Cardiac A &P Flashcards

1
Q

What does the left circumflex perfuse?

A

Supplies the left atrial wall, the posterior & lateral LV, anterolateral papillary muscle, the AV node in 10% of the population, and the SA node in 40-45% of the population.

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2
Q

What does the right coronary artery perfuse?

A

Supplies blood to the SA and AV nodes, the RA and RV, the posterior third of the interventricular septum, the posterior fascicle of the left bundle branch, and the interatrial septum.

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3
Q

Describe the position of the Heart within the sternum

A
  • Bounded anteriorly by the sternum and costal cartilages.
  • Positioned between Ribs 3, 4, and 5
  • Superior to diaphragm
  • Apex of the heart projects anteriorly
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4
Q

Normal volume of serous fluid in the pericardium. What is the function of this fluid?

A

10-25mL serous fluid
provides lubrication and free movement

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5
Q

From external to internal, what are the layers of pericardium?

A

Fibrous pericardium, parietal pericardium, and visceral pericardium

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6
Q

What chamber of the heart has the thinnest layer? Making is the easiest to lacerate during cardiac surgery.

A

Right Atrium ~2mm thick

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7
Q

The right atrium receives blood from?

A

IVC, SVC, and Coronary Sinus

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8
Q

The coronary sinus receives blood from the coronary veins, making it a useful cannulation location for cardioplegia for cardiac bypass. Is this retrograde or anterograde cardioplegia?

A

Retrograde. Send solution backward through coronary veins.

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9
Q

The coronary sinus is also used to place what kind of pacemaker?

A

Bi Ventricular Pacemaker. The third lead is threaded through the sinus down a vein that travels along the LV and then sits right outside the LV.

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10
Q

Atrial kick produces what percent of Left Ventricular End Diastolic Volume (LVEDV) in patients with a normal mitral valve

A

20%

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11
Q

When a patient has mitral stenosis, the atrial kick can be reduced up to what %?

A

40%!
Atrial kick provides up to 40% of LVEDV

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12
Q

What is the most common cause of RV failure?

A

LV Failure

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13
Q

RV wall thickness is how much thicker than RA wall thickness?

A

2x
~4-5mm thick

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14
Q

The left atrium receives oxygenated blood from the ____ pulmonary veins

A

FOUR

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15
Q

Do both atria contract or only one?

A

Both RA and LA contract during atrial systole

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16
Q

How thick is the LV wall?

A

~8-15mm. Needs to be the thickest to overcome SVR

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17
Q

What helps prevent the atrioventricular valves (TV and MV) from everting back into atria?

A

papillary muscles with chordae tendineae

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18
Q

The LAD primarily supplies blood to which parts of the heart?

A

Anterior 2/3 of interventricular septum
RBB and LBB
MV Papillary Muscles
and Anterior Lateral / Apical LV Walls

It also provides collateral circulation to the Anterior Wall of the RV.

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19
Q

What is the significance of the Sinus of Valsalva?

A

Small dilation above the aortic valve that allows the AV to open without occluding the (coronary ostia) openings of the coronary arteries.

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20
Q

Heart valves open and close due to?

A

changes in pressure gradients
Blood moves from an area of high pressure to lower pressure

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21
Q

Semilunar Valves (PV and AV) are composed of ____ cusps.

A

3
(bicuspid AV bad)

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22
Q

The left circumflex artery supplies blood to?

A

The posterior and lateral LV walls
Left atrial Wall
SA node in 40-45% population
AV node in 10% population

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23
Q

The right coronary artery (RCA) supplies blood to?

A

The SA and AV nodes
Posterior 1/3 of interventricular spetum

SA node - 50-60% population
AV node- 90% population

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24
Q

What is coronary artery dominance?

A

Pertains to what artery provides blood to the posterior descending artery (PDA).
50% of the population is via RCA
The other is sometimes LCA or LCx

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25
Q

The coronary sinus collects ~what % of blood from the LV

A

~85%

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26
Q

What are the Thebesian veins, and where to they drain?

A

veins that traverse the myocardium and drain directly into the RA, RV, and LV.

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27
Q

What are the cardioaccelerator fibers, and where do they originate?

