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Cardio-resp > Physiology > Flashcards

Physiology Flashcards

1
Q

7 phases of the cardiac cycle

A

1) Atrial contraction
2) Isovolumetric contraction
3) Rapid ejection
4) Reduced ejection
5) Isovolumetric relaxation
6) Rapid filling
7) Atrial systole

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2
Q

Intercalated discs

A

Allow action potential to pass from one cell to another without the need for a synapse

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3
Q

Four stages of cardiac muscle action potential

A

1) Depolarisation
2) Early repolarisation
3) Plateau phase
4) Final repolarisation

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4
Q

Plateau phase- cells involved and its importance

A

Plateau phase prevents tetanisation of cells
Has L-type calcium channels involved

**Very slow to open and very slow to close

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5
Q

What prevents the ventricle from contracting top-down?

A

Annulus fibrosis

Insulating activity

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6
Q

Conduction from SA node

A

Electrical activity begins at the pacemaker cells at the SA node
Travels from the right atrium to the left atrium
Travels down the Bundle of His
And terminates in Purkinje fibres

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7
Q

Resting potential of cardiac cells

A

Diagram says -85mV

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8
Q

What happens in each of the four phases of cardiac action potential

A

1) Depolarisation:
Cardiac cell at its resting potential. Fast Na+ channels open, Na+ comes in and reaches a threshold voltage of -70mV- self-sustaining Na+ current reached
L-type calcium channels open
Overshoots slightly above 0 mV

2) Early repolarisation:
Some K+ channels open and 0 mV reached

3) Plateau phase
L-type calcium channels still open, K+ flows out and this countercurrent maintains voltage at 0 mV

4) Final repolarisation
L-type calcium channels now close and K+ channels outflow exceeds Ca inflow. Resting potential of -85mV reached

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9
Q

SA node action potential

A

Spontaneous leaky Na+ channels have Na+ flowing in This is called the funny current
RMP is -60mV

At -55mV T-type Ca2+ channels open

At -40mV, threshold voltage, L-type calcium channels open and depolarise to 0mV

Brief plateau phase by K+ channels and then return to normal

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10
Q

Delay at AV node (0.16s) purposes

A

1) Delay conduction to ventricle, allows atria to contract fully
2) Acts as gate-keeper, limiting the transmission of ventricular stimulation during abnormal atrial rhythms

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11
Q

Chronotropy

A

Heart rate

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12
Q

Dual innervation of the heart

A

Parasympathetic NS innervates SA node

Similarly sympthathetic will have different effect on the chronotropy

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13
Q

ECG different components

A

P wave- atrial depolarisation
QRS complex- ventricular depolarisation
T wave- ventricular repolarisation

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14
Q

Heart block

A

Failure of stimulation of ventricles following atrial contraction

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15
Q

Time of one cardiac cycle

A

0.8 s

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16
Q

What causes the opening of the aortic valve

A

LV pressure increases more than aortic pressure

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17
Q

What causes mitral valve to shut

A

Ventricular pressure greater than atrial pressure

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18
Q

Normal resting cardiac output

A

5250 mL/min

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19
Q

CO

A

Cardiac output

CO = SV x HR

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20
Q

Things that can increase HR

Things that can decrease HR

A

Positive chronotropic factors

  • Sympathetic stimulation
  • Drugs
  • Hypocalcaemia
  • Anaemia

Negative chronotropic factors

  • Parasympathetic stimulation
  • Hypercalcaemia
  • Hypoxia
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21
Q

Things that can affect the stroke volume

A

Preload
Afterload
Contractility

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22
Q

Frank Starling Law

A

Amount of blood entering the heart will equal the amount of blood leaving the heart

EDV approximately same as SV

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23
Q

Afterload

A

Resistance blood must overcome to pump blood to the body

Inversely proportional to the stroke volume

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24
Q

Factors that increase contractility

Factors that decrease contractility

A

Positive inotropic factors

  • Sympathetic stimulation
  • Caffeine
  • Hypocalcaemia

Negative inotropic factors

  • Parasympathetic stimulation
  • Hypercalcaemia
  • Hypoxia
  • Hyperkalaemia
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25
Q

