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Yr 2 - Cardiology System > Cardiac Haemodynamics > Flashcards

Cardiac Haemodynamics Flashcards

1
Q

Why would this scan suggest pulmonary oedema?

A

More fuzzy –> less air = more fluid

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2
Q

Cardiac cycle of left side of heart

A
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3
Q

What is job of desmosomes in relation to heart?

A

Desmosomes stop separation during contraction by binding filaments, joining the cells together

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4
Q

How does the action potential spread between cardiac cells?

A

Gap junctions allow action potentials to spread between cardiac cells by permitting the passage of ions between cells, producing depolarization of the heart muscle

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5
Q

Structure of each muscle fibres in normal skeletal muscle

A
  • Skeletal muscles are composed of tubular muscle cells (myocytes called muscle fibers or myofibers) which are formed in a process known as myogenesis
  • Each muscle fibre composed of individual myofibrils which contain rows of adjacent sacromeres
  • Actin (thin) and myosin (thick) filaments overlap
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6
Q

What are sacromeres?

A

A sarcomere is the complicated unit of striated muscle tissue. It is the repeating unit between two Z lines

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7
Q

Describe calcium during this phase

A

Lots of calcium outside cell, calcium channels open, calcium comes into cell

Calcium can be used to help start new cardiac contraction

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8
Q

Describe interaction of actin, tropomyosin and troponin

A

Troponin is attached to the protein tropomyosin and lies within the groove between actin filaments in muscle tissue

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9
Q

What is purpose of tropomyosin-troponin complex in relaxed muscle?

A

Hides binding site of actin to myosin –> preventing contraction by blocking myosin-actin binding

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10
Q

Describe how muscle contraction works regarding troponin-tropomyosin complex

A
  1. Influx of Ca2+ as cell is depolarised by action potential
  2. Ca2+ binds to troponin-tropomyosin complex (binds to troponin C specifically) and causes it to change shape
  3. Change in shape exposes actin binding site
  4. Myosin binds to actin to form crossbridge and contraction begins
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11
Q

What happens when actin binding sites are exposed? What does this require?

A

Myosin heads can bind to actin –> requires ATP

Myosin exerts, ‘pulling’ action on actin and initials muscle contraction

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12
Q

How is chemical energy stored and then converted?

A

Within ATP, then converted into mechanical energy (ADP).

Results in:

  • Force generation
  • Myofilament shortening

Transforms basic mechanical energy into useful hydraulic function for the whole organ

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13
Q

How is blood ejection maximised (3D structure and orientation of cardiac muscle fibres)?

A
  • Longitudinal (top to bottom) filament shortening
  • Horizontal and circumfrential (around) thickening

This reduces LV chamber diameter, raising pressure and force aortic valve open

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14
Q

What are the different directions of myocardial contraction?

A
  • Longitudinal
  • Horizontal
  • Twisting (torsion)
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15
Q

Why does the system into which blood is propelled have inherent resistance?

A

It branches out into increasingly small and dense vessel networks

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16
Q

Why is a diastolic period essential?

A

The electrics repolarise, the myocardium relaxes and allows LV filling. Meanwhile the aortic valve shuts, the coronary sinuses fill so the coronaries are perfused, and the myocardium receives oxygen and glucose to allow more ATP to be generated.

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17
Q

What is cardiac reserve?

A

The capacity of heart to increase performace on demand (exercise, pregnancy, fluid overload)

Cardiac Reserve = Maximal Cardiax Output - Cardiac Output at Rest

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18
Q

What is equation for cardiac output?

A

Heart Rate x Stroke Volume

5 L/min at rest

Up to 20 L/min during exercise

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19
Q

What is effect of sympathetic innervation on heart rate?

A
  • Speeds up SA node depolarisation
  • More frequent action potentials
  • Increases conduction through AV node / Bundle of His
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20
Q

What is effect of B-agonists in heart?

A

Bind to β-receptors on cardiac and smooth muscle tissues

Overall, the effect of β-agonists is cardiac stimulation (increased heart rate, contractility, conduction velocity, relaxation)

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21
Q

How can sympathetic input affect calcium and overall increase cardiac output?

A
  • Prolonged opening of Ca2+ channels (more calcium binds to troponin and allow actin binding)
  • Enhances calcium action in excitation/contraction coupling mechanisms
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22
Q

What is preload?

