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Board Review > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Chronotropy:

A

HR

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2
Q

Inotropy

A

strength of contractility

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3
Q

dromotropy

A

conduction velocity (how fast an action potential travels per time)

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4
Q

lusitropy

A

Rate of myocardial relaxation (during diastole)

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5
Q

What is the function of the sodium-potassium pump?

A

Maintains the cardiac cell’s resting potential. It separates charge across the cell membrane keeping the inside of the cell relatively negative and the outside relatively positive

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6
Q

How does the sodium-potassium pump work?

see photo in cardiac AandP

A

It removes Na+ that enters the cell during depolarization.
It returns K+ that has left the cell during repolarization.

For every 3 Na+ ions it removes, it brings 2 K+ ions into cell

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7
Q

What are the 5 phases of the ventricular action potential?

see photo in cardiac A&P module

A 
Phase 0: Depolarization
Phase 1: Initial repolarization
Phase 2: Plateau
Phase 3: Repolarization
Phase 4: restoration of resting membrane potential
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8
Q

What is the ionic movement during Phase 0 of the ventricular action potential?

A

Na+ influx (depolarization)

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9
Q

What is the ionic movement during Phase 1 of the ventricular action potential?

A

K+ efflux and Cl- influx (initial repolarization)

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10
Q

What is the ionic movement during Phase 2 of the ventricular action potential?

A

Ca++ influx (plateau)

K+ efflux also

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11
Q

What is the ionic movement during Phase 3 of the ventricular action potential?

A

K+ efflux (repolarization)

K+ exits faster than Ca++ enters

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12
Q

What is the ionic movement during Phase 4 of the ventricular action potential?

A

Na+/K+ pump restores resting membrane potential

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13
Q

List the 3 phases of the SA node action potential.

see photo in cardiac A&P module

A

Phase 4: Spontaneous depolarization
Phase 0: Depolarization
Phase 3: Repolarization

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14
Q

What is the ionic movement during Phase 4 of the SA node action potential?

A

Leaky to Na+ (Ca++ influx at very end) (spontaneous depolarization)

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15
Q

What is the ionic movement during Phase 0 of the SA node action potential?

A

Ca++ influx (depolarization)

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16
Q

What is the ionic movement during Phase 3 of the SA node action potential?

A

K+ efflux (repolarization)

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17
Q

What determines the intrinsic heart rate?

A

rate of spontaneous phase 4 depolarization in the SA node

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18
Q

What physiologic factors can increase the intrinsic heart rate?

A
  • Increasing rate of spontaneous phase 4 depolarization (reaches TP faster)
  • TP becomes more negative (shorter distance between RMP and TP)
  • RMP becomes less negative (shorter distance between RMP and TP)
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19
Q

When the resting membrane potential and the threshold potential of the SA node are close it is __________ for the cell to depolarize.

A

easier

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20
Q

When the resting membrane potential and the threshold potential of the SA node are far it is __________ for the cell to depolarize.

A

harder

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21
Q

What is the calculation for MAP?

A

MAP= (SBP + 2DBP)/3
-or-
MAP= [(CO x SVR)/80] + CVP

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22
Q

What is normal MAP?

A

70-105 mmHg

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23
Q

What is the formula for SVR?

A

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

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24
Q

What is normal SVR?

A

800-1500 dynes/sec/cm^5

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25
Q

What is the formula for PVR?

A

PVR= [(MPAP-PAOP)/CO]x80

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26
Q

What is normal PVR?

A

150-250 dynes/sec/cm^5

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27
Q

What is the Frank-Starling relationship?

A

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

Increase preload–> increase myocyte stretch–> increase ventricular output, to a point.

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28
Q

What happens with overfilling and the frank-starling relationship?
(see photo in CV A&P module)

A

Additional volume overstretches ventricular sarcomeres, decreasing number of cross bridges that can be formed & ultimately CO is reduced. Contributes to pulmonary congestion and increased PAOP

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29
Q

What values can be used to represent ventricular volume (x-axis) in the Frank-Starling curve?