Cardiac work

A

Defined as the amount of work done by the ventricle to transport a volume of blood from a region of low pressure to a region of high pressure

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26
Q

SV equation

A

EDV- ESV

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27
Q

What affects stroke volume

A

EDV and ESV

EDV:

  • Venous filling pressure (preload)
  • Force of atrial contraction
  • Time to fill the ventricle
  • Distensibility of the ventricle wall

ESV:

  • Afterload
  • Force of ventricular contraction
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28
Q

Frank Starling mechanism

A

Increased venous pressure to the heart increases filling pressure which increases SV

The ability of the heart to change its contractility in response to changes in venous pressure

Length-tension relationship
Increase in length will result in increase in tension (force of contraction)

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29
Q

Resting sarcomere length

A

1.6 um

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30
Q

What influences preload

A

Peripheral venous tone
Gravity
Blood volume
Respiratory pump

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31
Q

What does gravity do to preload

A

Reduces it

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32
Q

Increased inotropy

A

Increased active tension at a fixed preload

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33
Q

Sympathetic inotropy

A

Adrenaline and NA bind to B1 receptors

They increase Ca2+ influx by releasing Ca from SR or increasing sensitivity of Ca for Trop C

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34
Q

Effect of hypertrophy on afterload

A

Hypertrophied ventricle = Low afterload

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35
Q

Afterload’s effect on preload

A

Increased afterload can cause increased preload

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36
Q

Effects of exercise

A

1) Increased contractility
2) Increased CO and increased preload
3) Increased afterload

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37
Q

Effect of preload and afterload on the curve

A

Increased afterload –> increased preload –> curve moves RIGHT

Decreased afterload –> decreased preload –> curve moves LEFT

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38
Q

What sense the arterial pressure

A

Baroreceptors

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39
Q

Where is the carotid sinus

A

Bifurcation of internal and external carotid arteries

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40
Q

How do baroreceptors work

A

They respond to stretching of the arterial wall where if there is an increase in BP, the arterial wall also increases leading to increased AP in the baroreceptors

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41
Q

How does the information from the baroreceptors go to the brain?

A

Carotid sinus baroreceptors- Innervated by sinus nerve of Hering (Glossopharyngeal nerve)
This synpases with nucleus tractus solitarius

Aortic baroreceptors innervated by the aortic nerve that combines with the vagus nerve

  • *Carotid sinus receptors control BP in brain
  • *Aortic sinus receptors control systemic BP
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42
Q

Mean arterial pressure

A

MAP- mean pressure over the entire cardiac cycle

“Driving force” for perfusion through tissue beds

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43
Q

Is mean arterial pressure the average of systolic and diastolic pressures?

A

No, as they are not of the same duration

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44
Q

Blood pressure (MAP)

A

P= QR

P- mean arterial pressure
Q- blood flow
R- Resistance (systemic vascular resistance)

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45
Q

BP equation

A

MAP = CO x SVR

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46
Q

To regulate BP- what three things can you regulate

A

CO
SVR
Blood volume

47
Q

What two things affect venous return

A

Skeletal muscle pump

Respiratory pump

48
Q

MAP is affected by:

A

CO
SVR
Blood volume
Distribution of blood between arteries and veins

49
Q

Systemic vascular resistance depends on:

A

Size of the lumen
Blood viscosity
Length of the blood length

50
Q

How is BP measured?

A

Short-term- Baroreceptors

Long-term- Renin-angiotensin system

51
Q

How is BP controlled?

A

Short-term- Baroreceptor reflex

Long-term- Renin/angiotensin/aldosterone hormonal control

52
Q

Atrial natriuretic peptide

A

Released by the cells of the atria

Lowers blood pressure by causing vasodilation and promoting loss of salt and water in the urine (lowers blood volume)

53
Q

Antidiuretic hormone (ADH) or vasopressin

A

Respond to dehydration or decreased blood volume

Cause vasoconstriction and increased water retention (increases blood volume and increases BP)

54
Q

Increased cardiac output in relation to venous pressure

A

Increases venous pressure

55
Q

There’s two ways of measuring venous pressure: Cardiac function curve and venous pressure curve

A

In cardiac function curve-
Increased venous pressure leads to increased CO

In venous pressure curve-
Increased CO leads to decreased venous pressure and hence, reduced pre-load

56
Q

When pressure in right atrium is 0 mmHg, what is the cardiac output

A

5L/min

57
Q

What enhances cardiovascular function curve?