A

At the end of atrial systole and just prior to atrial contraction, the ventricles contain approximately 130 mL blood in a resting adult in a standing position. This volume is known as the end diastolic volume (EDV) or preload.

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23
Q

Compare stretch of skeletal muscle to cardiac muscle

A

Cardiac muscle have narrower range (don’t stretch as much to have tension) but is more sensitive (don’t have to pull apart to have lots of tension)

Sarcomere lengths do not change very much in cardiac muscle compared to skeletal muscle; nevertheless, small changes in sarcomere length can produce large changes in tension development

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24
Q

What happens with increased sacromere length?

A
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25
Q

What is the cardiac myocyte and what is it composed of?

A
  • A specialised muscle cell composed of bundles of myofibrils that contain myofilaments
  • Myofibrils have distinct, repeating units (sacromeres)
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26
Q

What is the sacromere composed of?

A

Thick and thin filaments (myosin and actin)

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27
Q

What causes sacromere length to shorten?

A

Chemical and physical interactions between actin and myosin cause length to shorter (myocyte contracts)

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28
Q

What are the thin filaments of sacromeres composed of?

A

3 different types of protein: actin, tropomyosin and troponin

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29
Q

Describe changes in sacromere length related to tension and force of contraction

A

Changes in sarcomere length are an important mechanism by which the heart regulates its force of contraction (see Frank-Starling relationship). As a myocyte is stretched (as occurs with increased ventricular preload), the sarcomeres within the myofibrils are also stretched. With increased sarcomere length, there is an increase in the force of contraction (i.e., tension development by the muscle fibre)

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30
Q

How does LV end-diastolic volume (preload) relate to cardiac performance?

A

Increased preload = increased cardiac performace

Preload determines how stretched the LV wall is

31
Q

What happens to diameter of myofibrils as muscle stretches?

A

Is reduced

32
Q

How does reducing sacromere length (myofibril diameter) aid in contraction?

A

Thick and thin filaments (actin and myosin) are closer together so interaction is easier and more myosin heads can interact with actin

More contraction can occur with more force –> more cardiac output

33
Q

What is the Frank-Starling Law?

A
  • Represents the relationship between stroke volume and end diastolic volume
  • Stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction (the end diastolic volume), when all other factors remain constant.
  • As a larger volume of blood flows into the ventricle, the blood stretches the cardiac muscle fibers, leading to an increase in the force of contraction
34
Q

Why does venous return always correlate with cardiac output?

A

Equilibrates right and left heart output (LV CO = RV preload, and vice versa)

Venous return is the flow of blood back to the heart. Under steady-state conditions, venous return must equal cardiac output because the CVS is essentially a closed loop. Otherwise, blood would accumulate in either the systemic or pulmonary circulations.

35
Q

What causes a left shift in Frank-Starling curve?

A

Exercise, pharmacological stimulation (drugs)

36
Q

What causes a right shift in Frank-Starling curve?

A

Pharmacological depression (drugs), myocardial loss (e.g. infarction)

37
Q

How does noradrenaline and adrenaline result in muscle contraction? What effect does this have on Frank-Starling curve?

A

Noradrenaline and adrenaline stimulate cAMP, results in increased intracellular Ca2+, greater cross-bridge linking in sacromeres

Curve shifts to left

38
Q

What is equation for ejection fraction?

A

Ejection Fraction = Stroke Volume / End-diastolic volume

39
Q

What is physiological (rest) ejection fraction?

A

55-75% (can reach 90% in exercise)

40
Q

What is ejection fraction?

A

The proportion of blood ejected out of the heart related to how much was in it in the first place

41
Q

What does a failing heart show in relation to EF?

A

Reduced EF

42
Q

What can lead to myocardium contracting less?

A
  • Ischaemia –> scarred (dead) myocardium (thick, brittle, hard, doesn’t move or add to cardiac function)
  • Viral infection (inflammation of heart), alcohol –> wall thinning
  • Increased afterload –> chronic high-output
43
Q

How does the body try and compensate for a failing ventricle?

A
  • SNS overactivates
  • RAAS (renin-angiotensin-aldosterone system) kicks in
44
Q

These measures taken to try and compensate for a failing ventricle will work for a while but what happens when the heart stretches too much?

