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CP1.06_Cardio_ZACHOW > Lecture 2 > Flashcards

Lecture 2 Flashcards

1
Q

Label all:

A
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2
Q

What occurs during isovolumetric contraction?

A
  1. Left ventricular contraction (preload) increases to overcome afterload.
  2. Drastic pressure increase without a change in volume.
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3
Q

What is systolic ejection?

A
  • Starts when left ventricular preload overcomes aortic afterload.
  • Rapid at first and then tapers off.
  • Equivalent to stroke volume.
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4
Q

When does isovolumetric relaxation occur?

A
  • between end of systole and start of diastole.
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5
Q

What occurs if afterload (aortic pressure) increases?

A
  1. Increased peak- and end-systolic LV pressures.
  2. Decreased stroke volume.
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6
Q

What is the end-systolic pressure-volume relationship (ESPVR)?

A
  • ESP increases as aortic pressure increases because SV decreases.
  • If there is more volume in the left ventricle, ESP will be greater.
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7
Q

Draw graph of increased afterload.

LV pressure on Y-axis.

LV volume on X-axis.

A
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8
Q

What occurs if preload increases?

A
  1. Increased EDV.
  2. Increased stroke volume.

Ejection fraction remains the same (EF = SV/EDV).

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9
Q

When and how does preload increase?

A
  • Increases during physical exertion.
  • Due to increased ventricular filling.
  • More blood ejected from the heart (EF ratio remains the same).
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10
Q

Draw graph of increased preload.

LV pressure on Y-axis.

LV volume on X-axis.

A
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11
Q

What occurs during positive inotropy?

A
  • more blood ejected from left ventricle during systole.
  • SV increases.
  • ESV decreases.
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12
Q

What can induce positive inotropy?

A
  1. digoxin/digitalis: blocks Na+/K+ ATPase pump, NCX does not have required electrochemical gradient, sarcolemma calcium levels rise.
  2. SNS.
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13
Q

Draw graph of positive inotropy.

LV pressure on Y-axis.

LV volume on X-axis.

A
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14
Q

When does the heart exert the greatest force of contraction (i.e. shortening velocity)?

A
  • At the onset of systolic ejection
  • preload > afterload (aortic pressure)
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15
Q

Effect of increased afterload (aortic pressure) on left ventricle myocyte shortening velocity:

A
  • shortening velocity decreases.
    • now acting against more force (higher afterload).
  • less volume of blood ejected (SV decreases).
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16
Q

Effect of increased preload (aortic pressure) on left ventricle myocyte shortening velocity:

A
  1. shortening velocity remains relatively constant.
    • more volume moved, but opposing force (afterload) is the same.
  2. more blood volume being ejected - takes longer amount of time to eject.
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17
Q

Draw graph of increased preload and increased afterload effects on left ventricular myocyte shortening velocity.

Myocyte shortening velocity on Y-Axis.

LVV on X-Axis.

A
18
Q

What will occur to a heart working against abnormally high opposing pressures (i.e. afterload/systemic blood pressure) for an extended period of time?

A
  • left ventricle will work harder and hypertrophy.
  • may become pathological if chronic.
19
Q

Bradycardic heart rate, normal resting heart rate, and tachycardic heart rate:

A
  • Bradycardic: <60 BPM
  • Normal resting: 60-100 BPM
  • Tachycardic: >100 BPM
20
Q

Path of electrical conductivity through the heart from ANS afferents to ventricular myocytes. Label slow and fast fibers:

A
  1. ANS afferents
  2. SA node
  3. Internodal pathways, Bachmann’s (FAST)
  4. Atrial myocytes (SLOW)
  5. AV node
  6. Bundle of His (FAST)
  7. Right and Left Bundle Branches (FAST)
    • Left bundle branch gives off anterior and posterior fascicles (FAST)
  8. Purkinje fibers (FAST)
  9. Ventricular myocytes (SLOW)
21
Q

Label all:

A
22
Q

What is the only electrical connection between the atrium and the ventricles?