A
  • Increased inotropy
  • Decreased HR
  • Reduced afterload
58
Q

At zero CO, what is P(ra)?

A

8 mmHg

59
Q

Hilum

A

Renal artery, renal vein and ureter together

60
Q

Function of the glomerulus

A

Takes blood and turns it into a filtrate and lets the rest of the blood flow on
Efferent arteriole later on becomes the renal vein

61
Q

Bowmann’s capsule

A

Where the filtrate is collected

62
Q

Glomerular filtration rate and the diameters of afferent and efferent arterioles

A

Diameter of afferent arteriole is directly proportional to the filtration rate

Diameter of efferent arteriole is indirectly proportional to the filtration rate

63
Q

Effect of higher pressure on glomerular filtration rate

A

Increases it

64
Q

Proximal convulated tubule

A

Active resorption of glucose, Na+ and AA

65
Q

Descending part of the Loop of Henle

A

Only permeable to water- major part of water resorption

66
Q

Ascending part of Loop of Henle

A

Thick
Salts are actively pumped out to make the medulla really salty so water can flow out with it
Not permeable to water

67
Q

Distal convulated tubule

A

More reabsorption

Ends with a lot of waste that is collected into the collecting duct

68
Q

Collecting duct

A

Here, under the influence of ADH

More ADH, collecting duct is more porous and more water leaves- filtrate more concentrated

69
Q

Three sites of drug regulation in the kidney

A

1) Glomerulus
2) Distal convulated tubule
3) Collecting duct

70
Q

Two ways kidneys control BP

A

1) Cause arteries to constrict

2) Blood volume

71
Q

How does vasoconstriction occur in the kidneys

A

Specialised cells (juxtaglomerular cells- BP and macula densa- Na)

When BP drops, filtered Na drops

Juxtaglomerular cells release RENIN

Renin converts angiotensin I to angiotensin II (ACE)

Angiotensin causes blood vessels to constrict and raises BP

72
Q

How do kidneys cause an increase in blood volume

A

Angiotensin II stimulates the adrenal gland to release ADH. ADH increases retention of salt and water in the distal tubule, increasing blood volume

73
Q

Effect of angiotensin II on GFR

A

Increases it

74
Q

Pre-capillary sphincter

A

A band of smooth muscle at the beginning of a capillary which causes blood flow in capillaries to constantly change route

75
Q

Systemic vasoconstrictors

A

NA
Serotonin
Vasopressin
Angiotensin II

76
Q

Systemic vasodilators

A

Adrenaline
ACh
ANP

77
Q

Local vasoconstrictors

A

Serotonin

Endothelin

78
Q

Local vasodilators

A

NO
Histamine
Adenosine

79
Q

Adenosine

A

Local vasodilator

Released in hypoxic conditions

80
Q

Two types of hyperaemia

A

Active (increased metabolism)

Reactive (occlusion)

81
Q

What happens to coronary pressure when aortic pressure is high

A

Low coronary pressure

During systole, everything is contracting and blood doesn’t flow into coronary arteries

82
Q

Functions of the conducting zone of the respiratory system

A

1) Filter
2) Humidify
3) Warm

Conducting zone- respiratory passages that carry air to the site of gas exchange

Respiratory zone- where gas exchange occurs

83
Q

Functions of the pleura

A

Reduce friction
Create suction
Compartmentalisation

84
Q

Boyle’s Law

A

For air to go into the alveoli, their pressure must reduce below the atmospheric pressure- done through chest expansion

85
Q

What is the normal pleural pressure

A

Always has to be negative (-5 cm/H2O) to suck lungs into the chest wall
Expiration increases the pleural pressure close to 0

86
Q

Definitions of spirometry

A

Tidal volume- normal quiet breathing
Inspiratory reserve volume- forced inspiratory volume
Inspiratory capacity- maximum volume that can be inspired after normal expiration
Expiratory reserve volume- volume after normal exhalation
Residual volume- Air in the lungs after forced exhalation
Vital capacity- IRV + TV + ERV
Functional residual capacity- ERV + RV

