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Adv Principles 3 > Cards Review > Flashcards

Cards Review Flashcards

1
Q

Normal Tricuspid Area =

Symptoms begin @

A

Normal Tricuspid Area = 4-6cm2

Symptoms begin @ <1.5cm2

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2
Q

Normal Mitral Area =

Symptoms begin @

A

Normal Mitral Valve Area = 4-6cm2

symptoms begin @ 2-3cm2

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3
Q

Normal Area of Aortic Valve

Symptoms begin @

A

Normal area of AVA = 3-4cm2

Symptoms begin @ <1.5 cm2

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4
Q

Normal Pulmonic Area =

Symptoms begin @

A

Normal Pulmonic Valve Area = 4 cm2

Symptoms begin @ 2cm2

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5
Q

First Heart Sound =

A

Closing of the AV valves after atrial contraction, beginning of isovolumetric systole/contraction.

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6
Q

Second Heart Sound =

A

Sound of the SL valves closing, end of ventricular systole = isovolumetric diastole

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7
Q

Blood supply to the

  1. MYOCARDIUM
  2. EPICARDIUM
  3. ENDOCARDIUM
A

Blood supply to the

  1. MYOCARDIUM - Epicardial arteries (RCA/LCA)
  2. EPICARDIUM - Epicardial arteries (RCA/LCA)
  3. ENDOCARDIUM - blood within the chambers
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8
Q

LCA

  • branches
  • supplies
A

LCA

Left Coronary Artery arises from the left coronary sinus, LCA is short, left main arteria then bifurcates to

  1. Left Anterior Descending:
  • Diagonal branch,
  • septal perforating branch that supplies the anterior of LV, anterior 2/3 of interventricular septum, eventually anastomoses with RCA (right dominant system)
  • also called “anterior interventricular branch”
  • Also supplies part of RV
  • leads V1-V2 = septum
  • leads V3-V4 = anterior

2. Left Circumflex:

  • supplies the posterior + lateral LV
  • leads = I, AVL, V5, V6

LCA typically supplies:

  1. Most of the left ventricle [LAD, LCx]
  2. Part of the right ventricle [LAD]
  3. Anterior 2/3 of interventricule septum [LAD]
  4. AV bundle of conducting tissue
  5. SA node in 40% of people
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9
Q

RCA

  • branches
  • supplies
A

RCA

Right coronary artery arises from the right aortic ostia, runs along the coronary sulcus and branches into 1. SA nodal branch, 2. AV nodal branch, and 3. right marginal branch, 4. posterior descending artery/posterior intervenricular branch

  1. SA nodal branch
    * 60% of people supplies the SA node

2. AV nodal branch

  • feeds CRUX of the heart, junction of septa and walls of four chambers. Feeds AV node in 90% of people

3. Right Marginal Branch

  • feeds right border of heart

4. Posterior Descending Artery/Posterior Interventricular Branch

  • In right dominant heart feeds posterior 1/3 of interventricular septum and anastamoses with LAD
  • Lead I, II, AVF

RCA typically supplies:

  1. Right atrium
  2. Most of the right ventricle (some supplied by LAD)
  3. Part of left ventricle
  4. Posterior 1/3 of IV septum in right-dominant heart
  5. SA node in 60% of people - SA nodal branch
  6. AV node in 80-90% of people - AV nodal branch
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10
Q

Coronary Dominance Stats

A

Coronary Dominance Stats

  • Which artery crosses the crux o the heart to feed the posterior IV septum*
    1. In 50% of people it is the RCA
    2. In 20% of people it is the LCA
    3. in 30% of people it is a balanced pattern

APEX SAYS THAT 80% OF POPULATION IS RIGHT DOMINANT.

