Heart Physiology Flashcards

1
Q

what is the definition of the circulatory system?

A

oxygen system transporting O2, CO2, nutrients etc.

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2
Q

what are the characteristics of pulmonary circulation?

A

O2 depleted blood, passes from heart to lungs, returns oxygenated blood to heart

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3
Q

what are the characteristics of systemic circulation?

A

O2 rich blood, passes from heart to rest of body, returns deoxygenated blood to heart

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4
Q

what blood does the superior vena cava carry?

A

deoxygenated blood from head, neck and upper limbs

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5
Q

what blood does the inferior vena cava carry?

A

deoxygenated blood from below level of heart (abdomen, pelvis, lower limbs)

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6
Q

what blood does the coronary sinus contain?

A

venous blood from the heart

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7
Q

what septal defects can occur in the heart?

A

atrial, ventricular or atrioventricular (hole in the heart)
interventricular or interatrial

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8
Q

what conditions/diseases can result in end arterial coronary arteries?

A

coronary artery disease
ischaemia
angina pectoris
infarction

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9
Q

what is a coronary artery bypass graft?

A

redirecting blood supply if coronary arteries are blocked

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10
Q

what vessels can be used in a coronary artery bypass graft (CABG)?

A

saphenous vein
internal mammary artery
internal thoracic artery

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11
Q

what are the main functions of the cardiovascular system?

A

transport - nutrients, O2, waste, heat, hormones
buffers body pH
assists in infection response and urine filtration

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12
Q

what is each heart sound caused by?

A

first - AV valves closing
second - pulmonary/aortic valves closing

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13
Q

what is the formula for cardiac output?

A

stroke volume x heart rate
(per min)

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14
Q

what makes the heart contract?

A

SA node impulses spread across atria then ventricles
L/R sides contract at same time, resulting in a rise and fall of blood pressure in atria then ventricles

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15
Q

how does each node influence HR?

A

SA - determines HR (pacemaker)
AV - slows HR

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16
Q

how does K+ permeability affect HR?

A

increased permeability - longer time to threshold, fewer BPM, lower HR

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17
Q

how does Ca+ permeability affect HR?

A

increased permeability - shorter threshold time, more BPM, higher HR

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18
Q

what does Ca entry do to the cardiac muscle?

A

depolarisation then contraction

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19
Q

where is the vagal nerve and how does it influence HR?

A

terminates on nodal tissue (L = AV node, R = SA node)

releases ACl activating M2 receptors reducing HR and increasing K+ permeability

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20
Q

what is the cause of the atria-ventricular delay?

A

the annulus fibrosis acting as electrical insulator

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21
Q

what can carotid sinus syndrome be caused by?

A

vagus nerve overactivity
causes syncope/fainting

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22
Q

briefly explain the mechanisms of the cardiac cycle

A

a systole contraction then a diastole relaxation of the atria then the ventricles

blood flow controlled by valves and the diastole-systole sequence

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23
Q

what are the stages of the cardiac cycle?

A

atrial systole
atrial diastole
ventricular systole (1st phase)
ventricular systole (2nd phase)
ventricular diastole (early)
ventricular diastole (late)

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24
Q

what occurs during atrial systole?

A

atrial contraction forces blood into relaxed ventricles

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25
Q

what is the name of the contraction occuring during atrial diastole?

A

isovolumetric contractions

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26
Q

what occurs during ventricular systole? (1st phase)

A

ventricular contraction pushes AV valves closed
not enough pressure to open semilunar valves

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27
Q

what occurs during ventricular systole? (2nd phase)

A

ventricular pressure rises and exceeds arterial pressure, opening semilunar valves and ejecting blood

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28
Q

what occurs during ventricular diastole? (early)

A

ventricles relax
ventricular pressure drops
blood flows against cusps of semilunar valves forcing them closed
blood flows into relaxed atria

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29
Q

what type of relaxation occurs in ventricular diastole?

A

isovolumetric relaxation

30
Q

what occurs during ventricular diastole? (late)

A

all chambers are relaxed
ventricles fill passively

31
Q

what changes in the cases of a positive or negative inotropy?

A

preload of the heart

32
Q

what is the hearts membrane potential determined by?

A

ion concentration outside vs inside the cell

33
Q

explain the changes to the membrane potential when Na, K and Ca currents affect the heart cells

A

Na and Ca: positive inwards (depolarising)
K: positive outwards (repolarising)

34
Q

what occurs at phase 0 of the action potential?

A

upstroke: voltage gated Na channels open allowing Na in and depolarisation

35
Q

what occurs at phase 1 of the action potential?

A

notch: voltage dependant inactivation of Na
activation of outwards K causing repolarisation

36
Q

what occurs at phase 2 of the action potential?

A

plateau: balance of inwards Ca and outwards K

37
Q

what occurs at phase 3 of the action potential?

A

repolarisation: inwards currents are inactivated and outwards K channels repolarise cell

38
Q

explain the process of an excitation-contraction coupling

A

after excitation, the increase in Ca due to AP causes myofilaments to contract
(Ca channels in high concentration in t-tubules)

39
Q

what is the sarcoplasmic reticulum and what is its release mediated by?