A 
CVP
PAD
PAOP
LAP
LVEDP
LVEDV
RVEDV
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30
Q

What values can be used to represent ventricular output (y-axis) in the Frank-Starling curve?

A

CO
SV
LVSW
RVSW

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31
Q

What things increase cardiac contractility?

A
  • SNS stimulation
  • Catecholamines
  • Ca++
  • Digitalis
  • Phosphodiesterase inhibitors
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32
Q

What things decrease cardiac contractility?

A
  • Myocardial ischemia
  • Severe hypoxia
  • Acidosis
  • Hypercapnia
  • Hyperkalemia
  • Hypocalcemia
  • VA
  • Propofol
  • Beta-blockers
  • CCBs
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33
Q

Discuss excitation-contraction coupling in the cardiac myocyte:
(see photo in CV A and P)

A
  • myocardial cell membrane depolarizes.
  • Plateau of ventricular action potential (phase 2), Ca++ enters the cardiac myocyte through L-type Ca++ channels in the T-tubules.
  • Ca++ influx turns on the ryanodine-2 receptor –> releases Ca++ from sarcoplasmic reticulum (aka cal induced cal release)
  • Ca++ binds to troponin C (myocardial contraction)
  • Ca++ unbinds troponin C (Myocardial relaxation)
  • Most Ca++ is returned to sarcoplasmic reticulum via SERCA2 pump.
  • In SR, Ca++ binds to storage proteins called calsequestrin.
  • Repeat
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34
Q

What is afterload?

How do we measure it?

A

The force the ventricle must overcome to eject it stroke volume.

*In the clinical setting we use the systemic vascular resistance as a surrogate for LV afterload.

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35
Q

What law can be used to describe ventricular afterload?

A

Law of Laplace

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

intraventricular pressure pushes heart apart.
wall stress holds heart together.

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36
Q

Cardiac wall stress is reduced by:

A

Decreased intraventricular pressure
Decreased radius
increased wall thickness

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37
Q

3 conditions that set afterload proximal to the systemic circulation:

A

Aortic stenosis
Hypertrophic cardiomyopathy
Coarctation of the aorta

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38
Q

Relate the 6 stages of the cardiac cycle to the LV pressure-volume loop:
(see photo CV A and P)

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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39
Q

How do you calculate ejection fraction?

A

Stroke volume/ end-diastolic volume) x 100

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40
Q

How do you calculate stroke volume?

A

EDV - ESV = SV

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41
Q

Normal EF:

LV dysfunction EF:

A

Normal: 60-70%
Dysfunction: < 40%

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42
Q

Best TEE view for diagnosing myocardial ischemia:

see photo in CV A&p

A

Midpapillary muscle level in short axis

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43
Q

Calculate coronary perfusion pressure:

A

CPP = Aortic DBP - LVEDP

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44
Q

How can CPP be improved?

A

by increasing Aortic DBP or decreasing LVEDP (PAOP)

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45
Q

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

A

LV subendocardium.

It is best perfused during diastole. As aortic pressure increases, LV tissue compresses its own blood supply. High compressive pressure coupled with decreased coronary blood flow during systole increases coronary vascular resistance.

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46
Q

What factors decrease myocardial 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 O2 extraction:

  • left shift (decreased P50)
  • decreased capillary density
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47
Q

What factors increase myocardial oxygen DEMAND?