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11
Q

What Vessel Supplies the SA node? (stats)

A

What Vessel Supplies the SA node? (stats)

  1. RCA - SA nodal branch (60%)
  2. LCx - 40%
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12
Q

Table of EKG leads and vessels

A
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13
Q

Coronary Blood Flow =

A

Coronary Blood Flow =

  • 5% of CO or about 250 mL/min
  • Flow is determined by
    • duration of diastole
    • Cardiac Perfusion Pressure
    • LCA - flow mostly occurs during diastole
    • RCA - flow occurs during both diastole and systole
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14
Q

Cardiac Venous Saturation

A

Cardiac Venous Saturation

  • is the lowest in the body (30%)
  • cardiac myocardial oxygen consumption is very high
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15
Q

Cardiac Perfusion Pressure

  • Formula
  • Normal Values
A

Cardiac Perfusion Pressure

  • Formula
    • Diastolic BP - LV End Diastolic Pressure= CPP
  • Normal Values
    • 50-120 mmHg
    • autoregulated between 50-120 mmHg

Myocardial oxygen demand ALTERS autoregulation - O2 tension acting through adenosine, greatest dilation occurs in smallest vessels

LCA autoregulates more than RCA (LV only perfused during diastole)

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16
Q

What determines HR:

A

What determines HR:

  1. Intrinsic firing rate of the dominant pacemaker cells (SA node - P cells)
    1. “rate of spontaneous phase 4 depolarization of the SA node determines HR”
  2. Autonomic tone
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17
Q

Cardiac Conduction System:

A

Cardiac Conduction System:

  1. SA node - Pacemaker - P cells (spontaneous phase 4 depolarization)
  2. Internodal Tracts - within the atria, help to synchronize atrium
  • Anterior/Bachman’s Bundle = spetum
  • Middle/Wenckebach’s tract = SVC
  • Posterior/Thorel’s tract = septum
  1. AV node (moderator band/septomarginal trabeculae)
  2. Bundle of Hiss
  3. Left and Right Bundle Branches
  4. Purkinje Fibers
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18
Q

RMP vs Threshhold Potential

A

RMP vs Threshhold Potential

RMP:

  • Difference in electrical potential between the inside/outside of the cell [[inside of cell is negative r/t outside of cell]]

Threshhold Potential: [[-70mV]]

  • Internval voltage at which a cell depolarizes
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19
Q

Phases of Myocardial Action Potential:

A

Phases of Myocardial Action Potential: Five Phases

1. Phase 0: Depolarization/Upstroke

  • Depolarization = activation of Fast Na+ channels

2. Phase 1: Initiral Repolarization

    • inactivation of fast Na+ channels
      • Opening of K+ channels -> K+ efflux (slow)
      • Opening of Cl - channels -> chloride influx
  • Cells becomes slightly more negative

3. Phase 2: Plateau

  • Activation of slow voltagae-gated Ca+ channels - OPEN
  • Counters loss of K+ from open K+ channels
  • results in slow repolarization -> plateau
  • Na+ channels remain in active - prolongs absolute refractory time
  • sustained contraciton is necessary for heart’s pumping action

4. Phase 3: Repolarization

  • More K+ channels open (delayed rectifiers)
  • Slow Ca+ channels deactivate
  • This restores cell to RMP (-90 mV)

5. Phase 4: Resting

  • K+ channel leak as cell is permeable to K+
  • Na/K-ATPase: removes Na+ gained during AP, replaces K+ lost during repolarization
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20
Q

Absolute Refractory Period of Heart Muscle

A

Absolute Refractory Period of Heart Muscle

  • much longer absolute refractory period in cardiac muscle compared to nerve/skeletal muscle
  • limits frequency of AP - built in safety mechanism
  • PREVENTS tetanic contractions
  • NO tetanus in cardiac myocytes
  • prevents ectopic pacemakers from stimulating contraction and allows time for ventricle to fill
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21
Q

Phases of SA node Action Potential:

A

Phases of SA node Action Potential:

22
Q

Most of the stroke volume is ejected during

A

Most of the stroke volume is ejected during:

the first 1/3 of systole

23
Q

Phases of Cardiac Cycle:

A

Phases of Cardiac Cycle:

24
Q

Pressure-Volume Loop Cardiac Cycle

A
25
Q

Normal End Diastolic Volume

A

Normal End Diastolic Volume

~ 50 mL

26
Q

EF% Formula

A

EF% Formula

  1. (ESV - EDV) / EDV
  2. SV / EDV

normal EF% = 60-70%

27
Q

Wigger’s Diagram

A
28
Q

Preload =

A

Preload = The ventricular wall tension at the end of diastole

29
Q

Factors that Affect Contractility

A
30
Q

Law of LaPlace as it applies to ventricles (Apex)

A
31
Q

Myocardial Oxygen Extraction =

A

Myocardial Oxygen Extraction = 70%

  • therefore increasing O2 extraction is not a viable method of increasing oxygen supply.
  • Instead, coronary blood flow must increase to meet an increased metabolic demand.
32
Q

