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Cardiovascular Lectures > L2: Anatomy & Physiology Of The CV system > Flashcards

L2: Anatomy & Physiology Of The CV system Flashcards

1
Q

What is the biggest part of the heart?

A

The left ventricle - thicker wall than the right

Atria structures are thin

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2
Q

What is the role of the valves in the heart?

A

stop blood going the wrong way

increase efficiency of blood pumping through heart

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3
Q

Myocardial structure

- What 2 things does intercalated disks contain?

A
  1. Gap junctions- for cell to cell ion movement (rapid spread of electrical signal) –> contraction of heart
  2. Desmosomes - transfer force from cell to cell (end to end), when cells contract, heart contracts
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4
Q

What is the role of cardiomyocytes?

A

Consume lots of O2 in heart - most dense tissue for mitochondria

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5
Q

What is the structure of cardiomyocyte sarcomeres?

A

I band: actin (thin filaments)
H band: myosin (thick filaments
Titin: 2 way spring : helps cell relax after contracting

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6
Q

What is the cardiomyocyte length-tension relation?

A
  • increase in myofilament (actin + myosin) overlap = increase in force
  • more stretch (return of blood) = produces bigger contraction (increase in output of blood)
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7
Q

What is systolic and diastolic?

A

Systolic: contraction of heart
Diastolic: relaxation of heart

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8
Q

How is action potential conducted throughout the cardiomyocytes?

A

T-tubules allow conduction of rapid action potential

- releases calcium from Sarcoplasmic reticulum –> triggers synchronous contraction

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9
Q

What is the big structural difference btwn cardiac and skeletal myocytes?

A

Heart has much more mitochondria than skeletal - bc need to continuously move

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10
Q

Explain the cardiac excitation-contraction coupling process

A
  1. Ca enters cell during AP plateau
  2. Triggers release of more Ca from SR
  3. Ca binds to myofilaments (troponin-C)
  4. Activates cross-bridge cycling
  5. Cell shortens
  6. Most Ca pumped back in SR
  7. Some Ca exits cell by Na-Ca exchanger and sarcolemmal Ca pump
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11
Q

What is the role of the Troponin complex in the contraction and relaxation of cardiomyocytes?

A

Troponin complex = TnT + TnC + TnI

  1. Ca2+ binds to TnC
  2. TnC changes conformation
  3. TnI moves away from actin myosin binding site
  4. Actin binds to myosin and contraction occurs
  5. As [Ca2+] falls - Ca2+ dissociated from TnC
  6. TnI again blocks actin myosin binding site
  7. Relaxation occurs
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12
Q

What happens when TnI is phosphorylated by Beta adrenergic signalling?

A

Promotes dissociation of Ca2+ from TnC and myocyte relaxation

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13
Q

What is the difference btwn Cardiac and skeletal ECC?

  • no. of AP’s
  • Excitation
  • Regulation of force
  • Metabolism
A

Cardiac

  • One plateau (refractory period where heart cant contract again - prevent arrhythmia)
  • gap junction spread
  • Ca entry
  • oxidative only

Skeletal

  • many spikes
  • motor unit
  • AP freq and summation
  • oxidative and glycolytic
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14
Q

What happens during isovolumetric contraction?

A

The heart contract, there is no change in volume but there is change in pressure

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15
Q

How can we measure cardiac function?

A

Echocardiography - systolic function

- assessed by looking at cross sectional view of heart

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16
Q

How can we measure systolic function?

A

Echocardiography - systolic function

- assessed by looking at cross sectional view of heart

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17
Q

how can we measure diastolic function?

A

Echocardiography

- assessed by looking at longitudinal view of heart

18
Q

How can we measure diastolic function?

A

Echocardiography

- assessed by looking at longitudinal view of heart

19
Q

What does the doppler flow (mitral inflow) measure?

and what do the E and A waves represent?

A
  • measures blood flow velocity through mitral valve
  • E wave = blood flowing into ventricle by passive filling (due to pressure gradient)
  • A wave = blood flowing from atrium into ventricle by active filling (due to atrial contraction)
20
Q

Doppler flow (mitral inflow)

  • what is normal E/A?
  • What is impaired relaxation E/A?
A

normal: E/A > 1
- E wave bigger than A wave

Impaired relaxation: E/A < 1
- as heart stiffens, impaired diastolic function so E wave is similar to A wave

21
Q

What does tissue doppler (mitral valve movement) measure?

What is E’ wave and A’ wave represent?