A 
Tachycardia
HTN
SNS stimulation
Increased wall tension
Increased EDV
Increased afterload
Increased contractility
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48
Q

Nitric Oxide pathway:

see photo in CV A&P

A
  • Nitric oxide synthase catalyzes the conversion of L-arginine to NO.
  • NO diffuses from the endothelium to the smooth muscle.
  • NO activates guanylate cyclase
  • GC converts guanosine triphosphate (GTP) to cyclic guanosine monophosphate (cGMP).
  • Increased cGMP reduces intracellular calcium, leading to smooth muscle relaxation.
  • Phosphodiesterase deactivates cGMP to guanosine monophosphate (GMP) (this step turns off the NO mechanism)
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49
Q

Where do heart sounds match up on the LV pressure-volume loop?
(see photo CV valvular disease)

A

S1: closure of the mitral and tricuspid valves (marks onset of systole) (bottom right corner)
S2: Closure of Aortic and pulmonic vlaves (marks onset of diastole) (top left corner)
S3: may suggest systolic dysfunction (normal in kids and athletes) (bottom left corner)
S4: may suggest diastolic dysfunction (bottom right corner between S1 and S3

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50
Q

what are the 2 primary ways a heart valve can fail?

A

Stenosis:

  • fixed obstruction to forward flow during chamber systole.
  • Chamber must generate a higher than normal pressure to eject.

Regurgitation:

  • Vavle is incompetent
  • Some blood flows forwards and some blood flows backwards during chamber systole.
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51
Q

How does the heart compensate for pressure overload? Volume overload?
(see photo in CV valve disease)

A 
Stenosis:
pressure overload
Concentric hypertrophy
(walls thicken)
Sarcomeres added in parallel
Regurgitation: 
Volume overload
Eccentric hypertrophy
(chamber dilated)
Sarcomeres added in series
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52
Q

Hemodynamic goals for Aortic Stenosis:

A 
HR: slow normal
preload: increased
SVR: 0 to increased
contractility: 0
PVR: 0
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53
Q

Hemodynamic goals for Mitral Stenosis:

A 
HR: Slow normal
Preload: 0
SVR: 0
Contractility: 0
PVR: avoid increases
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54
Q

Hemodynamic goals for Aortic Insufficiency:

A 
HR: increased
Preload: 0 to increased
SVR: decreased
contractility: 0
PVR: 0
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55
Q

Hemodynamic goals for Mitral Insufficiency:

A 
HR: increased
Preload: 0 to increased
SVR: decreased
contractility: 0
PVR: avoid increase
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56
Q

what is the most common dysrhythmia associated with mitral stenosis?

A

Atrial fib

57
Q

6 risk factors for preoperative cardiac morbidity and mortality for non-cardiac surgery:

A

-High risk surgery
-H/O ischemic heart disease (unstable angina confers the greatest risk fo preoperative MI)
-H/O CHF
-H/O cerebrovascular dx
-DM
serum creatinine > 2mg/dL

58
Q

Risk of perioperative MI in pts with previous MI:

A

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

59
Q

What are the ACC/AHA guidelines for elective surgery after MI?

A

highest risk is greatest within 30 days. ACC/AHA guidelines recommend a minimum of 4-6 weeks before considering elective surgery.

60
Q

ACC/AHA categorized HIGH risk procedures according to cardiac risk:

A

Risk >5% :

  • Emergency surgery (especially in elderly)
  • Open aortic surgery
  • Peripheral vascular surgery
  • Long surgical procedures with significant volume shifts and/or blood loss
61
Q

ACC/AHA categorized INTERMEDIATE risk procedures according to cardiac risk:

A

Risk 1-5% :

  • CEA
  • Head and Neck surgery
  • intrathoracic or intraperitoneal
  • orthopedic
  • Prostate
62
Q

ACC/AHA categorized LOW risk procedures according to cardiac risk:

A

Risk <1% :

  • Endoscopic
  • Cataract
  • Superficial
  • Breast
  • Ambulatory
63
Q

Modified New York Association Functional Classification of Heart Failure:

A

Class I: Asymptomatic
Class II: Symptomatic with moderate activity
Class III: Symptomatic with mild activity
Class IV: Symptomatic at rest

64
Q

Cardiac enzymes:

A

Cells require O2 to maintain the integrity of its cell membrane. A cell deprived of O2 dies and releases its contents into the systemic circulation.