Autoregulation is the net effect of:

A

Autoregulation is the net effect of:

  1. Local Metabolism - most important
  • as MVO2 increases, coronary endothelium release adenosine as well as other vasodilatory substances.
  • Vasodilation decreases vascular resistance - leading to increased blood flow, increases coronary perfusion
  1. Myogenic Response
    * “Myogenic refers to the vessels innate ability to maintain a constant vessel diamete”
  2. Autonomic Nervous system:
  • causes of coronary constriction = alpha1(prinzmetal’s angina), histamine-1 - increase intracellular Ca++
  • causes of coronary artery dilation = beta 2, histamine 2, (decrease intracellular Ca++), muscarinic (increase NO)
33
Q

At rest, the myocardium consumes oxygen at rate of

A

At rest, the myocardium consumes oxygen at rate of :

8-10 mL/min/100g with an extraction ratio of 70%

The coronary sinus oxygen saturation is 30%

“Because of this, the myocardium cannot meaningfully increase its extraction ratio when oxygen demand increases. Instead, coronary blood flow and CaO2 must increase to be able to satisfy the demand.”

34
Q

most perioperative myocardial infarctions occur

A

24-48 hours following a surgery

35
Q

Aortic Stenosis Triad

A

Aortic Stenosis Triad

  1. Angina
    1. Due to increased O2 demand and decreased delivery r/t compression of subendothelial vessels r/t hypertrophy
  2. DOE
    1. due to decrease CO
  3. Syncope
    1. likely the result of exercise induced drop in SVR and uncompensated decrease in CO due to low SVR, SV is relatively fixed (r/t hypertrophy)
36
Q

Goals for Anesthesia with AORTIC STENOSIS

A

Goals for Anesthesia with AORTIC STENOSIS

  • Preload: FULL - very SV dependent
    • avoid hypotension r/t reflex tachycardia, decrease DBP = decrease CPP
  • Heart Rate: NORMAL / low normal
    • tachycardic -not enough time for perfusion
    • A.Fib - very dependent on atrial kick
    • bradycardic - decreases CO, cannot compensate bc SV is fixed
  • Afterload: Keep high because need DBP to be high enough to perfuse coronaries
  • Contractility: maintain
  • Rhythm: maintain NSR r/t atrial kick

Avoid decreases in SVR, etomidate > propofol

Avoid drugs that induce tachycardia (ketamine, pancuronium)

High opioid technique, half N2O, half volatile

Careful with DVL r/t catecholamine an tachycardia

Hypotension - tx with alpha agonist, avoid beta stim

37
Q

Hemodynamic Implications with AORTIC STENOSIS

A

Hemodynamic Implications with AORTIC STENOSIS

  • DECREASED ventricular compliance r/t hypertophy r/t pressure
  • Sensitivity to volume depletion, SV is fixed
  • Depend heavily on atrial kick for adequate ventircular filling pressure
  • Wide swings in ventricular filling pressure
  • PCWP will underesimate LVEDP
  • INCREASED LVEDP r/t hypertrophy, this will decrease CPP

Adequate diastolic time + perfusion pressure are key

  • maintain HR - avoid ischemia, SV is fixed so ensure adequate CO
  • maintain DBP - LVEDP is elevated, ensure adqueate CO
38
Q

Magnitude of Regurg in Aortic Regurg depends on

A

Magnitude of Regurg in Aortic Regurg depends on

  • HR - amount of time available for backward flow to occur
  • SVR -pressure gradient across arotic valve

Magnitude of aortic regurg is DECREASED by tachycardia and peripheral vasodilation

39
Q

Symptoms of Aortic Regurg

A

Symptoms of Aortic Regurg

  • symptoms usually minimal if regurg fraction <40%
  • severe with regurg fraction >60%
  • widened pulse pressure
  • decreased diastolic BP
  • bounding pulses
40
Q

Aortic Regurg can be either chronic or acute

A

Aortic Regurg can be either chronic or acute

  1. Chronic:
    * such as in rheumatic heart failure, persistent systemic HTN, or bicuspid aortic valve
  2. Acute:
  • infective endocarditis, trauma, dissection of thoracic aneurysm
  • Pts with acute onset regurg experience severe volume overload in a ventricle that has not had time to compensate (dilate). This typically results in coronary ischemia r/t increase wall stress, rapid deterioration in left ventricular function, decrease CO, pulm edema, and heart failure
41
Q