A

Eventually LV stretch exceeds physiological levels and we move to descending limb of sacromere tension curve (too much of a good thing is bad)

45
Q

In hospital, how can pulmonary oedma be treated?

A
  • High-flow oxygen –> lungs full of fluid from failing LV (not ideal gas exchange so low O2 saturation)
  • Morphine –> Relax pulmonary vessels to reduce preload and take strain off LV, also helps breathing, pain and relaxes patient
  • Furosemide –> Decreases pressure caused by extra fluid, reduces preload
46
Q

What is afterload?

A

The force or load against which the heart has to contract to eject the blood

47
Q

Ionotropy?

A

Contractility

48
Q

Chronotropy?

A

Heart rate

49
Q

Dromotropy?

A

Conduction velocity

50
Q

What does increased cAMP lead to?

A
  • Increased ionotropy (contractility)
  • Increased dromotropy (conduction velocity)
  • Increased chronotropy (heart rate)
51
Q

What is a muscle fibre called?

A

Myocytes

52
Q

What are myocytes composed of?

A

Myofibrils (

53
Q

What are myofibrils?

A

A basic rod-like unit of a muscle cell –> many chains of myofibrils make up myocytes

54
Q

How are myofibrils generated?

A

They are created during embryonic development in a process known as myogenesis.

55
Q

What are myofibrils composed of?

A

Long proteins including actin, myosin, and titin, and other proteins that hold them together –> these proteins are organised into thick and thin filaments called myofilaments which repeat along the length of the myofibril in sections called sacromeres

56
Q

What are sacromeres?

A

Repeated subunits along the length of the myofibril

57
Q

What are the 2 types of myofilaments?

A

Thin and thick filaments

58
Q

What do the thick filaments mainly consist of?

A

Myosin

59
Q

What do the thin filaments mainly consist of?

A

The protein actin

60
Q

How do muscles contract?

A

By sliding thin (actin) and thick (myosin) filaments along each other

61
Q

What type of muscle is cardiac muscle?

A

Striated

62
Q

What causes the muscle to appear striated?

A

The sarcomeric subunits of one myofibril are in nearly perfect alignment with those of the myofibrils next to it. This alignment gives rise to certain optical properties which cause the cell to appear striped or striated

63
Q

What are the boundaries of each sacromere?

A

Z-lines

64
Q

What are Z-lines?

A

dense protein discs that do not easily allow the passage of light.

65
Q

What can the area between the Z-lines be further divided into?

A

2 I-bands at either end and 1 A-band in the middle

66
Q

Describe and explain appearance of I bands

A

The I bands appear lighter because these regions of the sarcomere mainly contain the thin actin filaments, whose smaller diameter allows the passage of light between them

67
Q

Describe and explain appearance of A band

A

The A band contains mostly myosin filaments whose larger diameter restricts the passage of light.

68
Q

Where is troponin found? What is it attached to?

A

Troponin is attached to tropomyosin and lies between actin filaments in muscle tissue

69
Q

What is troponin? What is it a complex of?

A

Troponin is a complex of three regulatory proteins (troponin C, troponin I, and troponin T)

70
Q

What are adrenergic receptors?

A

a class of G protein-coupled receptors that are targets of many catecholamines like norepinephrine (noradrenaline) and epinephrine (adrenaline) produced by the body, but also many medications like beta blockers, β2 agonists and α2 agonists

71
Q

What does the binding of a catecholamine to an adrenergic receptor usually stimulate?

A

will generally stimulate the sympathetic nervous system

72
Q

What are the two principal signal transduction pathways involving the G protein-coupled receptors?

A
  1. the cAMP signal pathway
  2. the phosphatidylinositol signal pathway (IP3/DAG)
73
Q

What does the binding of noradrenaline / adrenaline to adrenergic receptors stimulate?

A

Gi and Gs (look at IMS) are linked to adenyl cyclase so agonist binding causes a rise in the intracellular concentration of the second messenger cAMP.

74
Q

what is Furosemide?

A

A loop diuretic (works on loop of Henle to increase water lost)

It’s used to treat high blood pressure, heart failure and oedema (a build up of fluid in the body)

Yr 2 - Cardiology System (25 decks)

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