65
Q

what are the 3 key biomarkers infarcted myocardium release:

A

Creatine kinase-MB
Troponin I
Troponin T

*Troponins are more sensitive than CKMB for diagnosing MI. These values must be elevated in the context of time with the patient’s EKG.

66
Q

CK-MB Initial elevation, Peak elevation, and return to baseline times:

A

Initial: 3-12hrs
Peak: 24hrs
Baseline: 2-3 days

67
Q

Troponin I Initial elevation, Peak elevation, and return to baseline times:

A

Initial: 3-12 hrs
Peak: 24hrs
Baseline: 5-10 days

68
Q

Troponin T Initial elevation, Peak elevation, and return to baseline times:

A

Initial: 3-12hrs
Peak: 12-48 hrs
Baseline: 5-14 days

69
Q

Tx of intraoperative MI should be focused on:

A

interventions that make the heart slower, smaller, and better perfused.

70
Q

Tx of intraoperative MI caused by increased O2 demand:

A
  • Increased HR: give BB to HR <80
  • Increased BP: increase depth of anesthesia, vasodilators
  • Increased PAOP: give Nitroglycerin
71
Q

Tx of intraoperative MI caused by decreased O2 supply:

A
  • Decreased HR: Anticholinergic, Pacing
  • Decreased BP: Vasoconstrictors, reduced depth of anesthesia
  • Increased PAOP: Nitroglycerin, Inotrope
72
Q

What factors reduce ventricular compliance? (the diastolic pressure-volume loop)
(see photo in CV pathophys)

A
  • Age >60
  • Ischemia
  • Pressure overload hypertrophy (aortic stenosis or HTN)
  • Hypertrophic obstructive cardiomyopathy
  • pericardial pressure (increased external pressure)

*higher filling pressures are required to prime the ventricle.

73
Q

What is systolic heart failure?

A

“The ventricle doesn’t empty well”
-Decreased EF with increased EDV

*volume overload commonly causes systolic dysfunction.

74
Q

What is diastolic heart failure?

A

“The ventricle doesn’t fill properly”
-heart is unable to relax and accept the incoming volume, b/c ventricular compliance is reduced.
Symptomatic heart failure with a normal EF.

75
Q

Hemodynamic goals of Systolic heart failure:

A

Preload: Already high (diuretics if too high)

Afterload: Decrease to reduce myocardial workload (SNP), Maintain CPP

Contractility: Augment with inotropes as needed (dobutamine)

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

76
Q

Hemodynamic goals of Diastolic heart failure:

A

Preload: volume required to stretch noncompliant ventricle (LVEDP) does not correlate with LVEDV (TEE is best)

Afterload: Keep elevated to perfuse a thick myocardium (Neo); Maintain CPP

Contractility: Usually normal

HR: slow/normal to increased diastolic time and CPP

77
Q

The problem with HTN:

A

high after load increases myocardial work and elevated arterial driving pressure damages nearly every organ in the body.

78
Q

6 complications of HTN:

A 
LV hypertrophy
Ischemic heart disease
CHF
Arterial aneurysm (aorta, cerebral)
Stroke
End-stage renal dx
79
Q

How does HTN contribute to CHF?

see photo in CV pathophys

A

HTN–> increased myocardial wall tension–> increased MVO2 and LVH.
LVH–>CHF and more increased MVO2.
Increased MVO2–>infarction and Dysrhythmias–>CHF

80
Q

What is the cerebral autoregulation curve?

A

the range of blood pressures where cerebral perfusion pressure remains constant.

81
Q

How does HTN affect cerebral autoregulation?

A

Chronic HTN shift curve to right.
Adaptions help the brain tolerate higher range of BP, however it can’t tolerate lower BPs.
BP past range of auto regulation is pressure dependent.

*Some text say the range of autoregulation remains the same in HTN pts, however evidence suggest it is actually narrowed.

82
Q

Risk of hypotension and malignant HTN on the brain?

A

Malignant HTN increases risk of hemorrhagic stroke and cerebral edema.

