Lecture 1 Flashcards

1
Q

Effective circulating volume (ECV) =

A
  • volume sensed by baroreceptor system which is available for perfusion.
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2
Q

Primary energy source of the heart

(non-stress scenario):

A
  1. Free fatty acid
  2. β-oxidation
  3. oxidative phosphorylation
  4. ATP
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3
Q

Secondary energy source of the heart

(stress scenario):

A
  1. Glucose
  2. Glycolysis
  3. Oxidative phosphorylation
  4. ATP
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4
Q

Heart source of energy in non-stress and in stress:

A
  • Non-stress: Free fatty acids
  • Stress: Glucose
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5
Q

The predominant differences between cardiac muscle and skeletal muscle:

A
  • cardiac muscle has:
    1. chronic work load
    2. high reliance on extracellular calcium
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6
Q

Type of calcium channels expressed in cardiac myocytes:

A
  • Type-L calcium channels.
    • Calcium enters myocytes through these channels to allow for cross-bridge cycling/contraction.
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7
Q

The two pathways in which an action potential in the heart can cause an influx of calcium into the sarcolemma of a myocyte:

A
  • Extracellular: Type L Ca2+ channels
  • Intracellular: T-tubules (DHPR and RyR)
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8
Q

The two sources of calcium for cardiac myocytes:

A
  • Extracellular:
    • enter sarcolemma via Type-L Ca2+ channels.
  • Intracellular:
    • enter sarcolemma via T-tubules (DHPRs and RyRs).
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9
Q

Phospholamban:

A
  • protein phosphorylated by PKA.
    • Unphosphorylated state: inhibits SERCA.
    • Phosphorylated state: SERCA activated.
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10
Q

Process of cardiomyocyte relaxation:

A
  1. Phospholamban phosphorylated; SERCA channels activated.
  2. Calcium efflux via SERCA channels and NCX ATPases.
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11
Q

What two structures are utilized by cardiomyocytes to cause calcium efflux from the sarcolemma and relaxation?

A
  1. SERCA channels
  2. NCX ATPase
    • secondary active transporter
    • sodium-calcium exchanger
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12
Q

Creatinine kinase function:

A
  • enzyme
  • converts creatine to phosphocreatine and ADP.
  • phosphocreatine + ADP = ATP.
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13
Q

Creatinine kinase expressed in myocardium:

A

CK-MB; “cardiac-specific CK.”

  • rises beginning around 3-8 h post-injury.
  • returns to normal within 48-72 h post-injury.
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14
Q

Troponins expressed in myocardium:

A

cTnI and cTnT

  • cardiac troponin I (cTnI)
  • cardiac troponin T (cTnT)
  • rise within around 3-4 h post-injury.
  • return to normal over 10-14 d post-injury.
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15
Q

What cardiac-specific markers increase in blood plasma levels post-myocardium injury?

A
  1. CK-MB (creatinine kinase)
  2. cTnI (cardiac troponin I)
  3. cTnT (cardiac troponin T)
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16
Q

Diastole characteristics (4):

A
  1. Phase of ventricular filling
  2. Myocardium relaxed
  3. Low intraventricular pressure
  4. Lowest arterial BP
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17
Q

The two values associated with diastole:

A
  1. End diastolic pressure (EDP)
  2. End diastolic volume (EDV)
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18
Q

Systole characteristics (4):

A
  1. Phase of ventricular emptying
  2. Myocardium contracting
  3. Highest intraventricular pressure
  4. Highest arterial BP
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19
Q

The two values associated with systole:

A
  1. End systolic pressure (ESP)
  2. End systolic volume (ESV)
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20
Q

When does the lowest arterial BP occur?

A

diastole

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21
Q

When does the highest arterial BP occur?

A

systole

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22
Q

Cardiac output (CO) =

A

CO = SV X HR

  • (stroke volume X heart rate)
  • SV = EDV - ESV
23
Q

Stroke volume (SV) =

A

SV = EDV - ESV

(end diastolic volume - end systolic volume)

24
Q

What are end diastolic volume (EDV) and end systolic volume (ESV)?

A
  • EDV = left ventricle volume after diastole (filling).
  • ESV = left ventricle volume after systole (emptying).
  • SV = EDV - ESV
25
Q

Mean arterial pressure (MAP) =

A

MAP = CO x TPR

(TPR = total peripheral resistance)

26
Q

Mean arterial pressure (MAP) represents the:

A
  • perfusion pressure; the driving force to maintain tissue perfusion (i.e. oxygenation).
27
Q

Cardiac output (CO) must be equal to:

A
  • venous return.
  • What goes out of the heart at the left ventricle must come back into the heart at the right atrium.
28
Q

What is occuring if cardiac output (CO) does not equal venous return?

