases coronary vascular resistance and predisposes it to ischemia
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25
Q

What factors reduce oxygen delivery?

A

Decreased Coronary Flow:

  • tachycardia
  • decreased aortic pressure
  • decreased vessel diameter (spasm or hypocapnia)
  • increased end diastolic pressure

Decreased CaO2:

  • hypoxemia
  • anemia

Decreased Oxygen Extraction:

  • left shift of Hgb dissociation curve (Decrease P50)
  • decreased capillary density
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26
Q

What factors increase oxygen demand?

A
  • Tachycardia
  • Hypertension
  • SNS stimulation
  • Increased wall tension
  • Increased end diastolic volume
  • Increased afterload
  • Increased contractility
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27
Q

What are the steps in the nitric oxide cGMP pathway?

A

Nitric Oxide = smooth muscle relaxant that induces vasodilation

  1. Nitric oxide synthase catalyzes conversion of L-arginine to nitric oxide
  2. Nitric oxide diffuses from endothelium to smooth muscle
  3. Nitric oxide activates guanylate cyclase
  4. Guanylate cyclase converts guanosine triphosphate (GTP) to cyclic guanosine monophosphate (cGMP)
  5. Increased cGMP reduces intracellular Ca2+, leading to smooth muscle relaxation
  6. Phosphodiesterase deactivates cGMP to guanosine monophosphate turning off the NO mechanism
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28
Q

Where do the heart sounds match up on the LV pressure volume loop?

A

S1: closure of mitral & tricuspid valves – bottom right corner of LV PV loop
S2: closure of aortic & pulmonary valves – top left corner of LV PV loop

S3: suggests flaccid/inelastic heart (think HF) – left side of bottom line of LV PV loop
*gallop rhythm (heard during middle 1/3 of diastole - after S2)
S4: caused by atrial systole – right side of bottom line of LV PV loop
*heard before S1
*may suggest decreased ventricular compliance

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29
Q

What are the two primary ways a heart valve can fail?

A

Stenosis: fixed obstruction to forward flow during chamber systole

  • chamber must generate higher than normal pressure to eject blood
  • leads to concentric hypertrophy (sarcomeres added in parallel)

Regurgitation: valve is incompetent (leaky)

  • some blood flows forward and some flows backward during chamber systole
  • leads to eccentric hypertrophy (sarcomeres added in series)
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30
Q

What is the following LV pressure volume loop?

A

Mitral Stenosis

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31
Q

What is the following LV pressure volume loop?

A

Aortic Stenosis

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32
Q

What is the following LV pressure volume loop?

A

Aortic Regurgitation

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33
Q

What is the following LV pressure volume loop?

A

Mitral Regurgitation

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34
Q

What are the hemodynamic goals for aortic stenosis?

HR, Preload, Contractility, SVR, PVR

A

HR: slow to normal

Preload: increased

Contractility: no change

SVR: no change or increased

PVR: no change

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35
Q

What are the hemodynamic goals for mitral stenosis?

HR, Preload, Contractility, SVR, PVR

A

HR: slow to normal

Preload: no change

Contractility: no change

SVR: no change

PVR: AVOID increase

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36
Q

What are the hemodynamic goals for aortic insufficiency?

HR, Preload, Contractility, SVR, PVR

A

HR: increased

Preload: no change or increased

Contractility: no change

SVR: decreased

PVR: no change

37
Q

What are the hemodynamic goals for mitral insufficiency?

HR, Preload, Contractility, SVR, PVR

A

HR: increased

Preload: no change or increased

Contractility: no change

SVR: decreased

PVR: AVOID increase

38
Q

What is the most common dysrhythmia associated with mitral stenosis?

A

Atrial Fibrillation

39
Q

What are the six risk factors for perioperative cardiac morbidity and mortality for non-cardiac surgery?

A
  • High-risk surgery
  • Hx of ischemic heart disease (unstable angina confers greatest risk of periop MI)
  • Hx of CHF
  • Hx of cerebrovascular disease
  • DM
  • Serum creatinine >2
40
Q

What is the risk of periop MI in the pt with a pervious MI?

