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BOARD REVIEW > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Define chronotropy, inotropy, dromotropy, and lusitropy

A

Chronotropy: heart rate

Inotropy: strength of contraction (contractility)

Dromotropy: conduction velocity (how fast the action potential travels per time)

Lusitropy: rate of mycardial relaxation (during diastole)

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2
Q

Describe the function of the sodium potassium pump

A

The Na+/K+ Pump maintains the cell’s resting potential. Said another way, it separates charge across the cell membrane keeping the inside of the cell relatively negative and the outside of the cell relatively positive

How it works:

  • it removes the 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 the cell
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3
Q

List the 5 phases of ventricular action potential and describe ionic movement during each phase

A

Phase 0: depolarization; Na+ influx

Phase 1: initial repolarization; K+ efflux & Cl- influx

Phase 2: Plateau; Ca+2 influx

Phase 3: Repolarization; K+ efflux

Phase 4: Na+/K+ pump restores resting membrane potential

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4
Q

List the 3 phases of the SA node action potential and describe the ionic movement during each phase

A

Phase 4: spontaneous depolarization; leaky to Na+

Phase 0: Depolarization; Ca+ influx

Phase 3: Repolarization; K+ efflux

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5
Q

What is the process that determines intrinsic heart rate, what physiologic factors alter it?

A

HR is determined by the rate of spontaneous phase 4 depolarization in the SA node

We can increase HR by manipulating 3 variable:

  1. The rate of spontaneous phase 4 depolarization increases (reaches TP faster)
  2. TP becomes more negative (shorter distance between RMP and TP)
  3. RMP becomes less negative (shorter distance btw RMP and TP)

When RMP and TP are CLOSE, it’s easier for the cell to depolarize

When RMP and TP are FAR, it’s harder for the cell to depolarize

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6
Q

What is the calculation for MAP? What is the normal value?

A

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

OR

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

Normal = 70 - 105 mmhg

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7
Q

What is the formula for SVR?

A

[(MAP - CVP) / CO] x 80

Normal = 800 - 1500 dynes/sec/cm^5

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8
Q

What is the formula for PVR?

A

[(MAP - PAOP) / CO] x 80

Normal = 150 - 200 dynes/sec/cm^5

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9
Q

Describe the Frank-Starling relationship

A

It describes the relationship btw vascular volume (preload) and ventricular output (CO)

  • increase preload > increased myocardial stretch > increased ventricular output (and vice versa)

Increasing preload increases ventricular output, put only to a certain point. To the right of the plateau, additional volume overstretches the ventricular sarcomeres, decreasing the number of cross bridges that can be formed and ultimately reducing cardiac output. This contributes to. Pulmonary congestion and increases PAOP.

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10
Q

What factor increase contractility? (5)

A

Just remember the that Chemicals affect Contractility - particularly Calcium (the three C’s)

Almost everything listed below either alters the amount of Ca+2 available to bind to the myofilaments or impacts the sensitivity of the myofilaments to Ca+2

  1. SNS stimulation
  2. Catecholamines
  3. Calcium
  4. Digitalis
  5. Phosphodiesterase inhibitors
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11
Q

What factors decrease contractility? (10)

A
  1. Myocardial ischemia
  2. Severe hypoxia
  3. Acidosis
  4. Hypercapnia
  5. Hyperkalemia
  6. Hypocalcemia
  7. Volatile anesthetics
  8. Propofol
  9. Beta-blockers
  10. Calcium-channel blockers
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12
Q

Discuss excitation-contraction coupling in the cardiac myocyte

A
  • the myocardial cell membrane depolarizes
  • during the plateau of the ventricular action potential (phase 2), Ca+2 enters the cardiac myocyte through L-type Ca+2 channels in the T-tubules
  • Ca+2 influx turns on the ryanodine-2 receptor, which releases Ca+2 from the SR (calcium-induced calcium-release)
  • Ca+2 binds to troponin C (myocardial contraction)
  • Ca+2 unbinds from the troponin C (myocardial relaxation)
  • most of the Ca+2 is returned to the SR via the SERCA2 pump
  • once inside the SR, Ca+2 binds to a storage protein called calsequestrin
  • the next time the cardiac myocyte depolarizes, the whole process repeats
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13
Q

What is afterload and how do you measure it in the clinical setting?

A

Afterload is the force the ventricle must overcome to eject its volume

We use SVR as a surrogate for LV afterload

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14
Q

What law can be used to describe ventricular afterload?

