Lecture 03 Heart Physiology 2 Flashcards

1. Understand myocardial contractility and how cardiac output is a function of stroke volume and heart rate 2. describe factors affecting stroke volume 3. understand the heart as an endocrine organ 4. describe how treatment is personalised to the patient

1
Q

How is Cardiac Output measured?

A

litres per minute

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2
Q

How is Cardiac Output calculated?

A

heart rate x stroke volume

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3
Q

What is Cardiac Output?

A

how much blood is being delivered through the circulation per minute

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4
Q

What is the blood volume?

A

5 litres

this is how much blood is pumped every minute at rest

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5
Q

What is the maximal blood volume with exercise?

A

35 litres

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6
Q

What is the Ejection Fraction (%)

A

refers to the percentage volume of blood ejected with each cardiac contraction
normally 55-60% at rest

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7
Q

What factors affect heart rate?

A

sympathetic stimulation
parasympathetic stimulation
circulating catecholamines
drugs

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8
Q

How does sympathetic regulation affect heart rate?

A

increases heart rate in response to NA

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9
Q

How does parasympathetic regulation affect heart rate?

A

decreases heart rate in response to vagus nerve

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10
Q

What is an example of a circulating catecholamine?

A

adrenaline

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11
Q

When (medically) is sympathetic and parasympathetic regulation irrelevant?

A

individuals with a heart transplant

no autonomic control

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12
Q

What factors affect stroke volume?

A
  1. intrinsic contractility

2. extrinsic contractility

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13
Q

What intrinsic factors affect stroke volume?

A
intracellular calcium 
oxygen 
free fatty acids
ATP 
muscle physiology
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14
Q

What extrinsic factors affect stroke volume?

A

preload/filling pressure
afterload/resistance to ejection
sympathetic activity

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15
Q

How would you increase a patient’s preload?

A

injection of saline increases their blood volume and therefore preload

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16
Q

What does intracellular calcium activate? What does this lead to?

A

ryanodine receptors on the sarcoplasmic reticulum

cascade reaction leading to further activation of ryanodine receptors and release of calcium

17
Q

How would sympathetic activity affect the stroke volume?

A

preload and after load kept the same

increasing sympathetic activity increases cardiac output

18
Q

How does calcium initiate contraction?

A

calcium attaches to troponin
leads to myosin to be exposed
actin binds to myosin
contraction

19
Q

How does contraction occur?

A
  1. myosin filaments have heads that form cross bridges when attached to actin filaments. ATP is hydrolysed when myosin head is unattached
  2. ADP+P are bound to myosin as myosin head attaches to actin
  3. ADP+P release causes head to change position and actin filament to move
  4. binding ATP causes myosin head to return to resting position
20
Q

Why is it important that the wave of depolarisation moves through the heart quickly?

A

so that the whole cardiac muscle can contract together

21
Q

What does the Frank-Starling Mechanism compare?

A

cardiac output and end-diastolic pressure

22
Q

What is end diastolic pressure?

A

volume of blood in the ventricles at the end of diastole

23
Q

What is the principle of the Frank-Starling Mechanism?

A

the bigger the stretch of the myocardial fibres the larger the contraction, this increases the stroke volume and therefore the cardiac output

24
Q

How does changes in the venous return affect the LVEDP and stroke volume?

A

increased venous return increases the volume and therefore the LVEDP, this will increase the stroke volume
decreased venous return decreases the volume and therefore the LVEDP, this decreases the stroke volume

25
Q

Frank Starling Mechanism - what determines how the ventricle operates?

A

a family of curves determined by afterload and contractility

26
Q

Frank Starling Mechanism - what happens if the curve shifts up and left?

A

increased contractility, stroke volume and resistance
decreased afterload
overall increase in cardiac output

27
Q

Frank Starling Mechanism - what happens if the curve shits down and right?

A

decreased contractility and stroke volume
increased afterload
overall line is flatter

28
Q

Frank Starling Mechanism - what effect does the preload have?

A

curve defined by afterload

move up and down that curve defined by preload

29
Q

What is Isoprenaline?

A

synthetic catecholamine similar to NA

30
Q

What does Isoprenaline do?

A

enhances calcium influx, increased intracellular calcium causes enhanced contraction
shift Frank Starling curve left and up to a higher cardiac output

31
Q

Frank Starling Mechanism - what does the curve look like for a failing heart? What does this mean?

A

curve to the right and down, much flatter
doesn’t matter how much preload is increased, the stroke volume is limited
increasing pressure has little-to-no effect

32
Q

How is high LVEDP in heart failure patients treated? Why?

A

diuretics - decrease filling pressure decreases LVEDP

33
Q

What is a symptom of low cardiac output (medical shock)? What can this lead to if untreated?

A

breathlessness

heart failure

34
Q

How is low cardiac output treated?

A

ACE inhibitors - vasodilation

shift curve left and up increasing CO and decreasing afterload