A
  • AV node / Bundle of His
    • AV node retards the electrical current.
23
Q

The two action potentials of the heart, and what cells they occur in:

A
  1. Plateau potential:
    • myocytes (atrial and ventricular)
    • Purkinje cells
  2. Pacemaker potential:
    • ​​Pacemaker cells of SA node
24
Q

Steps in pacemaker potential:

A
  1. Slow depolarization:
    • slow Ca2+ influx (T-type Ca2+ channels)
    • slow Na+ influx (HCN channel)
    • K+ efflux (HCN channel)
  2. Rapid depolarization:
    • Ca2+ influx (Type-T and Type-L Ca2+ channels)
  3. Repolarization, hyperpolarization:
    • K+ efflux (K+ channels)
25
Q

What current does the HCN channel of pacemaker cells produce?

A
  • funny current (If)
    • slow inward Na+
    • outward K+
26
Q

What type of AP is this, and where does it occur?

A
  • plateau potential
  • cardiac myocytes (atrial and ventricular)
  • purkinje cells
27
Q

What type of AP is this, and where does it occur?

A
  • Pacemaker potential (shark-fin appearance)
  • pacemaker cells in SA node
28
Q

Steps in plateau potential:

A
  1. Rapid depolarization:
    • Stimulus causes Na+ influx via VG-Na+ channels.
  2. Slow repolarization (plateau):
    • Two different VG-K+ channels open. K+ efflux.
    • Type-L Ca2+ channel opens. Ca2+ influx.
  3. Rapid repolarization:
    • Different VG-K+ channel opens. K+ efflux.
29
Q

Ions involved in the APs of plateau and pacemaker potentials at each step:

A
  • Plateau (myocytes; purkinje)
    1. Depolarization: Na+ in.
    2. Slow repolarization: K+ out; Ca2+ in.
    3. Rapid repolarization: K+ out.
  • Pacemaker (SA node)
    1. Slow depolarization: Ca2+ in; Na+ in; K+ out.
    2. Rapid depolarization: Ca2+ in.
    3. Rapid repolarization: K+ out.
30
Q

Effective refractory period:

A
  • Sodium channels recovering and completely inactive.
  • No stimulus will cause depolarization and opening of these channels.
31
Q

Relative refractory period:

A
  • sodium channels are somewhat recovered.
  • A strong stimulus can cause a depolarization.
32
Q

Relationship between plateau potentials and cardiomyocyte contraction:

A
  • Cardiomyocytes fire APs to cause contraction.
  • Myocyte sarcolemma calcium levels increase via Type-L calcium channels as depolarization occurs.
  • Contraction = slow repolarization.
  • Relaxation = repolarization/hyperpolarization.
33
Q

Opening and closing of voltage-gated Na+, Ca2+, and K+ channels determine depolarization and repolarization, which collectively orchestrates:

A
  • contraction (systole) and relaxation (diastole).
34
Q

Path of low and high pressure baroreceptors to medulla:

A
  • High pressure: carotid sinus/aortic arch.
  • Low pressure: right atrium.
  • Travel on vagus/glossopharyngeal to cardioacceleratory, cardioinhibitory, and vasomotor centers in the NTS, DMV, and NA nuclei in the medulla.
35
Q

How does the medulla cardioinhibitory center decrease HR?

A
  • PSNS (via Vagus).
  • decreases HR via ACh release binding to CM2 receptors in SA and AV nodes, atria, and ventricles.
36
Q

How does the medulla cardioacceleratory center increase HR?

A
  • SNS.
  • increases HR and contractile force via norepi binding to β1 adrenoreceptors in SA node, atria, and myocardium.
37
Q

How does the medulla vasomotor center increase vasoconstriction?

A
  • SNS.
  • vasoconstriction via norepi binding to α1 adrenoreceptors on VSM.
38
Q

Effect of increased SNS tone on SA pacemaker activity:

A
  1. Depolarization occurs quicker.
  2. Interval between subsequent depolarizations shortens (HR increases).

Norepi/epi causes conformational change in pacemaker ion channels.

39
Q

Effect of increased PSNS tone on SA pacemaker activity:

A
  1. Depolarization occurs more slowly.
  2. Interval between subsequent depolarizations is longer (HR decreases).
40
Q

Extrusion of positive charge from (or influx of negative charge into) an electrogenic cell will:

A
  • lower resting membrane potential and increase the time to reach threshold; and vice-versa.
    • PSNS on heart: lowers RMP.
    • SNS on heart: raises RMP.

CP1.06_Cardio_ZACHOW (10 decks)

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