Hypotension increases risk of cerebral hypoperfusion.

83
Q

What is Primary HTN?

A

“Essential” more common and has no identifiable cause (95% of all HTN)

84
Q

What is Secondary HTN?

A

Caused by some other pathology (5% of HTN)

85
Q

6 causes of secondary HTN?

APEX flashcard says 7 but only gives 6

A
  • Coarctation of aorta
  • Renovascular disease
  • Hyperadrenocorticism (Cushing’s syndrome)
  • Hyperaldosteronism (Conn’s disease)
  • Pheochromocytoma
  • Pregnancy-induced HTN
86
Q

2 major classes of CCBs?

A

Dihydropyridines

non-Dihydropyridines

87
Q

Dihydropyridines:

Target?

A

Vascular Smooth muscle (mostly)

88
Q

Dihydropyridines:

Clinical Effect?

A

Vasodilation–> decreased SVR

89
Q

Dihydropyridines:

Examples?

A

NifediPINE (Procardia)
Nicardipine (Cardene)
Nimodipine
Amlodipine (Norvasc)

90
Q

Non-Dihydropyridines:

Target?

A

Myocardium (mostly)

91
Q

Non-Dihydropyridines:

Clinical Effect?

A
  • Decreased Chronotropy
  • Decreased Inotorpy
  • Decreased Dromotropy
  • Decreased Coronary vascular resistance
92
Q

Non-Dihydropyridines:

Examples?

A

VerapAMil (class: phenylalkylAMIne)

DiltIAZEm (class: benzothIAZEpine)

93
Q

Describe the pathophysiology of constrictive pericarditis:

A

Caused by fibrosis or any condition where the pericardium becomes thicker.

During diastole, ventricle can’t fully relax, this reduces compliance and limits diastolic filling.
Ventricular pressure increases–>back pressure to the peripheral circulation–> ventricles adapt by increasing myocardial mass, but overtime this impairs systolic fx.

94
Q

Anesthetic management for constrictive pericarditis:

A

CO is dependent on HR (avoid bradycardia)

Preserved HR and contractility:

  • ketamine
  • pancuronium
  • VA with caution
  • opioids, Benzes, and etomidate ok

Maintain afterload
Aggressive PPV can decrease venous return and CO

95
Q

How is pericardial tamponade different than pericardial effusion?

A

fluid accumulated inside the pericardium (pericardial effusion) exerts and external pressure on the heart limiting its ability to fill and act like a pump (PT)

96
Q

Pathophysiology of pericardial tamponade:

see photo in CV pathophys

A

CVP rises in tandem with pericardial pressure.
As ventricular compliance deteriorates, left and right sided cardiac diastolic pressure (CVP and PAOP) begin to equalize.

97
Q

What is the best way to diagnoses tamponade?

A

TEE

98
Q

What is the best treatment for tamponade?

A

pericardiocentesis or pericardiostomy

99
Q

What is Kussmaul’s sign?
what does it indicate?
when is it the most pronounced?

A

It indicates impaired RV filling d/t poorly compliant RV or pericardium.

Blood essentially “backs up” which causes JVD and increased CVP.

It’s most pronounced during inspiration.

100
Q

2 conditions commonly associated with Kussmaul’s sign:

A

Constrictive pericarditis and pericardial tamponade.

*although it can occur with any condition that limits RV filling.

101
Q

What is Pulsus paradoxus?

what does this finding suggest?

A

An exaggerated decreased SBP during inspiration (fall more than 10mmHg).
Suggests impaired diastolic filling.

Negative intrathoracic pressure on inspiration–> increased venous return to RV–> bowing of ventricular septum towards LV–> decreased SV–> decreased CO–> decreased SB

102
Q

2 conditions usually associated with Pulsus Paradoxus:

A

Constrictive pericarditis
Pericardial tamponade.
(like kussmaul’s sign)

103
Q

what is Beck’s triad?

