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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.

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:

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
What current does the HCN channel of pacemaker cells produce?
* **funny current (If)** * slow inward Na+ * outward K+
26
What type of AP is this, and where does it occur?
* plateau potential * cardiac myocytes (atrial and ventricular) * purkinje cells
27
What type of AP is this, and where does it occur?
* Pacemaker potential (shark-fin appearance) * pacemaker cells in SA node
28
Steps in plateau potential:
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
Ions involved in the APs of plateau and pacemaker potentials at each step:
* **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
Effective refractory period:
* Sodium channels recovering and completely inactive. * No stimulus will cause depolarization and opening of these channels.
31
Relative refractory period:
* sodium channels are somewhat recovered. * A strong stimulus can cause a depolarization.
32
Relationship between plateau potentials and cardiomyocyte contraction:
* 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
Opening and closing of voltage-gated Na+, Ca2+, and K+ channels determine depolarization and repolarization, which collectively orchestrates:
* contraction (systole) and relaxation (diastole).
34
Path of low and high pressure baroreceptors to medulla:
* 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
How does the medulla cardioinhibitory center decrease HR?
* PSNS (via Vagus). * decreases HR via ACh release binding to CM2 receptors in SA and AV nodes, atria, and ventricles.
36
How does the medulla cardioacceleratory center increase HR?
* SNS. * increases HR and contractile force via norepi binding to β1 adrenoreceptors in SA node, atria, and myocardium.
37
How does the medulla vasomotor center increase vasoconstriction?
* SNS. * vasoconstriction via norepi binding to α1 adrenoreceptors on VSM.
38
Effect of increased SNS tone on SA pacemaker activity:
1. Depolarization occurs quicker. 2. Interval between subsequent depolarizations shortens (HR increases). ## Footnote **Norepi/epi causes conformational change in pacemaker ion channels.**
39
Effect of increased PSNS tone on SA pacemaker activity:
1. Depolarization occurs more slowly. 2. Interval between subsequent depolarizations is longer (HR decreases).
40
Extrusion of positive charge from (or influx of negative charge into) an electrogenic cell will:
* 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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