A

General Population: 0.3%
MI if > 6 months: 6%
MI if 3-6 months: 15%
MI if < 3 months: 30%

*highest risk of reinfarction is greatest within 30 days of an acute MI
*ACC/AHA guidelines recommend a minimum of 4-6 weeks before considering elective surgery

41
Q

What are considered HIGH risk surgical procedures according to cardiac risk? (4)

A
  • Emergency surgery (especially in elderly)
  • Open aortic surgery
  • Peripheral vascular surgery
  • Long surgical procedures with significant volume shifts and/or blood loss
42
Q

What are considered INTERMEDIATE risk surgical procedures according to cardiac risk? (5)

A
  • Carotid endarterectomy
  • Head and neck surgery
  • Intrathoracic or Intraperitoneal surgery
  • Orthopedic surgery
  • Prostate surgery
43
Q

What are considered LOW risk surgical procedures according to cardiac risk? (5)

A
  • Endoscopic procedures
  • Cataract surgery
  • Superficial procedures
  • Breast surgery
  • Ambulatory procedures
44
Q

What cardiac enzymes are released during an MI? When do you see elevation in the values?

A

Infarcted myocardium releases 3 key biomarkers: CK-MB, Troponin I, and Troponin T
-cardiac troponins are more sensitive than CK-MB for diagnosis of MI

CK-MB: initial elevation 3-12 hrs; Peak 24 hrs; Return to baseline 2-3 days
Troponin I: Initial 3-12 hrs; Peak 24 hrs; Return 5-10 days
Troponin T: Initial 3-12 hrs; Peak 12-48 hrs; Return 5-14 days

*these values must be evaluated in the context of the time of the pt’s EKG

45
Q

How do you treat intraop myocardial ischemia?

A

Focus on interventions that make the heart slower, smaller, and better perfused

Increased O2 Demand:

  • increased HR –> beta blocker
  • increased BP –> increased anesthesia depth, vasodilator
  • increased PAOP –> nitroglycerin

Decreased O2 Supply:

  • decreased HR -> anticholinergic, pacing
  • decreased BP –> vasoconstrictor, reduce anesthesia depth
  • increased PAOP –> nitroglycerin, inotrope
46
Q

What factors reduce ventricular compliance?

A

Diastolic pressure-volume relationship is affected by:

  • age >60
  • ischemia
  • pressure overload hypertrophy (aortic stenosis or HTN)
  • hypertrophic obstructive cardiomyopathy
  • pericardial pressure (increased external pressure)

*priming the ventricle requires higher filling pressures

47
Q

What is the difference between HFrEF (systolic) and HFpEF (diastolic) heart failure?

A

HFrEF – Ventricle doesn’t empty well
*hallmark of systolic HF is a decreased EF w/ an increased EDV (volume overload commonly causes systolic dysfunction)

HFpEF – Ventricle doesn’t fill properly
*occurs when heart can’t relax and accept the incoming volume because ventricular compliance is reduced
*defining characteristic of diastolic dysfunction is symptomatic HF w/ a normal EF

48
Q

What are the hemodynamic goals in a patient with HFrEF?

preload, afterload, contractility, HR

A

Preload: already high (diuretics if too high)

Afterload: decreased to reduce myocardial workload; maintain CPP

Contractility: augment w/ inotropes as needed (dobutamine)

HR: usually high d/t increased SNS tone; if EF is low, then a higher HR is needed to preserve CO

49
Q

What are the hemodynamic goals in a patient with HFpEF?

preload, afterload, contractility, HR

A

Preload: volume required to stretch noncompliant ventricle; LVEDP doesn’t correlate w/ LVEDV (TEE is best)

Afterload: keep elevated to perfuse a thick myocardium (Neo); maintain CPP

Contractility: usually normal

HR: slow/ normal to increase diastolic time and CPP

50
Q

What is the Modified New York Association Functional Classification of Heart Failure?