A

either losing blood or edema.

29
Q

Right atrial pressure (RAP)/central venous pressure (CVP):

A
  • pressure in the right atrium due to venous return.
  • lowest BP in body (0-2mm Hg).
30
Q

Average values of RAP/CVP and MAP:

A
  • RAP/CVP: 0-2mm Hg
  • MAP: 80-100mm Hg
31
Q

Functional important of the difference in MAP and RAP/CVP:

A
  • creates a pressure gradient favoring venous return to right atrium and normal blood flow.
32
Q

What will occur if RAP/CVP increases?

A
  • venous return impaired.
  • edema will manifest.
33
Q

If output to the lungs via the pulmonary trunk/right ventricle does not equal the input into the left atrium via the pulmonary veins, what occurs?

A

pulmonary edema

34
Q

What occurs to the atrium and ventricles during ventricular diastole?

A
  • Atrial systole.
  • Ventricular relaxation and chamber filling.
  • Blood flows through tricuspid/mitral valves.
35
Q

Normal ejection fraction (EF) percentage:

A

55-75%

36
Q

Normal regurgitant fraction:

A

0

37
Q

Ejection fraction (EF) =

A

EF = SV/EDV

(stroke volume/end diastolic volume)

38
Q

The ejection fraction (EF) is:

A
  • The fraction of blood from a given diastole that is ejected by the following systole.
  • Normal: 55-75%.
39
Q

In the heart, force = ?, and distance = ?

A
  • force = pressure
  • distance = Δvolume
40
Q

Conditions required for the left ventricle to eject blood:

A

preload (LV pressure) > afterload (aortic pressure)

41
Q

As the left ventricle begins to fill during diastole, what occurs to the cardiomyocytes?

A
  1. Begin to stretch. Passive tension develops.
  2. Stretch-induced calcium release. Influx of calcium.
42
Q

Isovolumetric contraction of the left ventricle:

A
  • Period in which left ventricle is contracting, but intraventricular pressure is less than aortic pressure. No movement of blood occurs.
  • When left intraventricular pressure overcomes aortic pressure, aortic valve snaps open and ejection occurs.
43
Q

Stretch-induced calcium release:

A
  • When left ventricular myocytes get stretched out during diastole, they begin to experience an influx of calcium in addition to an increase in passive tension.
44
Q

Afterload of the left ventricle and right ventricle, respectively:

A
  • Left ventricle: aortic pressure.
  • Right ventricle: pulmonary artery pressure.
45
Q

After PKA is activated by some stimulus, what does it activate via phosphorylation (3)?

A
  1. phospholamban
    • activates SERCA
    • relaxation
  2. Troponin I
    • dissociates calcium from tropononin C
    • relaxation
  3. Type-L calcium channels
    • influx of extracellular calcium
    • contraction
46
Q

What does PKA phosphorylate in order to induce ventricular relaxation?

A
  1. phospholamban
    • activates SERCA
    • relaxation
  2. Troponin I
    • dissociates calcium from tropononin C
    • relaxation
47
Q

What does PKA phosphorylate in order to induce ventricular contraction?

A
  1. Type-L calcium channels
    • influx of extracellular calcium
    • contraction
48
Q

Calcium efflux and influx are both happening at the same time due to PKA.

Whether or not contraction/relaxation occurs depends on:

A
  • Whether calcium levels are above or below threshold required for contraction.
  • Contraction occurs when the influx of calcium is greater than the efflux of calcium and above the required threshold for contraction.
49
Q

How does epi/norepi increase HR (2)?

A
  1. activation/phosphorylation of PKA via β1 adrenoreceptors.
  2. increased rate of SA nodal firing.
50
Q

NCX ATPase location and function:

A
  • Sodium-calcium exchanger on sarcolemma of ventricular myocytes.
  • Calcium efflux, sodium influx. RELAXATION.
  • Secondary active transporter.
  • Primary active transporter is Na+/K+ ATPase.
51
Q

NCX ATPase is a secondary active trasnporter. What is its required primary active transporter?

A

Na+/K+ ATPase.

  • Pumps sodium out.
  • Sets up favorable concentration gradient for NCX ATPase.
52
Q

What drug can inhibit Na+/K+ ATPase in ventricular myocytes, and what is the outcome?

A

Digitalis/digoxin.

  • Sarcolemma calcium levels rise, increased cardiac output.
53
Q

Digitalis/digoxin drug class and mechanism:

A
  • Positive inotrope. Increases cardiac output.
  • Inhibits Na+/K+ ATPase pump, reduces electrochemical driving force for NCX, sarcolemma calcium levels will rise, heart contracts harder.