A

Hypotension (decreased SV)
JVD (impaired venous return to right heart)
Muffled heart tones (fluid accumulation in the pericardial space attenuates sound waves)

104
Q

What conditions are associated with Beck’s triad?

A

Acute cardiac tamponade

105
Q

What are the best anesthetic techniques for a patient with acute pericardial tamponade undergoing a pericardiocentesis?

A

*LA is preferred technique d/t hemodynamics.

If general required, goal is to preserve myocardial function. SV is severely decreased and increased SNS tone (increased contractility and increased afterload) provide compensation.
Drugs that depress the myocardium or reduce after load can precipitate cardiovascular collapse.

106
Q

Drugs to avoid during pericardiocentesis for cardiac tamponade:

A 
Halogenated anesthetics
propofol
Thiopental
High dose opioids
Neuraxial anesthesia
107
Q

Drugs that are safe to use for pericardiocentesis for cardiac tamponade:

A

Ketamine (activation of SNS makes this the best choice)
Nitrous Oxide
Benzodiazepines
Opioids

108
Q

6 patient factors that warrant antibiotic prophylaxis against infective endocarditis:
(apex say list 7 but they only give 6)

A
  • Previous infective endocarditis
  • Prosthetic heart valve
  • unrepaired cyanotic congenital heart disease
  • Repaired congenital heart defect if the repair is <6months old
  • Repaired congenital heart disease with residual defects that have impaired endothelialization at the graft site
  • Heart transplant with valvuloplasty
109
Q

3 surgical procedures that warrant antibiotic prophylaxis against infective endocarditis:

A
  • Dental procedures involving gingival manipulation and/or damage to mucosa lining
  • Respiratory procedures that perforate the mucosal lining with incision or biopsy.
  • Biopsy of infective lesions on the skin or muscle
110
Q

What are 3 key determinants of flow through the LV outflow tract (LVOT)?

A

Systolic LV volume
Force of LV contraction
Transmural pressure gradient

111
Q

What factors tend to reduce CO in the patient with obstructive hypertrophic cardiomyopathy?

A

*things that distend the LVOT = good for CO

things that narrow LVOT = bad

112
Q

Conditions that Distend the LVOT:

A
  • increased systolic volume (increased preload or decreased HR)
  • decreased contractility
  • increased Ao pressure
113
Q

Conditions that Narrow the LVOT:

A
  • decreased systolic volume (decreased preload or increased HR)
  • increased contractility
  • decreased Ao pressure
114
Q

What hemodynamic conditions reduce CO in the patient with hypertrophic cardiomyopathy?

A
  • Increased HR (treat with BB or CCB)
  • Increased contractility (treat with BB or CCB)
  • Decreased preload (treat with volume)
  • Decreased afterload (treat with phenylephrine)
115
Q

How long should elective surgery be delayed for a patient with a bare metal stent?

A

30 days (3 months preferred)

116
Q

How long should elective surgery be delayed for a patient with a drug eluting stent?

A

Stable ischemic heart disease:
1st generation DES= 12 months minimum
current generation DES= 6 months minimum

Acute coronary syndrome: 12 months minimum

117
Q

How long should elective surgery be delayed for a patient s/p angioplasty?

A

2-4 weeks

118
Q

How long should elective surgery be delayed for a patient s/p CABG?

A

6 weeks (3 months preferred)

119
Q

How does temperature on Cardiopulmonary bypass effect our blood gases?

A

Solubility of a gas is a function of temperature, so hypothermia complicates our interpretation of blood gas results.
As temp decreases, more CO2 is able to dissolve in the blood. This effects the pH.

120
Q

What is an Alpha-stat blood gas?

A

it does not correct for patient’s temperature.
This technique aims to keep intracellular charge neutrality across all temperatures.
*associated with better outcomes in adults.

121
Q

What is a pH-state blood gas?

A

Correct for patient’s temp.
This technique aims to keep a constant pH across all temperatures.
*associated with better outcomes in PEDS.

122
Q

why is a LV vent used during CABG?