A

Class 1: asymptomatic

Class 2: symptomatic w/ moderate activity

Class 3: symptomatic w/ mild activity

Class 4: symptomatic at rest

51
Q

What are six complications of HTN?

A
  • LV hypertrophy
  • Ischemic heart disease
  • CHF
  • Arterial aneurysm (aorta, cerebral circulation)
  • Stroke
  • End-stage renal disease

*HTN is high afterload that increases myocardial work and an elevated arterial driving pressure damages nearly every organ in the body

52
Q

How does HTN contribute to CHF?

A

HTN –> Increased Myocardial Wall Tension –> LVH –> CHF

HTN –> Increased Myocardial Wall Tension –> Increased MVO2 –> Coronary insufficiency –> Infarction dysrhythmias –> CHF

53
Q

How does hypertension affect cerebral autoregulation?

A

Chronic HTN shifts cerebral autoregulation curve to the right

-this adaptation helps the brain tolerate a higher range of blood pressures – however, this comes at expense of not tolerative a lower BP

*malignant HTN increases risk of hemorrhagic stroke and cerebral edema
*hypotension increases risk of cerebral hypoperfusion

54
Q

What’s the difference between primary and secondary hypertension?

A

Primary (essential) HTN: has no identifiable cause (more common – 95%)

Secondary HTN: caused by some other pathology (5%)

55
Q

What are the 6 causes of secondary HTN?

A
  • Coarctation of the aorta
  • Renovascular disease
  • Hyperadrenocorticism (Cushing’s syndrome)
  • Hyperaldosteronism (Conn’s disease)
  • Pheochromocytoma
  • Pregnancy-induced HTN
56
Q

What are the two major classes of calcium channel blockers? Examples of each

A

Dihydropyridines: Nifedipine, Nicardipine, Nimodipine, Amlodipine, Clevidipine

  • target vascular smooth muscle (mostly)
  • vasodilation via decreasing SVR

Non-Dihydropyridines: Verapamil (phenylalkylamine) and Diltiazem (benzothiazepine)

  • target myocardium (mostly)
  • decrease chronotropy, inotropy, dromotropy, and coronary vascular resistance
57
Q

What is the pathophysiology of constrictive pericarditis?

A

Caused by fibrosis or any condition where the pericardium becomes thicker

  • during diastole, ventricles can’t fully relax – reduces compliance and limits diastolic filling
  • ventricular pressures increase – creates backpressure to peripheral circulation
  • ventricles adapt by increasing myocardial mass – over time this impairs systolic function
58
Q

What is the anesthetic management of constrictive pericarditis?

A

Avoid Bradycardia (CO is dependent on HR)

Preserve HR and contractility

  • ketamine
  • pancuronium
  • volatile agents w/ caution
  • opioids, benzos, and etomidate are ok

Maintain Afterload

Aggressive PPV can decrease venous return and CO

59
Q

What is the pathophysiology of pericardial tamponade? How is it diagnosed? What is the treatment?

A
  • Occurs when fluid accumulates inside the pericardium – the excess fluid exerts external pressure on the heart (limits ability to fill and function)
  • CVP rises in tandem w/ pericardial pressure (as ventricular compliance deteriorates - CVP and PAOP begin to equalize)

*TEE = best method of diagnosis
*Pericardiocentesis or Pericardiostomy = best treatment

60
Q

What is Kussmaul’s sign?

A

Indicates impaired right ventricular filling due to a poorly compliant RV or pericardium

-since RV filling is affected, blood “backs up” causing JUGULAR VENOUS DISTENTION and INCREASED CVP
*most pronounced during inspiration

61
Q

What two conditions are commonly associated with Kussmaul’s sign?

A

Constrictive Pericarditis and Pericardial Tamponade

*can occur w/ any condition limiting RV filling

62
Q

What is Pulsus Paradoxus?

A

Represents and exaggerated decrease in SBP during inspiration (suggests impaired diastolic filling)

  • SBP falls by more than 10mmHg during inspiration
  • negative intrathoracic pressure on inspiration –> increased venous return to RV –> bowing of ventricular septum toward LV –> decrease SV –> decreased CO –> decrease SBP
63
Q

What two conditions are commonly associated with pulsus paradoxus?

