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Cardio > Physiology > Flashcards

Physiology Flashcards

1
Q

What is oedema?

A

Accumulation of fluid in intersital space

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2
Q

What vessel regulates blood flow to capillaries?

A

Terminal arterioles

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3
Q

Where can you find capillaries with no pores?

A

BBB

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4
Q

Define Fick’s Law of Diffusion

A

The amount of gas that moves across a sheet of tissue in unit time is proportional to the area of the sheet but inversely proportionate to its thickness

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5
Q

O2 and CO2 are soluble in what and how do they transport across endothelium?
Same question for ions e.g. Na+, K+ etc.

A 
Gases = lipid soluble - transport across endo cells
Ions = water soluble - via pores in endo

(think about BBB - no pores to protect brain from ion imbalances but still need gases)

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6
Q

What pressures controls filtration in and out of cell

A

Favours filtration - capillary hydrostatic pressure (Pc)
Opposes filtration - capillary osmotic pressure (piec)
(H then O - alphabetical - out first then back in)
(if draw diagram of cell arrow of flow pointing into the cell is heading into the centre of the Pie)

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7
Q

How do you calculate net filtration pressure? Do arteries and veins have positive or negative NFP?

A 
NFP = Pc - PieC
Arteries = +ve (= favours filtration)
Veins = -ve (=opposes filtration)
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8
Q

How is excess fluid returned? Where is this particularly important?

A

Via lymphatic system as lymph

Lungs as low Pc

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9
Q

Match LV failure and RV failure to the site of oedema they cause

A

LVF - pulmonary

RVF - peripheral

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10
Q

What kind of clot formation follow Virchow’s Triad and what is it?

A

venous clots

Hypercoagulabilty
Blood stasis
Endothelial injury

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11
Q

What is the average resting potential for a cell?

What is the average resting potential for a cardiac cell?

A
  • 70mV

- 90mV

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12
Q

At what stage in the action potential of a cardiac cell does contraction occur? (actin moving over myosin)

A

Plateau - Phase 2

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13
Q

Explain the ion movements in relation to cardiac action potentials

A

Phase 0 - FAST influx of Na+

Phase 1 - Influx of Na+ stops
- K+ efflux starts

Phase 2 (plateau)

  • Influx of Ca2+ - via L-type Ca2+ channels
  • Efflux of K+

Phase 3

  • Ca2+ influx stops
  • K+ efflux takes over

Phase 4

  • resting potential
  • Na+/K+ ATPase acts
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14
Q

What is the refactory period and why is it important?

A

The time after an action potential in which it cannot produce another action potential

Prevents heart from being in constant contraction

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15
Q

How does cell to cell current travel in the heart?

A

Via gap junctions

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16
Q

What causes the thick and thin bands within a myofibril?

A

Thick and darker = myosin
Thin and lighter = actin

AM
A = like morning thin and light
M = like night thick and dark

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17
Q

Ca2+ is required to switch on cross-bridge formation. Ca2+ is released from sacroplasmic reticulum but only when?

Why is Ca2+ required for cross-bridge formation?

A

Ca2+ influx causes CICR (calcium induced calcium release) = contraction

Ca2+ binds with troponin C (Ca2+ -> C) to move troponin-tropomyosin complex aside and expose actin site for binding with myosin

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18
Q

Explain the structure inside a muscle fibre?

A

Muscle fibre -> myofibrils -> sacromeres -> actin and myosin

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19
Q

Define stroke volume and how is it calculated?

A

Volume of blood ejected PER ventricle PER heart beat

EDV - ESV

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20
Q

Define cardiac output and how is it calculated?

Average for man?

A

Volume of blood pumped by EACH VENTRICLE per minute

CO = SV x HR

5l

21
Q

What does the Frank-Starling curve/Starlings law of the Heart suggest?

What effect does the sympathetic system (noradernaline and adrenaline - released from adrenal glands) have on the graph?

What would cause a right shift?