A

The law of Laplace

Wall stress = (intraventicular pressures x radius) / ventricular thickness

  • intraventricular thickness is the force that pushes the heart apart
  • wall stress is the force that hold the heart together (it counterbalances intraventricular pressure)
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15
Q

What decreases wall stress? (3)

A
  1. Decreased intraventricular pressure
  2. Decreased radius
  3. Increased wall thickness
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16
Q

List 3 conditions that set afterload proximal to the systemic circulation

A
  1. Aortic stenosis
  2. Hypertrophic cardiomyopathy
  3. Coartication of the aorta
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17
Q

Relate the 6 stages of the cardiac cycle 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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18
Q

What is ejection fraction and how do you calculate it?

A

EF is a measure of systolic function (contractility). It is the percentage of blood that is ejected from the heart during systole. Said the other way, the EF is the stroke volume relative to the end-diastolic volume

  • normal EF: 60-70%
  • LV dysfunction is present when EF < 40%
  • SV is calculated as EDV-ESV
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19
Q

Calculate the stroke volume and or/ejection with a pressure volume loop

A
  • SV: width of the loop
  • EDV: right side of the loops at the x-axis
  • enter both variables into the equation in the previous question
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20
Q

What is the best TEE view for diagnosing myocardial ischemia?

A

Midpapillary muscle level in short axis

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21
Q

What is the equation for the coronary perfusion pressure?

A

CPP - aortic DBP - LVEDP

  • aortic DBP is the pushing force
  • LVEDP is the resistance to the pushing force

Therefore, CPP can be improved by increasing AoDBP or decreasing LVEDP (PAOP)

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22
Q

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

A

LV subendocardium is most susceptible to ischemia.

The LV subendocardium is best perfused during diastole. As aortic pressure increases, the LV tissue compresses its own blood supply and reduces blood flow. The high compressive pressure in the LV subendocardium coupled with a decreased coronary artery blood flow during systole increase coronary vascular resistance and predisposes this region to ischemia.

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23
Q

What factors increase myocardial oxygen demand? (7)

A
  1. Tachycardia
  2. HTN
  3. SNS stimulation
  4. increased wall tension
  5. Increased EDV
  6. Increased afterload
  7. Increased contractility
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24
Q

What factors decrease myocardial oxygen delivery? (8 w/in sub categories)

A
  • decreased coronary flow
    1. Tachycardia
    2. Decreased aortic pressure
    3. Decreased vessel diameter (spasm or hypocapnia)
    4. Increased EDP
  • decreased CaO2
    5. Hypoxemia
    6. Anemia
  • decreased oxygen extraction
    7. Left shift of Hgb dissociation curve ( decreased P50)
    8. Decreased capillary density
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25
Q

What is nitric oxide?

A

NO is a smooth muscle relaxant that induces vasodilation

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26
Q

Discuss the steps in the nitric oxide cGMP pathway

A
  1. NO synthase catelyzes the conversion of L-arginine to nitric oxide
  2. NO diffuses from the endothelium to the smooth muscle
  3. NO activates guanylate cyclase
  4. Gunylate cyclase converts guanosine triphosphate to cyclic guanosine monophosphate
  5. Increased cGMP reduces intracellular Ca+2 leading to smooth muscle relaxation
  6. Phophodiesterase deactivates cGMP to guanosine monophosphate (this step turns off the NO mechanism)
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27
Q

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

A

S1: closure of the mitral and tricuspid valves (marks onset of systole)

S2: closure of the aortic & pulmonic valves (marks onset of diastole)

S3: may suggest systolic dysfunction (normal in kids and theletes)

S4: may suggest diastolic dysfunction

Loop: think “MOM”

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28
Q

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

A
  1. Stenosis:
    - there is a fixed obstruction to forward flow during chamber systole
    - the chamber must generate a higher than normal pressure to eject the blood
  2. Regurgitation:
    - the valve is incompetent (its leaky)
    - some blood flows forward and some blood flows backward during chamber systole
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29
Q

How does the heart compensate for pressure overload?

A

Stenosis = pressure overload = concentric hypertrophy

**sarcomeres added in parallel

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30
Q

How does the heart compensate for volume overload?