A
  • measures velocity of tissue movement at mitral valve
  • E’ wave = passive LV filling
  • A’ wave = filling due to atrial contraction
22
Q

Diastolic function

- what happens to E/e’ ratio with increased severity of heart failure?

A

E/e’ ratio increases with severity
correlates with HF biomarkers
E/e’ ratio declines when heart failure improves

23
Q

How does electrical activation of myocardium/heart occur?

A
  1. Pacemaker in heart - SA node depolarizes the atria
  2. depolarizes septum (left to right)
  3. depolarize ventricular walls towards apex and up towards base
24
Q

What route does an AP travel through the conduction system of the heart?

A

Action potential travels from SA or AV node –> common bundle –> bundle branches –> purkinje fibres –> myocytes (cause contraction)

25
Q

ECG: what is… (refer to slides for diagrams)
P wave
QRS wave
T wave

A

P - due to atria contracting (depolarisation)
QRS - ventricles contracting (depolarisation)
T - ventricular repolarization

26
Q

What are the biomarkers of heart damage?

What is the process of their release?

A

Enzymes such as CK-MB, Troponin I (troponin free in cytoplasm, troponin complex released from actin filament), myoglobin
- used to diagnose myocardial infarction

  1. onset of myocardial infarction
  2. plasma membrane of necrotic (dead) myocytes become leaky
  3. mlcs leak out of cell and into circulation
27
Q

What is the difference in pressure btwn arterial and venous circuit?

A

Arterial circuit:
- high pressure

Venous circuit
- low pressure to deliver nutrients and O2 and remove waste

28
Q

Describe the venous return to the heart via calf muscle + role of valves

A
  • the calf muscle acts as pump for deep leg veins
  • calf muscle relaxed: valves prevent backflow, valves closed
  • calf muscle contracted : valve open, blood flow caused by muscle contraction
29
Q

What are the characteristics of the diff. blood vessels?

  • large arteries
  • small arterioles
  • capillaries
  • large veins
A

(refer to slides)

  • large arteries - pressure reservoir
  • small arterioles - resistance vessels
  • capillaries - exchange
  • large veins - volume reservoir
30
Q

Where is there the most blood volume distribution?

A

Most volume in systemic veins and venules

31
Q

What is distribution of cardiac output through vascular tree and organ beds?

A

Vascular tree: perfused in series
Organ beds: perfuse in parallel
At rest: highest flow to gut and kidney
Arterioles: control flow through each bed - by local and central signals

32
Q

What do the lymphatic vessels contain?

A

excess interstitial fluid, white blood cells, also transports fats from gut

33
Q

What is the role of the lymph nodes? How does lymph enter the blood?

A

Role: important in adaptive immune response
Transport: enters blood via lymphatic duct (right side), thoracic duct (left side) - aided by smooth muscle contraction + valves

34
Q

What happens to the venous and interstitial fluid during oedema?

A

Oedema: accumulation of interstitial fluid

  • increase in venous pressure
    e. g. with congestive heart failure
  • venous pooling
  • fluid accumulation in lung
  • increase in interstitial pressure
    e.g. lymph vessel blockage, parasitic infection, gross oedema of limbs
    caused by poor lymph drainage (not capillary dysfunction)
35
Q

What is blood pressure?

A

the driving force to push blood through circulation

36
Q

Role of pressure in resistance of vessels - systemic and pulmonary resistance

A 
Resistance systemic (narrower vessels) >> pulmonary resistance 
largest overall resistance in arterioles + biggest pressure drop
37
Q

How to calculate MAP (mean arterial pressure)?

A 
MAP = DP + 1/3 PP 
PP = SP - DP
38
Q

How does vasoconstriction and vasodilation occur?

A

Vasoconstriction: smooth muscle cells contract + increase resistance of vessel

Vasodilation: smooth muscle cells relax and decrease resistance of vessel

39
Q

Equation for:
Blood flow (velocity)
Cardiac output

A

Blood flow = pressure gradient (P2-P1)/ resistance

  • blood flow decreases with increased resistance
  • blood flow increases with increased pressure gradient

Cardiac output = mean arterial pressure / total peripheral resistance (TPR)
CO = HR x SV

40
Q

Role of Noradrenaline and Adrenaline in Sympathetic NS activation

A

Noradrenaline: - at smooth muscle cells
Receptor - alpha AR
Response - constrict

Adrenaline - at smooth muscle cells
receptor - beta 2 AR
response - dilate muscle

Cardiovascular Lectures (2 decks)

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