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Physiology > Cardiovascular physiology > Flashcards

Cardiovascular physiology Flashcards

1
Q

what is the pericardium (3)

A
  • the double layered membrane
  • surround the heart
  • providing protection and reducing friction as heart contracts
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2
Q

primary roles of the cardiovascular system (5)

A
  • distribution of oxygen and nutrients
  • transport of CO2 and metabolic waste products
  • distribution of water, electrolytes and hormones
  • thermoregulation
  • immune system infrastructure
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3
Q

what is the golden rule of the ECG?

A

the action potential is moving towards the positive input giving you an upward deflection

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4
Q

what is the 12 lead ECG? (2)

A
  • diagnostic test recording the electrical activity of heart from 12 different angles
  • more precise
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5
Q

how man electrodes and leads does the 12 lead ECG use?

A

10 electrodes
12 leads

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6
Q

the events of the cardiac cycle: (5)

A
  1. atrial systole (ventricular diastole)
  2. isovolumic contraction (ventricles)
  3. ventricular ejection
  4. isovolumic relaxation (ventricles)
  5. passive ventricular refilling
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7
Q

how is the heart a function syncytium? (2)

A
  • individual cells are electrically coupled together
  • cells are also mechanically coupled together due to flow of electrical events, which leads to the contractile events of the heart
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8
Q

what are the 2 main factors affecting heart rate?

A
  • autonomic nervous system
  • circulating hormones
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9
Q

why are HCN channels often referred to as ‘funny channels’? (2)

A
  • due to their unique property of producing inward currents
  • in response to hyperpolariation
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10
Q

why is an unstable resting membrane potential needed in SA nodal cells?

A

fundamental characteristic for their unique role as the hearts natural pacemaker

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11
Q

what are the sinus ‘brady/tachycardia conditions (3)

A
  • two different heart rhythms
  • characterized by variations in heart rate
  • generated by SA node
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12
Q

what medication can cause sinus bradycardia

A

beta-blockers

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13
Q

what medial conditions can cause sinus bradycardia? (2)

A
  • hypothyroidism
  • increased intracranial pressure
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14
Q

how do beta-blockers cause sinus bradycardia? (2)

A
  • blockage of Beta-1 adrenergic receptors
  • decreases sympathetic stimulation
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15
Q

what is a cardiac arrhythmia? (1) and what causes it (2)

A

an abnormal heart rhythm of rate generated by?
* abnormal impulse generation
* abnormal impulse conduction

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16
Q

what are excitable cells? (1)

A

a cell that is capable of generating and conducting electrical signals

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17
Q

what type of metabolic requirements are increased when we exercise? (4)

A
  • respiratory system
  • cardiovascular system
  • nervous system
  • endocrine system
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18
Q

what is the sympathetic and parasympathetic nervous system, and the key neurotransmitter involved in both

A

sympathetic:
* fight or flight system
* key nt - norepinephrine

parasympathetic:
* rest and digest system
* key nt - acetylcholine

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19
Q

how does the baroreceptor reflex regulate blood pressure? (2)

A
  • detecting changes in vessel stretch
  • sensing signals to CV centre
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20
Q

what does norepinephrine primarily act on in the heart?

A

beta-edrenergic receptors

21
Q

what do chemoreceptors do?

A

detect changes in chemical composition of blood

22
Q

the difference between dynamic (3) and resistance (2) exercise:

A

dynamic:
* rhythmical movements of limbs
* contraction/relaxation of skeletal muscle
* flexing of joints

resistance:
* sustained, isometrict contraction of specific muscles
* limited joint movement

23
Q

what is the TPR (total peripheral resistance)?

A
  • the overall resistance the blood encounters as it circulates through the artieres throughout the body
24
Q

does resistance training alone improve functional capacity of the CVS (cardiovascular system)?

A

no

25
Q

the use it or lose it concept, applied to aspects of life: (5)

A
  • muscular strength and endurance
  • cognitive function
  • joint flexibility
  • language skills
  • social skills
26
Q

what is aortic stenosis? (2)

A
  • narrowing of the aortic valve
  • resulting in increased pressure load on heart
27
Q

why non-functional hypertrophy is not one of the two main types of cardiac hypertrophy? (1)

A
  • non-functional hypertrophy does not primarily focus on the adaptive or maladaptive nature of hypertrophy
28
Q

consequences of inadequate cardiac output (3)

A
  • inadequate O2 distribution and CO2 removal
  • hypotension
  • circulatory collapse
29
Q

what does VO2 stand for?

A
  • oxygen consumption
30
Q

what is the VO2 max?

A
  • the maximum ability of the body to utilise oxygen during exercise
31
Q

what is VO2 max also known as?

A

aerobic capacity

32
Q

2 components affecting VO2 max? (2)

A
  • combined ability of the cardiovascular and pulmonary systems to transport oxygen to the muscular tissue system
  • the chemical ability of the muscular cellular tissue system to use oxygen in breaking down fuels
33
Q

is it possible to improve VO2 max, and if so by how much?

A

yes
10-15 %

34
Q

what is myocardial infarction? (3)

A
  • essentially a heart attack
  • whereby atherosclerotic plaque bocks one or more coronary arteries
  • restricts blood flow and oxygen to myocardium
35
Q

problem of large MI

A

cardiac arrest

36
Q

how can smaller MI’s be treated?

A
  • stents
  • fibrinolytic drugs
37
Q

long lasting effects of MI:

A
  • remodelling of heart for months, reducing pump function
38
Q

what is the role of t-tubules? (2)

A
  • transmits electrical impulses from cell surface into interior of cell
  • allowing for synchronized contraction of entire myocardium
39
Q

what is the myocardium? (3)

A
  • the middle layer of the heart wall
  • consists primarily oc cardiac muscle tissue
  • responsible for contraction of the heart
40
Q

how can one visualise calcium inside cells? (2)

A
  • laser scanning confocal microscopy
  • line scan recordings for fast Ca release events
41
Q

what happens if you lose t-tubules within the heart cells? (2)

A
  • delayed Ca2+ release
  • slow Ca2+ rise
42
Q

how was it thought to be possible to restory calcium release in cells with low, t-tubules, and why it was not a viable therapy

A
  • increased calcium entry through isoproterenol
  • has detrimental long term effects
43
Q

why is the notch important in the action potential of ventricular myocytes? (2)

A
  • brings membrane potential down to point where voltage gaed calcium channels are most active
  • consequently triggers much more Ca2+ release in cell
44
Q

where is the SERCA pump found (1) and what does the SERCA pump do? (3)

A
  • found in membrane of sarcoplasmic reticulum
  • pumps calcium against concentration gradient back into SR from cytoplasm
  • helps lower cytoplasmic calcium concentration
  • promoting muscle relaxation
45
Q

what are ventricular arrhythmias? (2)

A
  • rapid, disorganized activation of the ventricles
  • resulting in greatly reduced cardiac output
46
Q

what can ventricular arrhythmias cause? (2)

A
  • loss of consciousness
  • sudden cardiac death
47
Q

what are delayed afterdepolarizations (DADs) (3)

A
  • spontaneous Ca2+ release from SR
  • Ca2+ waves propagate by Ca-induced Ca release
  • Ca2+ removal by NCX generates depolarising current
48
Q

what happens in early after depolarizations? (3)

A
  • occur while action potential is still repolarising
  • prevents membrane potential from recovering down to rest
  • is due to change between inward and outward k+ curents
49
Q

what is the main factor triggering DADs and EADs

A

disrupted Ca2+ equilibrium

Physiology (10 decks)

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