A

Regurgitation = volume overload = eccentric hypertrophy

**sarcomeres added in series

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31
Q

List hemodynamic goals for the 4 common valvular defects

A
  1. Aortic stenosis: SLOW NORMAL
    - increase preload
  2. Mitral stenosis: SLOW NORMAL
    - avoid increased PVR
  3. Aortic regurg/insufficiency : FULL, FAST, FORWARD
    - decrease SVR
  4. Mitral regurg/insufficiency: FULL, FAST, FORWARD
    - decreased SVR
    - avoid increased PVR
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32
Q

What is the most common dysrhythmia associated with mitral stenosis?

A

Atrial fibrillation

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33
Q

List 6 risk factors for perioperative cardiac mobidity and mortality for non-cardiac surgery

A
  1. High risk surgery
  2. History of ischemic heart disease (unstable angina confers the greatest risk of perioperative MI)
  3. History of CHF
  4. History of CVA
  5. DM
  6. Serum creatinine > 2 mg/dL
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34
Q

What is the perioperative myocardial infarction in the pt with previous MI?

A
  • general population = 0.3%
  • MI if > 6 mo = 6%
  • MI if 3-6 mo = 15%
  • MI < 3 mo = 30%

**the highest risk of reinfarction is the greatest within 30 days of an acute MI. For this reason, the ACC/AHA guidelines recommend a minimum of 4-6 weeks before considering elective surgery in a pt with a recent MI

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35
Q

Categorize high risk surgical procedures according to cardiac risk

A

High risk = > 5%

  • emergency surgery (especially in the elderly)
  • open aortic surgery
  • peripheral vascular surgery
  • long surgical procedures with significant shifts and/or blood loss
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36
Q

Categorize intermediate risk surgical procedures according to cardiac risk

A

Intermediate risk = 1 -5%

  • carotid endarterectomy
  • head and neck surgery
  • intrathoracic or intraperitoneal surgery
  • orthopedic surgery
  • prostate surgery
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37
Q

Categorize low risk surgical procedures according to cardiac risk

A

Low risk = < 1%

  • endoscopic procedure
  • cataract surgery
  • superficial procedures
  • breast surgery
  • ambulatory procedures
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38
Q

What is the 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

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39
Q

How do you interpret cardiac enzymes in the pt with a suspected ischemic event?

A

A cell requires O2 to maintain the integrity of it cell membrane, and a cell deprived of oxygen dies and releases its contents into the systemic circulation

  • infarcted myocardium releases 3 key biomarker: creatinine kinase-MB, troponin I, and troponin T
  • cardiac troponins are more sensitive than CK-MB for the diagnosis of myocardial infarction
  • these values must be evaluated in the context of time the patient’s EKG
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40
Q

What is the timeframe for CK-MB, troponin I and troponin T

A

Initial elevation:

  • CK-MB: 3-12 hrs
  • Troponin I: 3-12 hrs
  • Troponin T: 3-12 hours

Peak elevation:

  • CK-MG: 24 hrs
  • Troponin I: 24 hrs
  • Troponin T: 12-48 hrs

Return to baseline

  • CK-MB: 2-3 days
  • Troponin I: 5-10 days
  • Troponin T: 5-14 days
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41
Q

How do you treat intraoperative myocardial ischemia?

A

Tx of myocardial ischemia should focus on interventions that make the hear slower, smaller, and better perfused

Increased O2 demand:
Cause:
- increased HR > Give BB’s to get a HR < 80 bpm
- increased BP > increase depth of anesthesia, vasodilator
- increased PAOP > nitroglycerin

Decreased O2 supply:
Cause:
- decreased HR > anticholinergic, pacing
- decreased BP > vasoconstrictor, reduce depth of anesthesia
- increased PAOP > nitroglycerin, inotrope

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42
Q

What factors reduce ventricular compliance?

A
  1. Age > 60 years
  2. Ischemia
  3. Pressure overload hypertrophy (aortic stenosis or HTN)
  4. Hypertophic obstructive cardiopmyopathy
  5. Pericardial pressure (increased external pressure)

**clinical takeway is that a higher filling pressures are required to prime the ventricle

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43
Q

What is the difference btw systolic and diastolic HF?

A

Systolic heart failure: the ventricle doesn’t empty well
- the hallmark is decreased EF with an increased end-diastolic volume. Volume overload commonly causes systolic dysfunction

Diastolic heart failure: the ventricle doesn’t fill properly
- diastolic failure occurs when the heart is unable to relax and accept the incoming volume, because ventricular compliance is reduced. The defining characteristic of diastolic dysfunction is symptomatic heart failure with a normal ejection fraction.