A

That as EDV is increased, SV will increase (as the heart muscle is stretched more it will pump harder and increased volume will be pushed out - think of rubber band - further you stretch it the harder it snaps back)

Left shift - as increases Ca2+ = increased contraction = increased SV

Heart failure as heart muscle is diseased (too weak or stiff (due to hypertrophy) and can no longer pump blood at same rate)

22
Q

Define intropic

Define chronotropic

A

Inotropic - affects strength of contraction
Chronotropic - affects HR

hr in chronotropic = HR

23
Q

Equation for resistance to blood flow

What has the biggest impact on blood flow?

A

R ∝ η.L/r^4

η = blood viscosity 
L = length of blood vessel 
r = radius of blood vessel

Radius

24
Q

How do you calculate pulse pressure?
What is the average?
What is a wide pulse pressure suggestive of?

A

Systolic-diastolic
~50mmHg
Valve regurgitation

25
Q

Define MAP and how is it calculated?

A

Mean arterial pressure during 1 CARDIAC CYCLE

2D+S/3

26
Q

Which vessel has the highest systemic vascular resistance?

A

Arterioles

27
Q

Define afterload

Define preload

A

Afterload = pressure that the heart must overcome to eject blood during systole

Preload = amount of sarcomere stretch experienced by myocytes at the end of ventricular filling during diastole (ventricular wall stretch)

28
Q

How is ejection fraction calculated and what is it?

A

SV/EDV x100%

Fraction of blood ejected from ventricle on each contraction

29
Q

What effect does stretch have on crossbridge formation?

A

Increases affinity of troponin for Ca2+

30
Q

Where is ACE (angiotensin converting enzyme) produced?

A

Lungs

31
Q

What effect does angiotensin II have?

A
  • Increases thirst
  • Increased ADH (anti-diuertic hormone) - retain more water
  • Vasoconstriction -> increase in SVR

Stimulates production of ALDOSTERONE by adrenal glands

  • Decreases Na+ and water secretion
  • Increases MAP
32
Q

Where is renin produced and what is its role?

A

juxtaglomerular cells in Kidneys

Converts angiotensinogen to angiotensin I

33
Q

What is the funny current associated with?

What is it?

A

Reaching threshold in pacemaker action potentials

Na + K influx

34
Q

What kind of troponin is released due to skeletal and cardiac muscle damage?

A

Troponin C

35
Q

When do coronary arteries fill?

A

During diastole

36
Q

What are expected oxygen sats in right atrium?

A

70%

37
Q

What effect does noradrenaline have on slope of pacemaker potential and what does this mean?

A

Increases slope of pacemaker potential -> increase HR

38
Q

In pacemaker cells what is responsible for depolarisation of the cell?

A

Ca2+ influx

paCemaker = Ca2+ influx

39
Q

What hormone has the ability to decrease BP by antagonising angiotensin II and aldosterone?
Where is it produced?
What is the other hormone that has the same ability but through different mechanisms?

A

ANP - artial nauetirtic peptide
Atria
BNP - brain nauetritic peptide (in response to increased ventricular stretch)

40
Q

Where are the two types of baroreceptors found and how do they both work to decrease BP?
What do they respond to?

A

Respond to increase in stretch due to increase BP

Arterial baroreceptors - aortic arch and carotid SINUS

  • dilation of arteries and veins (decrease TPR and decrease preload)
  • decrease HR

Cardiopulmonary (low pressure regions of heart e.g. RA)
- increase urine secretion

41
Q

Paraysympathetic innveration dominates during rest in heart. True or false?
What neurotransmitter is secreted and what does it act on?

A

True

ACh (acetyocholine) - M2 receptors

42
Q

How do calculate SVR?

A

MAP/CO

43
Q

How can you increase venous return hence increasing SV?

A

Resp inspiration
Increased venous pressure
Moving - muscular pump

44
Q

Where are the fastest conduction velocities in the heart?

A

Purkenjie fibres

45
Q

What is isovolumetric ventricular contraction defined as?

A

Period of time in heart when AV valves are shut and semilunar are yet to open

46
Q

What causes S1?

What causes S2?

A

Closing of AV valves

Closing of semilunar valves

47
Q

What is the minimum MAP required to perfuse essential organs?

A

60mmHg

48
Q

What effect does the vagus nerve have on the heart:

  • chronotropic
  • inotropic
A

Chronotropic - decreases HR

inotropic - no effect

Cardio (15 decks)

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