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BIOL 364 > Final: Circulation 5 > Flashcards

Final: Circulation 5 Flashcards

1
Q

how does depolarization travel through the heart (2)

A
  • specialized conducting pathways
  • directly between cardiomyocytes
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2
Q

specialized conducting pathways (3)

A
  • modified cardiomyocytes can spread action potential rapidly throughout the myocardium
  • these cells are elongated, lack contractile proteins, and are pale
  • they can undergo rhythmic depolarizations
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3
Q

depolarization directly between cardiomyocytes (2)

A
  • cardiomyocytes are electrically connected via gap junctions
  • allows electrical signals to pass directly from cell to cell
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4
Q

excitation-contraction coupling

A
  • the coupling of the action potential and the cardiomyocyte contraction
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5
Q

excitation-contraction coupling steps (8)

A
  1. action potential enters from adjacent cell
  2. voltage-gated Ca2+ channels open and Ca2+ enters the cell
  3. entry of Ca2+ triggers release of LOTS of Ca2+ from sarcoplasmic reticulum
  4. Ca2+ bind to troponin to initiate contraction
  5. relaxation occurs when Ca2+ unbinds from troponin
  6. Ca2+ is pumped back into sarcoplasmic reticulum for storage
  7. Ca2+ is exchanged with Na+
  8. Na+ gradient is maintained by Na+-K+-ATPase
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6
Q

conducting pathway in mammalian heart (4)

A
  1. SA node depolarizes, which spreads rapidly via the internodal pathway
  2. AV node delays the signals, while the depolarization spreads through atria via gap junctions and causes atria to contract
  3. depolarization spreads rapidly through bundles of His and Purkinje fibers
  4. depolarization spreads upward through ventricle, causes ventricle to contract
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7
Q

sequence of conduction pathway in mammalian heart (5)

A
  1. SA node
  2. internodal pathway
  3. AV node
  4. Bundle of His
  5. purkinje fibers
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8
Q

how do action potentials in cardiomyocytes differ from those in skeletal muscles

A
  • cardiomyocyte APs are extended, containing a plateau phase during repolarization
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9
Q

what is the purpose of the plateau phase (2)

A
  • to prevent tetanus by removing possibility for sustained contraction during rapid APs
  • allow the heart to refill with blood and relax
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10
Q

cardiomyocyte AP plateau phase (2)

A
  • extended repolarization that lasts as long as ventricular contraction
  • caused by Ca2+ entry via L-shaped channel and temporary reduced K+ permeability
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11
Q

electrocardiogram (ECG/EKG) (3)

A
  • composite recording of action potentials in cardiac muscle
  • contains the P wave, QRS complex, and T wave
  • used for clinical diagnosis of issues with conducting system
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12
Q

ECG: P wave

A
  • atrial depolarization
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13
Q

ECG: QRS complex

A
  • ventricular depolarization
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14
Q

ECG: T wave

A
  • ventricular repolarization
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15
Q

why is the T wave positive in the ECG if it represents a repolarization event

A
  • it is negative; ECG tracks change in membrane potential, not direction of change
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16
Q

heart sounds

A
  • opening and closing of heart valves
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17
Q

electrical and mechanical events in cardiac cycle

A
  • electrical events initiate contractile (mechanical) events
18
Q

electrical and mechanical events in left heart cardiac cycle: P-wave (2)

A
  • pressure is increasing in atrium and ventricle before P-wave
  • P-wave initiates atrial contraction and atrial BP peaks
19
Q

electrical and mechanical events in left heart cardiac cycle: QRS-complex (3)

A
  • QRS-complex initiates ventricular contraction and ventricular BP peaks
  • ventricular BP first exceeds atrial BP and then aortic diastolic BP
  • atrial relaxation occurs at same time
20
Q

electrical and mechanical events in left heart cardiac cycle: T-wave (2)

A
  • T-wave initiates ventricular realization and ventricular BP falls below aortic BP, then below atrial BP
  • energy stored in aorta is slowly released
21
Q

end-systolic volume (ESV)

A
  • volume after contraction
22
Q

end-diastolic volume (EDV)

A
  • volume before contraction
23
Q

cardiac stroke volume (SV) (2)

A

SV = EDV - ESV
- volume of blood pumped with each beat

24
Q

does a heartbeat fully empty the human ventricle

A
  • no, but more can be expelled during exercise/more intense contraction
25
Q

why does aortic blood pressure decrease during diastole

A
  • falls when heart is relaxed as blood is being transported away to the extremeties
26
Q

cardiac output (CO) (2)

A
  • volume of blood pumped per unit time
  • CO = HR x SV
27
Q

heart rate (HR)

A
  • rate of contraction (beats per minute)
28
Q

how can cardiac output be modified (2)

A
  • regulating heart rate
  • regulating stroke volume
29
Q

cardiac output modulation: heart rate (2)

A
  • modulated by autonomic nerves and adrenal medulla
  • activations of the parasympathetic (decreased HR) or the sympathetic system (increased HR)
30
Q

decreased HR

A
  • bradycardia
31
Q

increased HR

A
  • tachycardia
32
Q

cardiac output modulation: stroke volume (2)

A
  • modulated by various nervous, hormonal, and physical factors
  • nervous and endocrine system an cause heart to contract more forcefully, pumping more blood each beat
33
Q

control of stroke volume: pathway (8)

A
  1. binding of norepinephrine or epinephrine changes shape of beta1 adrenergic receptor, activating G protein
  2. G protein activates adenylate cyclase
  3. adenylate cyclase catalyzes ATP –> cAMP
  4. cAMP activates protein kinase A
  5. protein kinase phosphorylates L-type Ca2+, allowing Ca2+ to enter cell, stimulating contraction
  6. protein kinase phosphorylates Ca2+ channel on sarcoplasmic reticulum, allowing Ca2+ to move to cytoplasm, which stimulates contraction
  7. protein kinase phosphorylates myosin, stimulating contraction
  8. protein kinase phosphorylates sarcoplasmic Ca2+ ATPase speeding the removal of Ca2+ from cytoplasm during relaxation, decreasing relaxation time
34
Q

how is stroke volume increased by the sympathetic nervous sytem

A
  • more Ca2+ in cytoplasm increases contractile magnitude, promoting muscle contraction
35
Q

Frank-Starling effect (2)

A
  • increased end-diastole volume results in more forceful contraction and increased SV
  • heart automatically compensates for increases in volume of blood returning to the heart (autoregulation) due to length-tension relationship for muscle
36
Q

control of stroke volume: sympathetic activity levels and the Frank-Starling effect

A
  • levels of sympathetic activity shifts positions of cardiac muscle length-tension relationship
37
Q

Frank-Starling effect: increased sympathetic activity

A
  • intensifies Frank-Starling effect, increasing the possible range of the stroke volume
38
Q

Frank-Starling effect: decreased sympathetic activity

A
  • reduces Frank-Starling effect, reducing the possible range of the stroke volume
39
Q

what potentials are generated in the heart (5)

A
  • SA node
  • atrium
  • AV node
  • bundle of His
  • ventricular cardiomyocyte
40
Q

what potentials display a plateau phase in the heart (3)

A
  • atrium
  • bundle of His
  • ventricular cardiomyocyte
41
Q

what potentials don’t have a plateau phase in the heart (2)

A
  • SA node
  • AV node

BIOL 364 (44 decks)

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