A

Constrictive Pericarditis

Pericardial Tamponade

64
Q

What is Beck’s Triad? What conditions are associated with it?

A

Occurs in acute cardiac tamponade

S&S:

  • Hypotension (decreased SV)
  • Jugular venous distension (impaired venous return to the right heart)
  • Muffled heart tones (fluid accumulation in pericardial space)
65
Q

What are the best anesthetic techniques for the pt w/ acute pericardial tamponade undergoing pericardiocentesis?

A

Local anesthesia is preferred technique – because hemodynamics are minimally affected

If general is required – primary goal is to preserve myocardial function
-severely decreased SV and increased SNS tone (increased contractility/ increased afterload) provide compensation
*any drug that depresses myocardium or reduces afterload can precipitate CV collapse

66
Q

What drugs should be avoided in a pt w/ acute pericardial tamponade? What drugs are safer to use?

A

Drugs to Avoid:

  • halogenated anesthetics
  • propofol
  • thiopental
  • high dose opioids
  • neuraxial anesthesia

Safer to Use:

  • ketamine –best choice
  • nitrous oxide
  • benzos
  • opioids
67
Q

What 6 patient factors warrant antibiotic prophylaxis against infective endocarditis?

A
  • Previous infective endocarditis
  • Prosthetic heart valve
  • Unrepaired cyanotic congenital heart disease
  • Repaired congenital heart defect if the repair is <6 months
  • Repaired congenital heart disease w/ residual defects that have impaired endothelialization at the graft site
  • Heart transplant w/ vavuloplasty
68
Q

What are 3 surgical procedures that warrant antibiotic prophylaxis against infective endocarditis?

A

High risk procedures are thought to be “dirty” where risk of transient bacteremia outweighs risk of antibiotic therapy

  • Dental procedures involving gingival manipulation and/or damage to mucosa lining
  • Respiratory procedures that perforate mucosal lining w/ incision or biopsy
  • Biopsy of infective on the skin or muscle
69
Q

What are the 3 key determinants of flow through the LVOT?

A
  • Systolic LV volume
  • Force of LV contraction
  • Transmural pressure gradient
70
Q

What factors reduce cardiac output in the patient w/ obstructive hypertrophic cardiomyopathy?

A

Things that narrow LVOT = bad for CO

Increased obstruction and Decreased CO

  • decreased systolic volume (decreased preload or increased HR)
  • increased contractility
  • decreased aortic pressure
71
Q

What factors improve cardiac output in the patient w/ obstructive hypertrophic cardiomyopathy?

A

Things that distend LVOT = good for CO

Decreased obstruction and Increased CO

  • increased systolic volume (increased preload or decreased HR)
  • decreased contractility
  • increased aortic pressure
72
Q

How long should elective surgery be delayed in the patient after a percutaneous coronary intervention?

A
  • Angioplasty w/o Stent: 2-4 weeks
  • Bare Metal Stent: 30 days (3 months preferred)
  • Drug Eluting Stent (stable ischemic heart disease): 1st gen 12 months – Current gen 6 months
  • Drug Eluting Stent (acute coronary syndrome): 12 months minimum
  • CABG: 6 weeks (3 months preferred)
73
Q

What is the difference between alpha-stat and pH-stat blood gas measurement during cardiopulmonary bypass?

A

Alpha-stat – does NOT correct for pt temperature (aims to keep intracellular charge neutrality across all temps)
*associated w/ better outcomes in adults

pH-stat – corrects for pt temperature (aims to keep a constant pH across all temps)
*associated w/ better outcomes in peds

*as temp decreases, more CO2 will dissolve in the blood - by extension this affects pH

74
Q

Why is a left ventricular vent used during CABG surgery?

A

A LV vent removes blood from the LV – this blood usually comes from the Thebesian veins and bronchial circulation (anatomic shunt

75
Q

How does the intra-aortic balloon pump function throughout the cardiac cycle? How does it help the patient?

