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Year 1 LSS 1 > Cardiovascular System Facts > Flashcards

Cardiovascular System Facts Flashcards

1
Q

What are the dimensions of cardiomyocytes?

A

100um long and 15um wide.

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2
Q

What are the measures of pre-load?

A

End-diastolic volume/pressure

Right atrial pressure

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3
Q

What are the measures of after-load?

A

Diastolic arterial blood pressure (as this is the pressure the heart needs to overcome for ejection)

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4
Q

What is stroke work?

A

Stroke Volume X Pressure

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5
Q

What is Starling’s Law?

A

Increased diastolic fibre length increases ventricular contraction

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6
Q

What is the Law of Laplace?

A

When the pressure within a cylinder is held constant, the tension of its walls increases with increasing radius.

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7
Q

How is stroke volume calculated?

A

SV = End-diastolic volume - End-systolic volume

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8
Q

How is ejection fraction calculated?

A

SV/EDV

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9
Q

What is ejection fraction normally?

A

65%

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10
Q

How is Cardiac Output calculated?

A

HR X Stroke Volume

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11
Q

What factors determine stroke volume?

A

Pre-load
After-load
Contractility

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12
Q

What does the S4 heart sound indicate?

A
  • congestive HF
  • pulmonary embolism
  • tricuspid incompetence
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13
Q

What does the S1 heart sound indicate?

A

Closure of AV valves

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14
Q

What does the S2 heart sound indicate?

A

Pulmonary and Aortic valves closing

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15
Q

What does the S3 heart sound indicate?

A

Turbulent ventricular filling

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16
Q

What is the equilibrium potential for potassium?

A

-80mV

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17
Q

What is the equilibrium potential for sodium

A

+66mV

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18
Q

How long does a cardiac action potential last in comparison to a nerve action potential?

A

Nerve: 2ms
Cardiac: 280ms

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19
Q

What drugs aim to reduce blood pressure acting as calcium channel antagonists?

A

Nifendipine
Nitrendipine
Nisadipine

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20
Q

How can blood flow through a capillary be calculated? (F=….)

A

F = pressure gradient/vascular resistance

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21
Q

What factors influence vascular resistance?

A

Viscosity, Vessel length and Radius (1/r^4)

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22
Q

For what stimuli can the microvasculature respond to local needs?

A
  • Active hyperaemia
  • Change in temperature
  • An increase in blood pressure
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23
Q

How can MABP be calculated?

A

MAPB = CO X TPR

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24
Q

What are the Starling Forces?

A
  • Hydrostatic pressure

- Oncotic pressure

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25
Q

Where do the lymphatics eventually drain?

A

Right lymphatic duct
Thoracic duct
into the left/right subclavian veins

26
Q

How much lymph fluid drains in one day?

27
Q

What does a small and large square equal to in seconds on an ECG?

A
  1. 04s in small

0. 20s in big

28
Q

What are the leads in Einthoven’s Triangle

A

Lead 1: LA (+) -> RA (-)
Lead 2: LF (+) -> RA (-)
Lead 3: LF (+) -> LA (+)

29
Q

What is a normal cardiac axis?

A

-30 and 90 degrees

30
Q

What is right and left axis deviation?

A

> +90 is a right axis deviation

31
Q

What pathway does NO use to cause relaxation?

A

Upregulates guanylyl cyclase to covert GTP to cGMP. cGMP up-regulates protein kinase G.

32
Q

What pathway leads an endothelial cell to produce NO?

A

Phospholipase C -> IP2 stimulates endoplasmic release of Ca2+, which up regulates eNOS. eNOS converts L-argenine and O2 to L-citruline and NO.

33
Q

How does prostacyclin lead to relaxation?

A

Adenyl cyclase -> cAMP -> Protein kinase A -> relaxation.

34
Q

How do thromboxane receptors work?

A

TP(beta) receptors work by phospholipase C pathway. But IP3 causes constriction in smooth muscle cells NOT relaxation.
TP(alpha) receptors on platelets lead to platelet activation.

35
Q

What is the synthesis pathway of adrenaline?