A

an intracellular Ca store

mediated by ryanodine receptor

40
Q

explain the process of ventricular filling in diastole

A

driven by venous pressure
walls expand as they fill
atria contract adding 10-20% extra
end diastolic volume is ~120ml
once ventricular pressure exceeds atrial, AV valves shut

41
Q

name the brain and spinal nerves associated with CVS regulation and whether they are sympathetic or parasympathetic

A

glossopharyngeal (P)
vagus (P)
vasomotor (S)
cardiac accelerator (S)

42
Q

what structure does the sympathetic and parasympathetic nervous activity impact in the heart?

A

SA node

43
Q

explain the sympathetic response to HR regulation

A

nerve terminals release noradrenaline as response to stimulation
downstream effects mediated by messenger system involving cAMP production

44
Q

explain the parasympathetic response to HR regulation

A

nerve terminals release ACl in response to stimulation
downstream effects mediated by ACl-regulated K channels coupled to muscarinic receptors (ACl binds to these)

45
Q

why is ACl rapidly decayed in the parasympathetic HR response?

A

SA and AV nodes contain cholinesterase (hydrolyses ACl)

46
Q

what is resting HR regulated by?

A

parasympathetic response (stronger than sympathetic)

47
Q

what is stroke volume determined by?

A

contractility

48
Q

in what ways is stroke volume regulated?

A

sympathetic - increases stroke volume, magnitude and force rate generated

parasympathetic - decreases stroke volume and weakens contractions

49
Q

where are baroreceptors found and what do they detect?

A

found in carotid sinus and aortic arch

detect stretch and pressure changes

50
Q

what does stretch in arterial baroreceptors do?

A

increases receptor firing
inhibits sympathetic outflow from pressure origin

51
Q

explain the result of excitatory and inhibitory post-synaptic potentials

A

excitatory (EPSP) - depolarises target neuron
inhibitory (IPSP) - hyperpolarises target neuron

52
Q

what is a convergence neuron?

A

a neuron influenced by many other neurons

53
Q

what is a divergence neuron?

A

many neurons influenced by 1 neuron

54
Q

what nerves affect HR?

A

vagus (P) - decreases HR
cardiac accelerator (S) - increases HR and contractility

55
Q

which parts of the brain control CVS input?

A

higher brain centres
proprioreceptors
baroreceptors
chemoreceptors

56
Q

explain the input function of each relevant part of the brain

A

higher brain centre - cerebral cortex, limbic system and hypothalamus

proprioreceptors - joint movements

baroreceptors - BP

chemoreceptors - blood acidity

57
Q

what changes are seen in the heart during exercise?

A

increase:
cardiac output (25l/min)
HR (140bpm)
stroke volume (180ml)

decrease:
filling time (33%)

58
Q

compare the ECG times of a resting HR and an exercised HR

A

resting:
AV systole - 0.48s
diastole - 0.32s

exercised:
AV systole - 0.3s
diastole - 0.1s

59
Q

how is BP controlled during exercise?

A

when CO increases, skeletal muscle vascular beds dilate reducing PR

60
Q

what does TPR depend on and what is it controlled by?

A

depends on arteriole diameter

controlled by local metabolic factors
low O2 and high CO2 levels act on smooth muscle to relax/dilate

61
Q

why does BP increase during static exercise?

A

increase in SV with no change in TPR

62
Q

where do the parasympathetic nerves regulating HR originate from and where do they act?

A

vagal motor nuclei in brainstem (medulla)
left side acts on AV node
right side acts on SA node

63
Q

describe the course of the sympathetic nerves affecting HR and where they supply

A

cardiac sympathetic fibres exit spinal cord at T1-5
long nerve fibres run along great vessels
left side supplies ventricles
right side supplies atria

64
Q

what is the sympathetic neurotransmitter increasing HR and what does it do?

A

noradrenaline - binds to a1 adrenoreceptors

increases AV conduction, decreases myocyte AP length, increases SV and increases relaxation rate

65
Q

what is the parasympathetic neurotransmitter decreasing HR?

A

ACl - activates M2 muscarinic receptor hyperpolarising SA node and reducing AP’s generated

66
Q

what is the SA node firing rate affected by?

A

changes in autonomic nerve activity
circulating hormones (hyper/hypothyroidism)
serum ion concentration (hyper/hypokalaemia)
cellular hypoxia
drugs

67
Q

explain the bruce protocol

A

fitness test involving different stages of exercise in 3 minute intervals
speed/gradient are gradually increased to measure cardiac work and identify areas of poorly perfused myocardium

68
Q

explain how hypoxia from exercise can appear on an ECG

A

O2 consumption increases with exercise, O2 delivery cant keep up
ST segment on ECG shows electrophysiological changes in O2 delivery

69
Q

how do nitrates work in reducing cardiac work?

A

venodilation
reduces venous pressure and preload

70
Q

what can be the problem of an increased preload? (venous return to RV)

A

heart has to work harder to pump blood out
can result in heart failure, coronary artery disease and angina