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250-S1 > 7.1 Cardiac Cycle > Flashcards

7.1 Cardiac Cycle Flashcards

1
Q

What are systole and diastole?

A 
Systole = ventricular contraction, pumping blood out of the heart
Diastole = ventricular relaxation, filling with blood
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2
Q

What is the sequence of electrical excitation?

A 
SA node
AV Node
Bundle of His (AV bundle)
Bundle branches (in inter ventricular septum)
Purkinje fibers (in walls of ventricles)
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3
Q

Where is the SA node?

What is its intrinsic rate?

A

Right atrial wall

75-100

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4
Q

Where is the AV node?

What is its intrinsic rate?

A

Inferior inter-atrial septum

40-60

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5
Q

Where is the AV bundle?

What is its intrinsic rate?

A

Super inter-ventricular septum

20-40

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6
Q

What is happening in the heart during the P-wave?

A

Atrial depolarization

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7
Q

What is happening during the QRS complex?

A

Ventricular depolarization

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8
Q

What is happening during the T-wave?

A

ventricular repolarization

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9
Q

What are the 3 stages of the cardiac cycle?

A

1- Mid to late ventricular diastole
2- Ventricular systole
3- Early ventricular diastole

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10
Q

In mid to late ventricular diastole, what is going on with: ICS, valves, chambers?

A 
ICS: pause, then SA Node fires
P-wave
atria: relaxed, then contracted
squeezes last bit of blood into ventricles
ventricles: relaxed
AV valve: open
SL valve: closed
Ventricle volume: filling to maximum
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11
Q

In ventricular systole, what is going on with ICS, valves, chambers?

A

ICS: AV Node fires, spreads through Bundle of His, Bundle branches, Purkinje fibers
QRS wave
atria: relaxed
ventricles: contract
AV valve: closed
SL valve: closed, then opens as pressure increases
when both valves are closed, no blood is leaving -> ISOVOLUMETRIC CONTRACTION
then, opens and blood is ejected
Ventricle volume: blood leaving, volume decreases to minimum

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12
Q

In early ventricular diastole, what is going on with ICS, valves, chambers?

A

ICS: repolarize and pause
T-wave
atria: relaxed
ventricles: relaxed
AV valve: closed, then opens as pressure increases
when both valves are closed, no blood is filling the ventricle –> ISOVOLUMETRIC RELAXATION
then, opens and blood is filling ventricle
SL valve: closes
Ventricle volume: low, then begins to fill

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13
Q

What is EDV?

A

End diastolic volume
=how much blood in ventricle after after diastole, before pumping
=Max fill

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14
Q

What is ESV?

A

End systolic volume

= how much blood is in ventricle after pumping

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15
Q

What is the equation for cardiac output?

A

CO= HR x SV

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16
Q

What is the equation for stroke volume?

A

SV= EDV-ESV

= End diastolic - end systolic

17
Q

What is the definition of preload?

A

is the amount of blood in the heart at the end of diastole=EDV

18
Q

What is the main contributor to preload? Why is it significant?

A

Venous return:
filling causes stretch of ventricle wall
muscle fibers contract best at optimal length due to maximal crossbridge formation
resting cardiac muscle is kept below optimal length, as stretch or filling increases, cardiac muscle strength increases

19
Q

What is the Frank-Starling law?

A

Higher Preload = Higher Stroke Volume

= the more you fill it, the stronger it gets

20
Q

Other than venous return, what contributes to preload?

A

HR: time to fill decreased heart rate gives the heart more time to fill allowing more blood to enter the heart
skeletal muscle pump skeletal muscle contraction presses on the veins, more blood returns to heart
respiratory pump inhaling increases abdominal pressure, decreases thoracic pressure more blood returns to heart
SNS constriction of veins contraction of vein walls presses on the veins, more blood returns to heart

21
Q

At a general level, what is responsible for the force of contractility?

A

Ion changes

22
Q

What increases contractility?

A

Increase Ca2+ in heart muscle cells
SNS
Hormones: epi, thyroxine, glucagon
Increased serum Ca2+

23
Q

What decreases heart contractility?

A

via multiple ion changes
acidosis, increased blood H+
increased blood K+
decreased blood Ca2+

24
Q

What is after load?

A

the resistance, back pressure exerted on the ventricles by the arteries, must be overcome in order to eject blood

25
Q

What is the primary result of after load? When is it most clinically important?

A

Decreases stroke volume
Mainly relevant during disease, hypertension
pulmonary hypertension: high pressure in the pulmonary arteries
right ventricle must work harder to pump through the pulmonary trunk
systemic hypertension: high pressure in the systemic arteries
left ventricle must work harder to pump through the aorta

26
Q

How does the SNS increase HR?

A

through epinephrine
Increased Na+ via voltage gated Na+ channels
Increased Ca2+ via fast and slow Ca2+ channels
Faster to threshold due to + ions entering ICS cells
Faster to peak depolarization in ICS and cardiac muscle cells
SA node fires more often, AV node delay decreased
Increased speed of atria and ventricle contraction

27
Q

What is the Bainbridge reflex?

A

increased filling of the atria stretches atrial muscle, this causes stimulation of the SA node and a reflex via stretch receptors in the atria, increasing heart rate.
does not have a pronounced effect on contractility of the heart

28
Q

How does the PNS decrease HR?

A

acetylcholine:
open K+ channels
Depresses Na+ and Ca2+ entry through If and T-type channels
Increased hyperpolarization
Takes longer to get to threshold
Decreased firing at SA node
Decreases AV node excitability, increased AV node delay
Shorter plateau phase of atria, weaker atrial contraction

29
Q

What is vagal tone (in heart)?

A

Vagal tone= PNS, from vagus nerve
SA Node alone-100 bpm
At rest, Vagal tone lower BPM to 75

Ex: heart transplant, vagus nerve not reconnected, therefore higher resting HR

250-S1 (44 decks)

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