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44
Q

Discuss the pathophysiology of systolic HF

A

Preload: already high (diuretics if too high)

Afterload: decrease to reduce myocardial workload (SNP); maintain CPP

Contractility: augment with inotropes as needed (dobutamine)

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

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45
Q

Discuss the pathophysiology of diastolic HR

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: ususally normal

HR: slow/normal to increase diastolic time and CPP

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46
Q

List the 6 complications of hypertension

A

The problem with HTN: a high afterload increase myocardial work and an elevated arterial driving pressure damages nearly every organ in the body

  • left ventricular hypertrophy
  • ischemic heart disease
  • CHF
  • arterial aneurysm (aorta, cerebral circulation)
  • stroke
  • ESRD
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47
Q

How does HTN contribute to CHF?

A

HTN > increased myocardial wall tension > increased MVO2 > coronary insufficiency > CHF

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48
Q

How does HTN affect cerebral autoregulation?

A

The cerebral autoregulation curve describes the range of blood pressures where cerebral perfusion pressure remains constant

Chronic HTN ahifts this curve to the right. This adaptation helps the pt’s brain tolerate a higher range of BP, however, this comes at the expense of not being able to tolerate a lower BP. Remember that BP past the range of autoregulation is pressure dependent.

  • malignant HTN increases the risk of hemorrhagic stroke and cerebral edema
  • hypotension increases the risk of cerebral hypoperfusion
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49
Q

What’s the difference btw primary and secondary HTN?

A
  • primary (essential) HTN is more common and has no identifiable cause (95% of all HTN cases)
  • secondary hypertension is caused by some other pathology (5% of all HTN cases)
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50
Q

List 6 causes of secondary HTN

A
  1. Coartication of the aorta
  2. Renovascular disease
  3. Hyperadrenocorticism (Cushing’s syndrome)
  4. Hyperaldosteronism (Conn’s disease)
  5. Pheochromocytoma
  6. Pregnancy-induced HTN
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51
Q

What are the 2 major classes of calcium channel blockers? List examples of each

A
  1. Dihydropyridines: target vascular smooth muscle to cause vasodilation > decreased SVR
    - ex: nifedipine, nicardipine, nimodipine, amlodipine
  2. Non-dihydropyridines: target myocardium (mostly) to decrease chronotropy (HR), inotropy, dromotropy (conduction velovity) and coronary vascular resistance
    - ex: verapamil, diltiazem
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52
Q

Describe the pathophysiology of constrictive pericarditis

A

Constrictive pericarditis is cause by fibrosis or any condition where the pericardium becomes thicker

During diastole, the ventricles cannot fully relax, and this reduces compliance and limits diastolic filling. Ventricular pressures increase, which creates a backpressure to the peripheral circulation. The ventricles adapt by increasing myocardial mass, but over time this impairs systolic function

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53
Q

Describe the anesthetic management of constrictive pericarditis

A
  • CO is dependent of HR > avoid bradycardia
  • preserve HR and contractility > ketamine, pancuronium, volatile agents w/ caution
  • *opioids, benzos, and etomidate OK
  • maintain afterload
  • aggressive PPV can decrease venous return & CO
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54
Q

Describe the pathophysiology of pericardial tamponade

A

Cardiac tamponade occurs when fluid accumulates inside the pericardium. What separates it from a pericardial effusion is that the excess fluid exerts an external pressure on the heart limiting its ability to fill and act like a pump

CVP rises in tandem with pericardial pressure. As ventricular compliance deteriorates, left and right sided cardiac diastolic pressure (CVP and PAOP) begin to equalize. TEE is the best method of diagnosis, and the best treatment is pericardiocentesis or pericardiostomy

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55
Q

What is Kussmaul’s sign?

A

Kussmaul’s sign indicates impaired right ventricular filling d/t a poorly compliant RV or pericardium. Since RV filling is affected, the blood essentially “backs up” which causes jugular vein distention and an increased CVP. IT is most pronounced during inspiration.

56
Q

List 2 conditions commonly associated with Kussmaul’s sigm

A
  1. Constrictive pericarditis
  2. Cardiac tamponde

**both limit RV filling

57
Q

What is pulsus paradoxus?