Anesthetic Implications of Aortic Regurg

A

Anesthetic Implications of Aortic Regurg

“Fast HR, Full Volume, Forward Flow”

“Normal to elevated HR, normal to low BP“

  • Preload: maintain - increase to maximize foward flow/CO
  • HR: normal to high normal (>80 bpm)
    • Bradycardia will increase the duration of diastole which is when regurg occurs, will increase LVEDV, tx bradycardia promptly
  • Contractility: minimize myocardial depression- may disrupt compensation

If LV failure DOES occur -> treat with vasodilator to decrease afterload and inotrope to increase contractility

“overall modest decreases in SVR and modest increases in HR are reasonable goals for aortic regurg + anesthesia”

If using high opioid technique - AVOID bradycardia

42
Q

Underlying patho of hemodynamic changes in [chronic] aortic regurg:

A

Underlying patho of hemodynamic changes in [chronic] aortic regurg:

  • dilation of aortic root and chronic regurg leads to chronic volume overload
  • chamber size [LV] increases gradually
  • Increased wall stress r/t increased LVEDV
  • decrease in forward left ventricular SV r/t regurg
  • eccentric hypertrophic - chamber enlargement + increased wall thickness
  • increase in diastolic chamber compliance - dilation - thus LVEDP is maintained - less risk for ischemia in chronic compared to acute
43
Q

Hemodynamic changes of mitral stenosis

A

Hemodynamic changes of mitral stenosis

  • LV is not subject to pressure or volume overload, actually LV is underloaded.
  • Instead, LA pressures rise -> LA enlargement -> prone to a.Fib
  • Decreasein CO is from decreased LV filling and also if a.fib develops
  • when CO increases - DOE(?) - from increased LA volume
  • severe MS can lead to CHF -> pulm edema
  • pulm. congestion can lead to RV failure, pulm HTN
44
Q

Anesthetic Goals of Mitral Stenosis managment

A

Anesthetic Goals of Mitral Stenosis managment

  • slow, tight/HIGH, full
  • preload: enough to maintain flow across stenotic valve
  • slow: HR, ensure atrial kick is maintained, allow time for ventriuclar filling
  • BP: tight control, avoid decreases in BP because CO is already compromised, maintain slightly higher BP r/t this.
  • prevention or treatment of events that can decrease CO or lead to pulmonary edema
  • AVOID rapid transfusions, careful with lithotomy positions
    *
45
Q

Symptoms of MS

A

Symptoms of MS

  • dyspnea on exertion
  • A. Fib
  • orthopnea, paroxysmal noctural dyspnea
  • P. Mitrale on EKG
46
Q

most common valve dx in the US: (2)

A

most common valve dx in the US: (2)

  1. Aortic stenosis (calcifcication, bicuspid valve)
  2. Mitral regurg
47
Q

MR is associated with:

A

MR is associated with:

  1. Mitral stenosis, usually in the context of rhuematic heart dx
  2. ISOLATED MR is associated with IHD, hx of inferior MI, papillary muscle dysfunction
48
Q

Severe MR is classified as

A

Severe MR is classified as

MR >60%

<30% = Mild Symptoms

30-60% = Moderate Symptoms

>60% = Severe Symptoms

49
Q

Chronic MR can develop…

A

Chronic MR can develop…

  • asymptomatically because the LA will expand to accomodate volume.
50
Q

Acute MR presents as

A

Acute MR presents as

  • Usually in the setting of inferior MI
  • papillary muscle rupture
  • acute pulm edema
  • cardiogenic shock
  • holosystolic murmur
51
Q

Can monitor degree of MR via

A

Can monitor degree of MR via :

V wave on CVP

52
Q

Anesthetic Goals of MR

A

Anesthetic Goals of MR

  • Full, Fast, Forward,
  • Preload: Full - ensure enough forward flow
  • HR: Fast, less time for regurg
  • afterload: low, normal, ensure forward flow
  • Contractility - maintain
  • Rhythm - NSR, normal/fast, less reliant on atrial kick

Avoid sudden decreases in HR - more time for regurg

Prevent bradycardia

Adv Principles 3 (2 decks)

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