87
Q

Dead space

A

Some inspired air doesn’t contribute to gas exchange
Made of anatomical dead space and alveolar dead space
Hence, total dead space

88
Q

Alveolar ventilation efficiency

A

Getting more air into the lungs is more effective in getting tissues more oxygenated when compared to increased the frequency

89
Q

Elastic resistance and non-elastic resistance- name two viscous resistance factors

A

1) Viscous resistance

2) Diameter of the tube

90
Q

Compliance

A

How easily something can be stretched

*Ease with which the lungs expand

91
Q

Elastance

A

Tendency to recoil to initial size after distention

92
Q

What are residual volume and total lung capacity dependent on?

A

Chest wall

93
Q

Function of Alveolar Type II cells

A

Surface tension between air and liquid is inwards, it reduces the diameter and opposes alveolar expansion
These cells produce surfactant that reduces surface tension

Lack of surfactant can cause Infant Respiratory Distress Syndrome (IRDS)

94
Q

Low compliance

A

Stiff lung- cannot expand- fibrosis, TB, Pulmonary oedema

95
Q

High compliance

A

Floppy lung due to loss of elastic tissue
Extra work is needed to exhale
Emphysema/COPD, Bronchitis

96
Q

Histamine receptors

A

H1- increases secretions
H2- increases viscosity

**Mucosal oedema

97
Q

Airway smooth muscle tone

A

Airways constrict with:
- Increased ACh

Airways dilate with:
- Decreased ACh

98
Q

Most common index of resistance

A

FEV1/FVC

99
Q

On a flow volume chart- what is positive flow?

A

Expiration

100
Q

Causes of restrictive lung disease

A

Parenchymal

  • Sarcoidosis
  • Pulmonary fibrosis
  • Pneumonia

Extraparenchymal

  • Diaphragmatic problems
  • Myasthenia gravis
  • Lobectomy
  • Obesity
  • Ankylosing spondylitis
101
Q

Restrictive lung disease

A

Reduced lung capacity
Smaller lung volume
Increased flow rate
Increased FEV1/FVC

102
Q

Obstructive lung disease

A

Increased resistance causing airway obstruction
Reduced flow rate
Larger lung volume
Reduced FEV1/FVC

103
Q

Diffusion rate is affected by four things

A

1) Surface area
2) Concentration gradient
3) Membrane thickness
4) Diffusion constant

104
Q

How long does it take for gases to reach equilibrium

A

0.24 s

105
Q

Limitations to pulmonary gas exchange

A 
Low O2 conc
Hypoventilation 
Diffusion limitations
V/Q mismatching
Right --> Left shunts
106
Q

What is VA/Q at rest?

A

0.84

107
Q

Dead space

Shunt

A

Dead space- Impaired perfusion (high VA/Q)

Shunt- Impaired ventilation (low VA/Q)

108
Q

Autoregulation of arteriole and bronchiole diameter

A

O2- arteriole (high O2, arterioles dilate)
CO2- bronchiole (high CO2 bronchioles dilate)

**This is to match the mismatched V/Q

109
Q

Regional differences in Va/Q

A

Top half of the lungs under perfused
Bottom half of the lungs under ventilated

Two things do this:

1) Hydrostatic pressure (pushing blood into capillary beds)
2) Alveolar expansion (alveoli squished on expiration)

110
Q

What is the V/Q ratio in pulmonary embolism

A

HIGH

111
Q

O2 dissociation factors

A

More O2 unloaded:

  • High temp
  • High CO2
  • High H+ (low pH)

More O2 loaded

  • Low temp
  • Low CO2
  • Low H+ (high pH)
112
Q

Where does the dorsal respiratory group feed to?

A

Nucleus of tractus solitarius

113
Q

Pneumotaxic centre

A

Limits inspiration

Controls the switch off point of inspiratory ramp

114
Q

Hering Breur inflation reflex

A

Responds to lung stretching too much to switch off the inspiratory ramp
When tidal volume is 3x

Cardio-resp (4 decks)

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