A

Preganglionic SNS fibers that originate from T1-T4.

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28
Q

Increased SNS activity leads to what cardiac effects

A

Increased HR (chronotropy)
Increased force of contraction (inotropy)
Increased rate of AV node discharge (dromotropy)

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29
Q

At rest, does the parasympathetic NS or Sympathetic NS tone predominate?

A

PNS - heart is “resting”

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30
Q

Which vagus nerve controls the SA node?

A

the right vagus nerve

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31
Q

Which vagus nerve controls the AV node?

A

the left vagus nerve

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32
Q

An increase in PNS tone, ex: vagal stimulation, leads to? How can this be treated intraop?

A

Primarily decreased HR and, to a lesser degree, decreased contractility.

Tx: atropine or glycopyrolate

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33
Q

Which usually has a faster response, SNS stimulation or vagal PNS stimulation?

A

Vagal stimulation and response on cardiac innervation is commonly very rapid in onset whereas sympathetic stimulation is more gradual in onset.

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34
Q

Resting membrane potential is determined/regulated by what electrolyte?

A

Potassium

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35
Q

Threshold membrane potential is determined/regulated by what electrolyte?

A

Calcium

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36
Q

The AV node has “slower” transmission of action potentials to?

A

Allow sufficient time for atrial contraction

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37
Q

Resting Membrane Potential is the difference between?

A

The electrical potential between the inside and outside of the cell.
(Na primary extracellular ion, K primary intracellular ion)

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38
Q

What is threshold potential?

A

the internal voltage at which the cell will depolarize

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39
Q

When RMP is closer to TP, is the cell easier or harder to depolarize?

A

Easier

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40
Q

When RMP is further from TP, is the cell easier or harder to depolarize?

A

Harder

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41
Q

What does hypo and hyperkalemia do to RMP

A

HyPOkalemia decreases RMP
HyPERkalemia increases RMP (when you have high K, you have high risk of dysrhythmias due to frequent depolarizations)

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42
Q

What do hypo and hypercalcemia do to TP?

A

HyPOcalcemia decreases TP
HyPErcalcemia increases TP

43
Q

Phase 0 of ventricular APs are related to the _________ into the cell

A

Influx of Sodium (Na)

44
Q

Phase 1 Initial Repolarization of the ventricular action potential is related to?

A

Chloride influx into cell and Potassium efflux out of cell

45
Q

The Phase 2 Plateau of the ventricular action potential is related to?

A

Calcium Influx and Potassium Efflux

46
Q

The Phase 3 Final Repolarization of the ventricular action potential is related to?

A

Potassium efflux

47
Q

The Phase 4 Resting Phase of the ventricular action potential is related to?

A

Sodium efflux via the sodium-potassium ATPase pump

48
Q

What is the difference between the relative and absolute refractory periods

A

Relative: time during the action potential when a second stimulus can result in another action potential

Absolute: Time during which a conducted action potential can not be evoked. Lasts from Phase 0 to middle of Phase 3

49
Q

Relative Refractory Period coincides with what on an EKG? Why is this clinically relevant?

A

Coincides with the T wave. Can cause R-on-T phenomenon and lead to Vfib or VT.
This is why we sync for cardioversions.

50
Q

What are the similarities and differences between the SA node and Ventricular depolarizations

A

Differences:
SA node does NOT have a phase 1 (initial repolarization) or phase 2 (plateau phase).
Phase 0 Depolarization for the SA node: is predominantly from calcium influx
Phase 4 Spontaneous Depolarization: Due to leaky sodium (and calcium) channel influx.

Similarities - Both have:
Phase 0: Depolarization
Phase 3 Repolarization due to Potassium Efflux

51
Q

What things increase cardiac conduction velocity?

A

SNS activation
Adrenergic agonists - Epi, Norepi, Isoprel

52
Q

What things decrease cardiac conduction velocity?

A

Parasympathetic NS stimulation
Cholinergic Drugs - Neostigmine
Myocardial Ischemia

53
Q

What are the two systolic phases of the cardiac cycle?

A

Isovolumetric ventricular contraction
Ventricular Ejection (Rapid, then reduced ejection)

54
Q

What are the four diastolic phases of the cardiac cycle?