A

It is a counterpulsation device that improves myocardial oxygen supply while reducing myocardial oxygen demand

Diastole: pump inflation augments coronary perfusion – inflation correlates with the dicrotic notch on the aortic pressure waveform

Systole: pump deflation reduces afterload and improves CO – deflation correlates with R wave on EKG

76
Q

What are 4 contraindications to the intra-aortic balloon pump?

A
  • Severe aortic insufficiency
  • Descending aortic disease
  • Severe peripheral vascular disease
  • Sepsis
77
Q

Describe the Crawford classification system of aortic aneurysms.

A
  • Type 1: all or most of descending thoracic aorta / only upper abdominal aorta
  • Type 2: all or most of descending thoracic aorta / most abdominal aorta
  • Type 3: only lower descending thoracic / most abdominal aorta
  • Type 4: no descending thoracic aorta / most abdominal aorta
78
Q

Describe Stanford classification system of aortic dissection.

A

Stanford Type A: involves ascending aorta

Stanford Type B: does not involve ascending aorta

79
Q

Describe DeBakey classification system of aortic dissection.

A
  • Type 1: tear in ascending aorta + dissection along entire aorta
  • Type 2: tear in ascending aorta + dissection only in ascending aorta
  • Type 3a: tear in proximal descending aorta + dissection is limited to thoracic aorta
  • Type 3b: tear in proximal descending aorta + dissection along thoracic and abdominal aorta
80
Q

Which law describes the relationship between aortic diameter and risk of aortic rupture in a pt w/ an abdominal aortic aneurysm?

A

Law of Laplace

  • wall tension = transmural pressure x vessel radius
  • increased diameter –> increased transmural pressure –> increased wall tension

*mortality increases significantly once AAA reaches 5.5cm
*surgical correction is recommended when aneurysm exceeds 5.5 cm or if it grows more than 0.6-0.8cm a year

81
Q

How does the aortic cross clamp contribute to the risk of anterior spinal artery syndrome?

A

Aortic cross clamp placed above the artery of Adamkiewicz may cause ischemia to the lower portion of the anterior spinal cord – can result in anterior spinal artery syndrome (Beck’s Syndrome)

82
Q

How does anterior spinal artery syndrome present?

A
  • Flaccid paralysis of lower extremities
  • Bowel and bladder dysfunction
  • Loss of temp and pain sensation
  • Preserved touch and proprioception
83
Q

What is amaurosis fugax?

A

Blindness in one eye –> sign of impending stroke

*emboli travel from internal carotid artery to ophthalmic artery, which impairs perfusion of optic nerve and causes retinal dysfunction

84
Q

What information does an EEG monitor give you?

A
  • Monitors cortical electrical function (does not detect subcortical problems)
  • Risk of cerebral hypoperfusion w/ loss of amplitude, decreased beta-wave activity and/or appearance of slow wave activity

*High incidence of false-negatives

85
Q

What conditions can lead to false conclusions on a EEG?

A

Increased Frequency:

  • mild hypercarbia
  • early hypoxia
  • seizure activity
  • ketamine
  • N2O
  • light anesthesia

Decreased Frequency:

  • extreme hypercarbia
  • hypoxia
  • cerebral ischemia
  • hypothermia
  • anesthetic overdose
  • opioids
86
Q

What regional technique can be used for the patient undergoing carotid endarterectomy? What levels must be blocked?

A
  • Cervical plexus block (superficial or deep)
  • Local infiltration

-Must cover C2-C4

87
Q

What reflex can be activated during carotid endarterectomy or following carotid balloon inflation?

A

Baroreceptor reflex

88
Q

A patient in the PACU develops a hematoma following right endarterectomy. Her airway is completely obstructed. What is the best treatment at this time?

A

Pt requires emergency decompression of the surgical site
-if surgeon isn’t immediately available – you must do it

Cricothyroidotomy may be required

APEX Study Guide (13 decks)

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