Cardiac Output (Pt2): Mechanical events and Stroke Volume Flashcards

1
Q

systole

A

ventricular contraction and blood ejection

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2
Q

Diastole

A

ventricular relaxation and blood filling

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3
Q

Do the ventricles have the same SV

A

yes

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4
Q

what is the cardiac cycle predominately driven by

A

Pressure changes in the ventricles (minor part played by atrial contraction)

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5
Q

What drives opening/closing of valves

A

pressure changes in the 4 compartments

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6
Q

Systole: isovolumetric ventricular contraction

A

AV valves closed
Pressure ventricles>atria
Aortic and pulmonary valves closed
Pressure ventricles

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7
Q

Systole: ventricular ejection

A

AV valves closed and pressure ventricles > atria

Aortic and pulmonary valves open and pressure ventricles > arteries

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8
Q

Diastole: isovolumetric ventricular relaxation

A

AV valves closed and pressure ventricles > atria

Aortic and pulmonary valves closed and pressure ventricles < arteries

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9
Q

Diastole: ventricular filling

A

Negative pressure in ventricles (90%):
AV valves open, pressure ventricles < atria
A and P valves closed and pressure ventricles < arteries

Atrial contraction (10%):
AV valves open
A and P closed

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10
Q

Pressure and volume changes during the cardiac cycle

A

During systole, BP rising in ventricles, SL valves open and blood passes out
In diastole pressure in arteries gets higher than in the heart, then SL valves close and heart starts relaxing.
As it relaxes, creates a vaccuum in the bottom of the heart, and the low pressure flips open the AV valves

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11
Q

SV=

A

EDV (end diastolic volume) - ESV (end systolic volume)

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12
Q

heart sounds caused by

A

closure of heart valves

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13
Q

1st sound

A

closure of AV valves

onset of systole (contraction)

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14
Q

2nd sound

A

closure of pulmonary and aortic valves

onset of diastole (relaxation)

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15
Q

Regulation of SV

A
  • filling pressure (reload)- starling’s law of the heart
  • arterial pressure opposing ejection (afterload)
  • contractility: sympathetic nerves, circulating agents
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16
Q

what is end-diastolic ventricular volume (pre load) determined by

A

CVP - central venous pressure

17
Q

What is CVP determined by

A

skeletal muscle pump (blood squeezed back towards heart leading to incr CVP)
Blood volume (reduced BV leads to reduced CVP)
Gravity (posture)- when standing, gravity leads to pooling in legs and reduces volume and CVP
Sympathetic nerves- contraction of central and peripheral veins leads to incr CVP
Respiratory pump (breathing)- inspiration = incr CVP, expiration = decr CVP

18
Q

frank starling mechanism

A

ventricles contract with more force (ie incr stroke volume) if it contains more blood (ie incr end-diastolic ventricular volume)

19
Q

What is frank starling mechanism determined by

A

length-tension relationship in the muscle ie greater stretch = more tension developed in the cardiac muscle

20
Q

What is the main function of the frank starling mechanism

A

maintains balance between left and RHS of the heart and stops accumulation of blood in lungs

21
Q

How does F-S stop blood accumulating in the lungs

A

if incr venous return to right ventricle then incr contraction
more blood to lungs
If incr venous return to left ventricle then incr contraction
Incr stroke volume
Blood doesn’t accumulate in lungs

22
Q

Contractility

A

sympathetic only, not para, controls SV
Symp release noradrenaline, activate B1 adrenergic receptors, incr force and speed of cardiac muscle contraction and incr ventricular contraction at any given end-diastolic ventricular volume

23
Q

arterial pressure opposing ejection

A

Higher arterial BP, harder heart is to open

Hypertension (high BP) makes it more difficult to open valves and eject blood, leading to heart failure

24
Q

congestive heart failure

A

reduced CO
tiredness and shortness of breath
Fluid retention via kidneys to incr CO ( venous return)

25
Q

systolic dysfunction

A

coronary heart disease leading to ischaemic heart disease and heart attack
Heart attack damages heart muscle, decr ventricular contractility so lower SV

26
Q

Diastolic dysfunction

A

Hypertension
stiffening of ventricular wall - incr ventricular muscle- inr cardiac resistance- incr arterial pressure- high BP/ hypertension

27
Q

Diastolic dysfunction

A

Hypertension
stiffening of ventricular wall - incr ventricular muscle- inr cardiac resistance- incr arterial pressure- high BP/ hypertension
Also stiffening leads to decr in end-diastolic ventricular volume, leads to decr in stroke volume