A

Isovolumetric ventricular relaxation
Rapid ventricular filling
Reduced ventricular filling
Atrial systole

55
Q

During Isovolumetric Ventricular Contraction, what valves are closed and why?

A

-Aortic and Mitral Valve are closed.
-LV Pressure is greater than LA pressure, which closes the mitral valve.
-LV pressure continues to increase until it surpasses aortic pressure.

56
Q

During Ventricular Ejection, what valve is open and which is closed? What is ejected?

A

AV open and MV closed

LV Pressure exceeds Aortic Pressure, which opens the AV.

Stroke volume is ejected into the aorta.

57
Q

During ventricular ejection, what part/fraction of ejection moves the most volume?

A

The first 1/3 of ejection

58
Q

During Diastole, what valves are closed during Isovolumetric Ventricular Relaxation? Why?

A

Both the AV and MV are closed.

Aortic Pressure is greater than LV pressure closing the AV. (seen as dicrotic notch)
The LV pressure continues to decrease.

59
Q

During Diastole, what valves are open/closed during rapid ventricular filling? Why?

A

AV Closed, MV Open

LA Pressure > LV pressure forcing MV open
LV Volume increases (~80% of LV filling) but still less than Aortic Pressure, so AV stays closed

60
Q

During Diastole, what valves are open/closed during reduced ventricular filling? Why?

A

AV Closed, MV Open

LV filling continues at a slower rate

61
Q

During Ventricular Diastole, what valves are open/closed during Atrial Systole? Why?

A

AV Closed, MV Open

Atrial contraction - atrial kick contributes the remaining 20% of LV filling.
LA pressure still greater than LV pressure (MV open)

LV Pressure still < than aortic pressure (AV still closed)

62
Q

End of atrial systole correlates with?

A

End diastolic volume

63
Q

Both the AV and MV are closed during which phases of the cardiac cycle?

A

Systole: Isovolumetric Ventricular Contraction
Diastole: Isovolumetric Ventricular Relaxation

64
Q

What phase of the cardiac cycle does the dicrotic notch occur during?

A

Diastolic Isovolumetric Ventricular Relaxation

65
Q

What is the Cardiac Output formula? What are normal values?

A

HR x SV
5-6 L/min

66
Q

What are the primary determinants of Stroke Volume that we can effect?

A

Preload
Afterload
Contractility

67
Q

What are two factors that influence stroke volume that we cannot control?

A

Regional Wall Abnormalities
Valvular Pathology

68
Q

How does calcium increase cardiac contractility?

A

The magnitude of Calcium Influx during phase 2 depolarization is directly related to myocardial contraction.
Inc. intracellular calcium increases contractility.

69
Q

How does cyclic AMP influence calcium?

A

cAMP raises intracellular calcium

70
Q

How does Milrinone work regarding calcium?

A

Milrinone is a Phosphodiesterase Inhibitor. This means it prevents Phosphodiesterases from breaking down intracellular cAMP, which is essential for intracellular calcium movement.

71
Q

How do our volatile anesthetics cause myocardial depression?

A

Depress cardiac contractility by decreasing the entry of Calcium into cells during depolarization. (dose-dependent)

72
Q

Ketamine seems to have the _____ direct depressant effect.

73
Q

Cardiac Index Formula and Normal Value

A

CO/BSA

2.8-4.2 L/min/(meters squared - dont care but added for completeness)

74
Q

MAP Calculation

A

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

or

(CO x SVR / 80) + CVP

75
Q

SVR formula and normal values

A

(MAP-SVR / CO) x 80

800-1500dynes/sec/cm^3

76
Q

PVR formula and normal values

A

(MPAP-PAOP/CO) x80

150-250dynes/sec/cm^3

77
Q

SV formula and normal values

A

SV= EDV-ESV

Normal 50-110mL/beat

78
Q

Preload is a measurement of?

A

Muscle length prior to contraction

(muscle length influenced by amt of volume stretching the ventricle)

79
Q

Afterload is a measurement of?

A

Tension against which the ventricle muscle must contract.
Most often estimated with SVR

80
Q

Contractility is a measurement of?