A

Pulsus paradoxus represents an exaggerated decrease in SBP during inspiration (SBP falls more than 10 mmHg during inspiration). This finding suggest impaired diastolic filling

Negative intrathoracic pressure on inspiration > increased VR to RV > bowing of ventricular septum toward LV > decreased SV > decreased CO > decreased SBP

58
Q

Describe the anesthetic management of constrictive pericarditis

A
  • CO is dependent on HR > AVOID bradycardia
  • Preserve HR and contractility > ketamine, pancuronium, volatile agents with caution
  • *opioids, benzos and etomidate OK
  • maintain afterload
  • aggressive PPV can decrease venous return and CO
59
Q

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

A

Associated with acute cardiac tamponade

  1. Hypotension (decreased stroke volume)
  2. Jugular vein distention (impaired venous return to right heart)
  3. Muffled heart tones (fluid accumulation in the pericardial space attenuates sound waves)
60
Q

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

A

Local anesthetics is the preferred choice because they do not alter hemodynamics.

If a general anesthetic is required, your primary goal is to preserve myocardial function. SV is severely decreased and increased SNS tone (increased contractility and increased afterload) provide compensation. Any drug that depresses the myocardium or reduces afterload can precipitate CV collapse.

61
Q

What drugs are safe to use for pericardiocentesis? (4)

A
  1. Ketamine (activation of the SNS makes this the best choise)
  2. Nitrous Oxide
  3. Benzos
  4. Opioids
62
Q

What drugs do you avoid to use for pericardiocentesis? (5)

A
  1. Halogenated anesthetics
  2. Propofol
  3. Thiopental
  4. High dose opioids
  5. Neuroaxial anesthesia
63
Q

List 6 pt factors that arrant abx prophylaxis against infective endocarditis

A
  1. Previous infective endocarditis
  2. Prosthetic heart valve
  3. Unrepaired cyanotic congenital heart disease
  4. Repaired congenital heart defect if the repair is < 6 months old
  5. Repaired congenital heart disease with residual defects that have impaired endothelialization at the graft site
  6. Heart transplant with valvuloplasty
64
Q

List 3 surgical procedures that warrant abx prophylaxis against infective endocarditis

A

High risk procedures are thought to be “dirty” procedures where the risk of transient bacteria outweighs the risk of abx therapy:

  1. Dental procedures involving gingival manipulation and/or damage to mucosa lining
  2. Respiratory procedures that perforate the mucosal lining with incision or biopsy
  3. Biopsy of infective lesions on the skin or muscle
65
Q

What are the 3 key determinants of flow through the left ventricular outflow tract?

A
  1. Systolic LV volume
  2. Force of LV contraction
  3. Transmural pressure gradient
66
Q

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

A

Things that tend to distend the LV outflow (LVOT) are good for cardiac output, while things that narrow at the LVOT are bad

67
Q

What conditions distend the LVOT?

A

Conditions that distend the LVOT (decrease obstruction and increase CO)

  • increased systolic volume (increased preload or decreased HR)
  • decreased contractility
  • increased aortic pressure (increased transmural pressure gradient > pressure distends the LVOT)
68
Q

What conditions narrow the LVOT?

A

Conditions that narrow the LVOT )increased obstruction and decrease CO)

  • decreased systolic volume (decreased preload or increased HR)
  • increased contractility
  • decreased aortic pressure (transmural pressure gradient)
69
Q

What hemodynamic conditions reduce cardiac output in the pt with hypertrophic cardiomyopathy

A
  1. Increased HR (tx w. BB’s or CCB’s)
  2. Increased contractility (tx with BB’s or CCB’s)
  3. Decreased preload (treat with volume)
  4. Decreased afterload (tx w/ phenylephrine)
70
Q

How long should elective surgery be delayed in the pt with a bare metal stent? Drug eluting stent? S/p angioplasty? S/p CABG?

A
  1. Angioplasty: 2-14 weeks
  2. Bare metal stent: 30 days (3 months preferred)
  3. Drug eluting stent:
  • stable ischemic heart disease (SIHD): 1st generation DES = 12 months; current generation DES = 6 months
  • Acute coronary syndrome (ACS): 12 months minimum

CABG: 6 weeks (3 months preferred)

71
Q

What is the difference btw alpha-stt and pH-stat blood gas measurement during CPB?

A

Because the solubility of a gas is a function of temperature, it should make sense that hypothermia complicates out interpretation of blood gas results during CBP. As temp decreases, more CO2 is able to dissolve in the blood. By extension this effects the pH. Knowing this poses an interesting question about how to best management blood pH during CBP with hypothermia.

  • Alpha-stat does not correct for the pt’s temperature; this technique aims to keep charge neutrality across all temperatures; it is associated with better outcomes in adults
  • pH-stat: corrects for the pt’s temperature; this technique aims to keep a constant pH acress all temps; it is associated with better outcomes in peds.
72
Q

Why is a left ventricular vent used during CABG surgery?

