Cardiac Output 2 Flashcards

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1
Q

how will the parasympathetic nervous system impact the heart at rest

A

decrease heart rate but not effect on stroke volume

decrease Na+ current by inhibiting HCN channels

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2
Q

intrinsic regulation

A

CVS is a closed system
amount of blood returning must = vol. blood ejected
Venous return = Cardiac Output

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3
Q

frank-Starling law

A

hearts intrinsic ability to adapt to changes in blood volume

greater degree of stretch = greater force of contraction of myocytes

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4
Q

how did otto frank and Ernest H Starling investigate the law

A

independent experiments investigating effects of filling pressure on stroke volume

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5
Q

mechanics of starling law

A

Actin and myosin are brought together as myocardium is stretched
– increased filling increases the stretch
increased overlap = more cross bridges formed -> more force made

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6
Q

the muscle stretch relationship with cross bridge relationship is similar to

A

force-length

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7
Q

preload

A

umbrella term to describe ventricular filling during diastole
– it is a catch term all to describe the end diastolic volume

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8
Q

what is ventricular filling affected by

A

the pressure in the atria, venous pressure, gravity and the volume of blood in the circulation

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9
Q

what will ventricular filling impact

A

stroke volume and cardiac output

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10
Q

great veins function

A

capacitance vessels for the storage of blood

– veins contain 60-70% of total blood volume at any given time

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11
Q

how does increased blood volume change venous pressure and preload

A

increased central venous
pressure and hence increased preload
– equally an increased venous tone will also increase the central venous pressure

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12
Q

how does gravity affect the blood returning to the heart

A

blood returning to the heart has to work against gravity

e.g. arterial blood to the brain

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13
Q

when upright, what factor is gravity for venous return and what is it the basis for

A

this is negative factor for venous return

– this is the basis for postural hypotension on standing

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14
Q

how is venous return affected in supine position

A

In the supine position venous return is increased
– this can contribute to pulmonary congestion and orthopoea (breathlessness when
lying flat) in heart failure

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15
Q

where do large veins pass through in limbs

A

• In limbs large veins pass between muscle blocks and are compressed as the muscle contracts
– to a lesser extent this happens as an adjacent artery pulsates

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16
Q

how does compression in veins affect blood distribution

A

This compression displaces the blood and the presence of the valves
mean it must go back toward the heart
– think of squeezing a tube of toothpaste

17
Q

how does the thoracic and abdominal pressure change during inspiration

A

diaphragm flatten
raises abdominal pressure
lowers thoracic pressure
blood from abs to thorax

18
Q

how does the thoracic and abdominal pressure change during inspiration

A

thoracic pressure increases
abdominal pressure decreases
stays below abdomen in legs

19
Q

how do muscle and thoracic pump contribute to cardiac output in exercise

A

increase cardiac output in exercise

20
Q

The Starling Law of the heart increases stroke volume by

A

changing the orientation of the fibres

21
Q

what do iontropes increase and how

A

increase contractility by changing

Ca2+ signalling

22
Q

what do changes in preload effect

A

the filling of the ventricle

– as preload increases so does filling

23
Q

how will increased afterload affect the cardiac output

A

decrease cardiac output short term

24
Q

as the stroke volume drops …

A

the end systolic volume rises
– atrial filling remains unchanged
– the end diastolic volume is increased

25
Q

Increased end diastolic pressure, increases …

A

increases stretch of the ventricles
leading to a more forceful contraction
– cardiac output is maintained at greater work

26
Q

typical daily water intake

A

~2.5 L most lost via kidney

27
Q

how is water intake categorised

A

body water compartments
intracellular - 67%
extracellular 33%

28
Q

Physiological control of blood volume

A

renin-angiotensin system
Antri-diuretic hormone
Atrial Natriuretic Peptide

29
Q

RAS

A

Ang II - potent vasoconstrictor (increases resistance)
– stimulates aldosterone, increasing Na+ and water reabsorption from urine.
– net effect is expansion of blood volume and increase in blood pressure

30
Q

ADH

A

released in response to high osmolality and/or low blood volume
– drives water reabsorption from kidney (decreases diuresis)

31
Q

Atrial Natriuretic Peptide (ANP)

A

one of many natriuretic peptides (includes brain or BNP)

– opposite of the other two, inhibits salt reabsorption so promotes salt and water loss

32
Q

heart failure

A

inability to maintain cardiac output
decrease cardiac output = decreased blood pressure
activate baroreceptor reflex
SNS induced increase in renin-angiotensin system

33
Q

when there is heart failure how does the problem try to be address by activating SNS induced ATS

A

maintain stroke volume by volume expansion

will be a point where no further volume expansion can maintain stroke volume

34
Q

excess blood volume

A

increased blood volume stretches atria activating sensory afferents to medulla
decrease SNS = less RAS, ADH greater filtration in kidney
also triggers release of ANP and BNP