A

intrinsic property of the muscle to force a contraction unrelated to preload or afterload

81
Q

EF formula and normal values

A

EF=(EDV-ESV)/EDV x 100

or
EF = (SV/EDV) x 100

Normal 60-65%

82
Q

Ejection Fraction is?

A

Percentage of end-diastolic volume that is ejected during systole

83
Q

An EF < than ____% is associated with significant left ventricular impairment

84
Q

How do hypocalcemia, B-adrenergic blockade, and calcium channel blockers impact cardiac function?

A

Can potentiate cardiac depression

85
Q

What is happening at point A on the LV pressure-volume loop?

A

Aortic Valve Closes

86
Q

What is happening at point B on the LV pressure-volume loop?

A

Mitral Valve Opens

87
Q

What is happening at point C on the LV pressure-volume loop?

A

Mitral Valve Closes

88
Q

What is happening at point D on the LV pressure-volume loop?

A

Aortic Valve Opens

89
Q

What is happening at Phase 1 on the LV pressure-volume loop?

A

Ventricular Filling (Diastole)
- End-Systolic Volume ~50mL
- MV opens leading to ventricular filling
- LV is compliant, and there is little to no change in LV pressure
- Atrial kick will increase filling volume 20% and increase pressure 5-7mmHg
- LVEDV ~120mL

90
Q

What is happening at Phase 2 on the LV pressure-volume loop?

A

Isovolumetric Contraction (Systole)
- LV is stimulated to contract
- LV pressures > LA pressure now and MV closes
- LV pressure continues to increase and build tension
- No change to LV volume. (we are stretching/contracting but no volume changes)

91
Q

What is happening at Phase 3 on the LV pressure-volume loop?

A

Ventricular Ejection (Systole)
- LV pressure > Aortic Pressure which opens AV
- MV remains closed
- LV ejects stroke volume ~70mL
- Stroke volume is ejected into the aorta and LV volume decreases
- Normal end-systolic volume ~50mL (volume left in LV after ejection)

92
Q

What is happening at Phase 4 on the LV pressure-volume loop?

A

Isovolumetric Relaxation (Diastole)
- Aortic Pressure > LV pressure forces AV closure
- MV remains closed
- LV volume does not change, pressure decreased to pre-filling pressures
- LV remains with volume of ~50mL

93
Q

What is the normal coronary blood flow at REST?

A

4-7% of CO, or ~225-250mL/min

94
Q

What are some things that increase oxygen supply to the myocardium?

A

-Decrease HR (more time for LCA to supply heart during diastole)
-Increase in blood flow (decreasing HR, increases blood flow)

95
Q

What are some ways to decrease oxygen demand?

A

Decrease HR - the heart has a high metabolic demand. (Faster HR, more demand, and more O2 extraction.)

96
Q

What does Poiseuille’s Law say about the relationship between radius and flow?

A

Changes in the radius of a tube (vessel) change the flow to the FOURTH power of the radius.

97
Q

When does coronary blood flow through the RV and LV? Why?

A

RV: CBF occurs throughout the cardiac cycle
LV: CBF occurs mainly throughput diastole (~80-90%)
- During systole, the LCA blood flow is decreased due to compression and stretch of the subendothelial vessels

98
Q

What is the myocardial extraction % of O2 ?

A

Very high. 65-70% of )2 from hemoglobin

99
Q

Factors that increase myocardial oxygen demand (consumption)?

A

Increased HR
increased preload, inc. afterload, inc. contractility, SNS stimulation

100
Q

Factors that decrease myocardial oxygen supply?

A

Increased HR
increased end-diastolic pressures
decreased coronary diameter (ischemia)
decreased extraction (anemia, hypoxemia)
Decreased MAP

101
Q

Coronary vasculature will autoregulate at a MAP of?

A

60-140mmHg

102
Q

What is the main determinant of coronary blood flow?

A

Diastolic BP

103
Q

Coronary Perfusion Pressure = ?

A

DBP - LVEDP

104
Q

What cardiac reflexes most commonly cause vagal stimulation (causing bradycardia and hypotension)?

A

Baroreceptor Reflex
Oculocardiac Reflex
Celiac Reflex
Bezold-Jarisch Reflex