A

It removes blood from the LV which usually comes from the Thebesian veins and bronchial circulation (anatomic shunt).

123
Q

How does the IABP help patients?

A

Its a counter pulsation device that improves myocardial O2 supply while reducing myocardial O2 demand.

124
Q

How does the IABP function during the cardiac cycle?

A

Diastole:

  • Pump inflation augments coronary perfusion.
  • Inflation correlates with the dicrotic notch on the aortic pressure wave form.

Systole:

  • Pump deflation reduces after load and improves CO.
  • Deflation correlates with R wave on EKG.
125
Q

4 contraindications to IABP:

A
  • Severe aortic insufficiency
  • Descending aortic disease
  • Severe peripheral vascular disease
  • Sepsis
126
Q

Describe the Crawford classification system of aortic aneurysms:
(see photo in CV pathophys)

A

Type 1: All/most descending thoracic; upper only abdominal
Type 2: All/most descending thoracic; most abdominal
Type 3: lower only descending thoracic; most abdominal
Type 4: None descending thoracic: most abdominal

127
Q

Describe the DeBakey classification system of aortic aneurysms:
(see photo in CV pathophys)

A

Type 1: Tear in ascending aorta + dissection along entire aorta
Type 2: Tear in ascending aorta + dissection only in ascending aorta
Type 3: Tear in proximal descending aorta with:
-Type 3a: dissection is limited to thoracic aorta
-Type 3b: dissection along thoracic and abdominal aorta

128
Q

Describe the Stanford classification system of aortic aneurysms:
(see photo in CV pathophys)

A

Type A: involves ascending aorta

Type B: Doesn’t involve ascending aorta

129
Q

Which law describes the relationship between aortic diameter and risk of aortic rupture in the patient with an abdominal aortic aneurysm?

A

Law of Laplace.

wall tension = transmural pressure X vessel radius
Increased diameter–> increased transmural pressure–> increased wall tension

130
Q

When is surgical repair recommended for aortic aneurysms?

A

Mortality increases significantly once AAA reaches 5.5cm.

Surgical correction once AAA reaches 5.5cm or if it grows more than 0.6-0.8cm/year.

131
Q

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

A

aka Beck’s syndrome (different from Beck’s triad)

Placed above the artery of Adamkiewicz may cause ischemia to the lower portion of the anterior spinal cord.

132
Q

How does anterior spinal artery syndrome present?

A
  • Flaccid paralysis of lower extremities
  • Bowel and bladder dysfunction
  • Loss of temperature and pain sensation
  • Preserved touch and proprioception
133
Q

What is amaurosis fugax?

A

Blindness in one eye.
It is a sign of impending stroke.
Emboli travel from the internal carotid artery to the ophthalmic artery, which impairs perfusion of optic n. and causes retinal dysfunction.

134
Q

EEG during CEA. What does the monitor tell you?

A
  • Monitors cortical electrical function (doesn’t detect subcortical problems)
  • Risk of cerebral hypo perfusion with loss of amplitude, decreased beta-wave activity, and/or appearance of slow wave activity.
135
Q

There is a high incidence of false negatives in EEG possibly caused by things that INCREASE frequency (Hz) such as:

A 
Mild hypercarbia
Early hypoxia
Seizure activity
Ketamine
N2O
Light anesthesia
136
Q

There is a high incidence of false negatives in EEG possibly caused by things that DECREASE frequency (Hz) such as:

A 
Extreme hypercarbia
Hypoxia
Cerebral ischemia
Hypothermia
Anesthetic overdose
Opioids
137
Q

What regional technique can be used for CEAs?

What levels must be blocked?

A

Cervical plexus block (superficial or deep)
Local infiltration

Must cover C2-C4

138
Q

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

A

Baroreceptor reflex

139
Q

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

A

Emergency decompression of surgical site.
If surgeon isn’t immediately available, this falls on you.
Cricothyroidotomy maybe required.

Board Review (8 decks)

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