A

A left ventricular vent removes blood from the LV; the blood usually comes from the Thebasian veins and bronchial circulation (anatomic shunt).

73
Q

How does the intra-aortic balloon pump function throughout the cardiac cycle? How does this help the pt?

A

The IABP is a counter pulsation 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 cardiac output
  • deflation with R wave on the EKG
74
Q

List 4 contraindications fo IABP

A
  1. Severe aortic insufficiency
  2. Descending aortic disease
  3. Severe peripheral vascular disease
  4. Sepsis
75
Q

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

A

Applying the Law of Laplace, we know the diameter of the AAA correlates with the risk of rupture

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

Since mortality increases significantly once the AAA reaches 5.5 cm, surgical correction is recommended when the aneurysm exceeds 5.5 cm or if it grow more than 0.6 - 0.8 cm/yr

76
Q

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

A

An aortic cross clamp placed above the artery of Adamkiewicz may cause to the lower portion of the anterior spinal cord. This can result in spinal artery syndrome, otherwise known as Beck’s syndrome.

77
Q

How does anterior spinal artery syndrome present? (4)

A
  1. Flaccid paralysis of the lower extremities
  2. Bowel and bladder dysfunction
  3. Loss of temperature and pain sensation
  4. Preserved touch and proprioception
78
Q

What is amaurosis fugax?

A

Amaurosis fugax (blindness in one eye) is a sign of a impending stroke. Emboli travel from the internal carotid artery to a ophthalmic artery, which impairs perfusion of the optic nerve and causes retinal dysfunction

79
Q

A pt is undergoing carotid endarterectomy with EEG monitoring. What does this monitor tell you, and what conditions can lead to false conclusions?

A

EEG: monitors cortical electrical function (does not detect subcortical problems)

  • risk of cerebral hypoperfusion with loss of amplitude, decreased beta-wave activity, and/or apperance of slow wave activity
  • high incidence of false-negatives
80
Q

List 6 causes of increased frequency of EEG monitoring

A
  1. Mild hypercarbia
  2. Early hypxia
  3. Seizure activity
  4. Ketamine
  5. N2O
  6. Light anesthesia
81
Q

List 6 causes of decreased frequency of EEG monitoring

A
  1. Extreme hypercarbia
  2. Hypoxia
  3. Cerebral ischemia
  4. Hypothermia
  5. Anesthetic overdose
  6. Opioids
82
Q

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

A

Techniques for regional anesthesia for a pt undergoing CEA include:

  1. Cervical plexus block (superficial or deep)
  2. Local infiltration

Regional anesthesia must cover C2-C4

83
Q

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

A

Baroreceptor reflex

84
Q

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

A

This pt requires emergency decompression of surgical site. If the surgeon isn’t immediately available, this falls on you. Cricothyroidotomy may be required.

85
Q

Describe three facts about ventricular myocytes

A
  1. Resting membrane potential is -90mV
  2. Hypokalemia decreases resting membrane potential
  3. They contain more mitochondria than skeletal myocytes
86
Q

Which phase of the ventricular action potential is calcium conductance the greatest?

A
  • Phase 2 - Plateau phase
87
Q

Which current is responsible for slow phase four depolarization in the SA node

A

I-f

  • the funny current is the primary determinant of the pacemaker’s intrinsic heart rate; said another way, it sets the rate of spontaneous phase 4 depolarization in the SA node
88
Q

What is the normal oxygen delivery in a 70-kg adult?

A

1000 mL/min

89
Q

Blood flow is inversely proportional to what?

A

hematocrit

90
Q

Which variables are related by the Frank-Starling mechanism?

A

Pulmonary artery occlusion pressure and stroke volume

91
Q

What three factors impair cardiac contractility?

A
  1. Hypoxia
  2. Hypercapnia
  3. Hyperkalemia
92
Q

A decrease in what would most likely cause stroke volume to increase?

A

Afterload

93
Q

Which phase of the cardiac cycle is characterized by an open mitral valve and closed aortic valve? (3)

A
  1. Rapid ventricular filling
  2. Diastasis
  3. Atrial systole
94
Q

Which two drugs cause coronary vasodilation?

A
  1. Adenosine

2. Beta-2 stimulation

95
Q

Which condition increases myocardial oxygen consumption?

A

Decreased diastolic filling

96
Q

How does nitric oxide work?

