Lecture 2 Flashcards
Label all:
What occurs during isovolumetric contraction?
- Left ventricular contraction (preload) increases to overcome afterload.
- Drastic pressure increase without a change in volume.
What is systolic ejection?
- Starts when left ventricular preload overcomes aortic afterload.
- Rapid at first and then tapers off.
- Equivalent to stroke volume.
When does isovolumetric relaxation occur?
- between end of systole and start of diastole.
What occurs if afterload (aortic pressure) increases?
- Increased peak- and end-systolic LV pressures.
- Decreased stroke volume.
What is the end-systolic pressure-volume relationship (ESPVR)?
- ESP increases as aortic pressure increases because SV decreases.
- If there is more volume in the left ventricle, ESP will be greater.
Draw graph of increased afterload.
LV pressure on Y-axis.
LV volume on X-axis.
What occurs if preload increases?
- Increased EDV.
- Increased stroke volume.
Ejection fraction remains the same (EF = SV/EDV).
When and how does preload increase?
- Increases during physical exertion.
- Due to increased ventricular filling.
- More blood ejected from the heart (EF ratio remains the same).
Draw graph of increased preload.
LV pressure on Y-axis.
LV volume on X-axis.
What occurs during positive inotropy?
- more blood ejected from left ventricle during systole.
- SV increases.
- ESV decreases.
What can induce positive inotropy?
- digoxin/digitalis: blocks Na+/K+ ATPase pump, NCX does not have required electrochemical gradient, sarcolemma calcium levels rise.
- SNS.
Draw graph of positive inotropy.
LV pressure on Y-axis.
LV volume on X-axis.
When does the heart exert the greatest force of contraction (i.e. shortening velocity)?
- At the onset of systolic ejection
- preload > afterload (aortic pressure)
Effect of increased afterload (aortic pressure) on left ventricle myocyte shortening velocity:
-
shortening velocity decreases.
- now acting against more force (higher afterload).
- less volume of blood ejected (SV decreases).
Effect of increased preload (aortic pressure) on left ventricle myocyte shortening velocity:
-
shortening velocity remains relatively constant.
- more volume moved, but opposing force (afterload) is the same.
- more blood volume being ejected - takes longer amount of time to eject.
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.
What will occur to a heart working against abnormally high opposing pressures (i.e. afterload/systemic blood pressure) for an extended period of time?
- left ventricle will work harder and hypertrophy.
- may become pathological if chronic.
Bradycardic heart rate, normal resting heart rate, and tachycardic heart rate:
- Bradycardic: <60 BPM
- Normal resting: 60-100 BPM
- Tachycardic: >100 BPM
Path of electrical conductivity through the heart from ANS afferents to ventricular myocytes. Label slow and fast fibers:
- ANS afferents
- SA node
- Internodal pathways, Bachmann’s (FAST)
- Atrial myocytes (SLOW)
- AV node
- Bundle of His (FAST)
- Right and Left Bundle Branches (FAST)
- Left bundle branch gives off anterior and posterior fascicles (FAST)
- Purkinje fibers (FAST)
- Ventricular myocytes (SLOW)
Label all:
What is the only electrical connection between the atrium and the ventricles?
- AV node / Bundle of His
- AV node retards the electrical current.
The two action potentials of the heart, and what cells they occur in:
-
Plateau potential:
- myocytes (atrial and ventricular)
- Purkinje cells
-
Pacemaker potential:
- Pacemaker cells of SA node
Steps in pacemaker potential:
-
Slow depolarization:
- slow Ca2+ influx (T-type Ca2+ channels)
- slow Na+ influx (HCN channel)
- K+ efflux (HCN channel)
-
Rapid depolarization:
- Ca2+ influx (Type-T and Type-L Ca2+ channels)
-
Repolarization, hyperpolarization:
- K+ efflux (K+ channels)
What current does the HCN channel of pacemaker cells produce?
-
funny current (If)
- slow inward Na+
- outward K+
What type of AP is this, and where does it occur?
- plateau potential
- cardiac myocytes (atrial and ventricular)
- purkinje cells
What type of AP is this, and where does it occur?
- Pacemaker potential (shark-fin appearance)
- pacemaker cells in SA node
Steps in plateau potential:
-
Rapid depolarization:
- Stimulus causes Na+ influx via VG-Na+ channels.
-
Slow repolarization (plateau):
- Two different VG-K+ channels open. K+ efflux.
- Type-L Ca2+ channel opens. Ca2+ influx.
-
Rapid repolarization:
- Different VG-K+ channel opens. K+ efflux.
Ions involved in the APs of plateau and pacemaker potentials at each step:
-
Plateau (myocytes; purkinje)
- Depolarization: Na+ in.
- Slow repolarization: K+ out; Ca2+ in.
- Rapid repolarization: K+ out.
-
Pacemaker (SA node)
- Slow depolarization: Ca2+ in; Na+ in; K+ out.
- Rapid depolarization: Ca2+ in.
- Rapid repolarization: K+ out.
Effective refractory period:
- Sodium channels recovering and completely inactive.
- No stimulus will cause depolarization and opening of these channels.
Relative refractory period:
- sodium channels are somewhat recovered.
- A strong stimulus can cause a depolarization.
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.
Opening and closing of voltage-gated Na+, Ca2+, and K+ channels determine depolarization and repolarization, which collectively orchestrates:
- contraction (systole) and relaxation (diastole).
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.
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.
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.
How does the medulla vasomotor center increase vasoconstriction?
- SNS.
- vasoconstriction via norepi binding to α1 adrenoreceptors on VSM.
Effect of increased SNS tone on SA pacemaker activity:
- Depolarization occurs quicker.
- Interval between subsequent depolarizations shortens (HR increases).
Norepi/epi causes conformational change in pacemaker ion channels.
Effect of increased PSNS tone on SA pacemaker activity:
- Depolarization occurs more slowly.
- Interval between subsequent depolarizations is longer (HR decreases).
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.