A

Tyrosine -> DOPA by tyrosine hydroxylase
DOPA -> Dopamine by DOPA decarboxylase
Dopamine -> Noradrenaline by Dopamine beta hydroxylase
Noradrenaline -> Adrenaline by phenyl-N-methyl transferase

36
Q

Where are the different beta adrenoreceptors found?

A

beta-1 receptors are found in cardiac muscle and smooth muscle of the GI tract.
beta-2 receptors are located on bronchial, vascular and uterine smooth muscle.
beta-3 receptors are found on fat cells.

37
Q

Where are the different alpha adrenoreceptors found?

A

alpha-1 are located on post-synaptic effector cells, mainly on resistance vessels.
alpha-2 are located on the presynaptic nerve terminal membranes. Some alpha-2 receptors are also found in vascular smooth muscle cells.

38
Q

What is the sheer rate?

A

The velocity gradient at any point

39
Q

How is sheer stress calculated?

A

Sheer rate X Viscosity.

40
Q

How do you calculate pulse pressure?

41
Q

How do you calculate mean blood pressure?

A

DBP + 1/3PP

42
Q

What is the windkessel effect?

A

During ejection, blood enters the aorta faster than it leaves them.

43
Q

How many times greater is venous compliance compared to arteriolar compliance?

A

10-20 times

44
Q

What is the definition of hypertension?

A

more than 140/90mmHg

45
Q

What are the stages of haemostatic plug formation?

A
  1. Vessel contraction
  2. Unstable platelet plug (primary haemostasis)
  3. Stabilisation of plug with fibrin (secondary haemostasis)
  4. Vessel repair and dissolution of clot.
46
Q

What are the inhibitory mechanisms to prevent clotting?

A
  • Tissue Factor Pathway Inhibitor
  • Protein C anticoagulant pathway
  • Antithrombin
47
Q

Explain the mechanism behind fibrinolysis

A

Plasminogen binds to the fibrin clot. It is converted to Plasmin via a Tissue Plasminogen Activator. Plasmin degrades fibrin.

48
Q

How does heparin work?

A

Accelerates antithrombin

49
Q

Define atherosclerosis

A

The build-up of fibrous and fatty material inside the arteries.

50
Q

What is the pathogenesis of atherosclerosis?

A

1) Endothelial dysfunction
2) Fatty streak formation
3) Formation of advanced lesion

51
Q

What are the four key aspects of atherosclerosis?

A

Thrombosis
Senescence
Leukocyte recruitment
Permeability

52
Q

How do statins work?

A

HMG-CoA reductase inhibitor: lowers cholestrol synthesis.

53
Q

How do macrophages still bind to mLDLs in LDLR-negative patients?

A

Through scavenger receptors.

54
Q

What do macrophages secrete when activated by mLDLs?

A

Cytokines that recruit more monocytes
Chemoattractants and growth factors of VSMC
Proteinases that degrade tissue
Tissue factors

55
Q

What are the free radixes produced by macrophage enzymes?

A 
NADPH Oxidase (superoxide O2)
Myeloperoxidases (HOCL and HONOO)
56
Q

How do macrophages influence VSMC in atherosclerosis?

A
  • Platelet derived growth factor causes VSMC chemotaxis from Tunica media, VSMC survival and proliferation
  • Transforming growth factor beta causes VSMC to become more synthetic, producing collagen and matrix deposition
57
Q

What percent of CHD can be attributed to the common risk factors?

58
Q

At what point does intermyocardial artery compensation for stenosis fail?

A

When stenosis is larger than 70%

59
Q

Differentiate between the two types of thombus

A

White thrombus: platelet rich, common in arteriole thrombosis, benefit from anti platelet therapy
Red thrombus: firebird rich (with trapped erythrocytes), common in venous or low pressure circulations, benefit from anticoagulative therapy

60
Q

What is the prognosis for heart failure?

A

50% dead in 3 years

61
Q

What are the different types of cardiomyopathy?

A
  • Dilated
  • Restrictive
  • Hypertrophic
  • Arrhythmic right ventricular

Year 1 LSS 1 (3 decks)

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