A
  1. It reduces right ventricular afterload

2. It is inactivated by hemoglobin

97
Q

Describe the S1 heart sound

A
  • closure of the mitral & tricuspid valves
  • marks onset of systole
  • end of LV filling and beginning of isovolumetric contraction
  • volume proprtional to force of contracting ventricle
  • LOUDER: vigorously contracting ventricle
  • SOFTER: poorly contracting ventricle
98
Q

Describe the S2 heart sound

A
  • closure of aortic & pulmonary valves
  • marks onset of diastole
  • end of LV ejection and beginning of isovolumetric relaxation
  • volume proportionate to LV pressure decrease at the end of systole
  • LOUDER: hypertension
  • SOFTER: hypotension
99
Q

Describe the S3 heart sound

A
  • suggests flaccid and inelastic heart - think heart failure
  • heard during middle 1/3 of diastole, after S2
  • gallop rhythm; described as a rumbling sound
100
Q

Describe the S4 heart sound

A
  • caused by atrial systole

- heard before S1

101
Q

Which valve diseases are associated with eccentric hypertrophy?

A
  1. Mitral regurgitation

2. Aortic regurgitation

102
Q

Following aortic valve repair, what will happen to the left end-systolic volume?

A

It decreases d/t a reduction in the impedance to ventricular ejection

103
Q

At what number is aortic stenosis considered severe? What are the most common causes?

A

< 0.8 cm2

Common causes:

  1. Calcification of valve leaflets
  2. Rheumatic fever
  3. Infective endocarditis
104
Q

What are the symptoms of aortic stenosis?

A

Think SAD:

  1. Syncope
  2. Angina
  3. Dyspnea
105
Q

What is anesthetic management of aortic stenosis?

A

“SLOW NORMAL”

  1. HR: 70-80 bpm and NSR
  2. Preload: increase; adequate LVEDP is required to fill the non-compliant LV
  3. SVR: maintain or increase; SV is fixed by the stenotic valve, therefore, CO is dependent on HR
    - hypotension > decreased aortic root pressure > decreased CPP > myocardial ischemia

**hypotension should be treated with an alpha-1 agonist; this will increase SVR and coronary perfusion pressure without increasing HR

  1. Contractility: maintain
  2. PVR: usually normal

**AVOID spinal anesthesia!

106
Q

Which drugs are likely to contribute to hemodynamic instability in the pt with symptomatic severe mitral stenosis?

A
  1. Ephedrine; increases HR and CO
  2. Nitrous oxide; increases PVR, increasing the workload on the RV

**anesthetic goals for MS: FULL, SLOW, CONSTRICTED

107
Q

What drugs should be used to treat severe mitral stenosis?

A
  1. Phenylephrine

2. Furosemide

108
Q

What are some common causes of mitral stenosis?

A
  1. RA
  2. Systemic lupus erythematous
  3. Congenital defect
  4. Left atrial myxoma
  5. Carcinoid syndrome
  6. Iatrogenic following mitral valve repair
109
Q

What is the anesthetic management of mitral regurgitation?

A

FULL, FAST, FORWARD

  • Minimize the regurgitant volume
110
Q

What things make mitral valve regurgitation worse? (3)

A
  1. Decreased HR
  2. Increased SVR
  3. Increased LV to LA pressure gradient
111
Q

What are some common causes of mitral valve regurgitation?

A
  1. Rheumatic fever
  2. Ischemic heart rate
  3. Endocarditis
  4. Ruptured chordae tendineae
  5. MVP
  6. SLE
  7. RA
  8. Carcinoid syndrome
112
Q

What makes the size of regurgitant volume worse in aortic regurgitation?

A

FULL, FAST, FORWARD

Made worse by:

  1. Bradycardia
  2. Increased SVR (increased aortic-LV pressure gradient)
  3. Large valve orifice (larger area for the floor to return through)
113
Q

Which valvular disorder are associated with a systolic murmur?

A
  1. Mitral insufficiency

2. Aortic stenosis

114
Q

Describe the mnemonic for all 4 murmurs:

A
  1. ASSS: aortic stenosis is a systolic murmur heard at the right sternal border
  2. ARDS: aortic regurgitation is a diatolic murmur heard at the right sternal border
  3. MSDA: mitral stenosis is a diastolic murmur heard at the apex of the left axilla
  4. MRSA: mitral regurgitation is a systolic murmur heard at the apex and left axilla
115
Q

What is the formula for coronary perfusion pressure?

A

CPP = aortic diastolic pressure - LVEDP

**PAOP is a surrogate for LVEDP

116
Q

What factors decrease cardiac compliance?

A
  1. Age >60 year
  2. Ischemia
  3. Pressure overload hypertrophy (aortic stenosis or HTN)
  4. Hypertrophic obstructive cardiomyopathy
  5. Pericardial pressure (increased external pressure)
117
Q

What factors increase cardiac compliance?

A
  • factors that dilate the heart:
  1. Chronic aortic insufficiency
  2. Dilated cardiomyopathy
118
Q

Which finding would be the most likely to occur in a pt with congestive heart failure?

A

Increased sympathetic tone

  • pt’s with CHF rely on elevated levels of circulating catecholamines (increased SNS tone)
119
Q

What are three complications r/t chronic HTN?

A
  1. Left ventricular hypertrophy
  2. Dysrhythmias
  3. Increased myocardial oxygen consumption

**will NOT see decreased diastolic time; this is determined by HR

120
Q

What is the most common cause of secondary HTN?

A

Secondary = identifiable cause

  • renal artery stenosis
121
Q

A pt with a history of CAD and an ejection fraction of 35% has developed atrial fibrillation with RVR. What is the best tx for this pt?

A
  • Diltiazem

**in the pt with impaired contractility, diltiazem is a better choice than verapamil

122
Q

Describe two things that occur during during constrictive pericardititis

A
  1. Kussmaul’s sign is usually present

2. Bradycardia should be avoided

123
Q

Describe Beck’s triad

A
  1. Muffled heart tones: d/t fluid accumulation in the pericardial sac
  2. Jugular vein distension: d/t decreased venous return to the right heart
  3. Hypotension: d/t decreased stroke volume

**use ketamine for induction!

124
Q

What drugs are safe to use for cardiac tamponade?

A
  1. Ketamine
  2. N2O
  3. Benzos
  4. Opioids
125
Q

What drugs to avoid for cardiac tamponade?

A
  1. Halogenated anesthetics
  2. Propofol
  3. Thiopental
  4. High dose opioids
  5. Neuroaxial anesthesia

**pt’s are HR dependent

126
Q

Which procedure puts a pt with a history of infective pericarditis at the highest risk of an adverse outcome?

A
  • dental implant

**should receive preoperative abx for any dirty procedure (Dental procedure, respiratory procedures that perforate the mucosal lining with incision or biopsy, biopsy of infective lesions on the skin or muscle)

127
Q

What reduces outflow obstruction in obstructive hypertrophic endocarditis?

A
  1. Phenylephrine
  2. Esmolol
  3. 500 mL of 0.9% NaCl bolus

**things that distend the LVOT are GOOD, things that narrow the LVOT are BAD

  • nitroglycerine reduces preload which causes the LVOT to narrow, thereby worsening the obstruction
128
Q

What is SAM? When does it occur?

A

SAM: systolic anterior motion

  • caused by the Venturi effect as blood rapidly flows across the LVOT; remember that velocity increases through a point of stricture
  • diagnosed with TEE
  • can occur following mitral valve repair (NOT replacement)
129
Q

How long should a pt wait to have elective surgery after bare metal stent placement?

A
  • 30 days
130
Q

Priming the CBP machine with a balanced salt solution decrease what? (3)

A
  1. Oxygen carrying capacity
  2. Plasma drug concentration
  3. Blood viscosity
  4. Blood hematocrit

**does NOT decrease microvascular flow

131
Q

When is awareness most likely to occur ruing CABG?

A
  • sternotomy
132
Q

What two statements describe an IABP?

A
  1. It is contraindicated in severe aortic insufficiency

2. It inflates during diastole and increased myocardial oxygen supply

133
Q

What increases following cross clamp removal during abdominal aortic aneurysm?

A
  1. Total body oxygen consumption
  2. Pulmonary vascular resistance

**when the clamp is release, ischemic tissues release acid and vasoactive substances into systemic circulation; this increases PVR and PAP

134
Q

Occlusion of the artery of Adamkiewicz causes what to occur?

A
  1. Loss of temperature and pain sensation
  2. Flaccid paralysis of the LE’s
  3. Bowel and bladder dysfunction

**does NOT cause loss of propioception

135
Q

What is the best monitor of neurologic integrity during a CEA?

A
  • an awake patient
136
Q

In the pt with right subclavian steal syndrome, arterial flow is diverted from the:

A

Right vertebral artery to the right subclavian artery

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