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Physiology Flashcards

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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
Cardiac work
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
26
SV equation
EDV- ESV
27
What affects stroke volume
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
28
Frank Starling mechanism
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)
29
Resting sarcomere length
1.6 um
30
What influences preload
Peripheral venous tone Gravity Blood volume Respiratory pump
31
What does gravity do to preload
Reduces it
32
Increased inotropy
Increased active tension at a fixed preload
33
Sympathetic inotropy
Adrenaline and NA bind to B1 receptors | They increase Ca2+ influx by releasing Ca from SR or increasing sensitivity of Ca for Trop C
34
Effect of hypertrophy on afterload
Hypertrophied ventricle = Low afterload
35
Afterload's effect on preload
Increased afterload can cause increased preload
36
Effects of exercise
1) Increased contractility 2) Increased CO and increased preload 3) Increased afterload
37
Effect of preload and afterload on the curve
Increased afterload --> increased preload --> curve moves RIGHT Decreased afterload --> decreased preload --> curve moves LEFT
38
What sense the arterial pressure
Baroreceptors
39
Where is the carotid sinus
Bifurcation of internal and external carotid arteries
40
How do baroreceptors work
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
41
How does the information from the baroreceptors go to the brain?
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
42
Mean arterial pressure
MAP- mean pressure over the entire cardiac cycle | "Driving force" for perfusion through tissue beds
43
Is mean arterial pressure the average of systolic and diastolic pressures?
No, as they are not of the same duration
44
Blood pressure (MAP)
P= QR P- mean arterial pressure Q- blood flow R- Resistance (systemic vascular resistance)
45
BP equation
MAP = CO x SVR
46
To regulate BP- what three things can you regulate
CO SVR Blood volume
47
What two things affect venous return
Skeletal muscle pump | Respiratory pump
48
MAP is affected by:
CO SVR Blood volume Distribution of blood between arteries and veins
49
Systemic vascular resistance depends on:
Size of the lumen Blood viscosity Length of the blood length
50
How is BP measured?
Short-term- Baroreceptors | Long-term- Renin-angiotensin system
51
How is BP controlled?
Short-term- Baroreceptor reflex | Long-term- Renin/angiotensin/aldosterone hormonal control
52
Atrial natriuretic peptide
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
Antidiuretic hormone (ADH) or vasopressin
Respond to dehydration or decreased blood volume | Cause vasoconstriction and increased water retention (increases blood volume and increases BP)
54
Increased cardiac output in relation to venous pressure
Increases venous pressure
55
There's two ways of measuring venous pressure: Cardiac function curve and venous pressure curve
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
When pressure in right atrium is 0 mmHg, what is the cardiac output
5L/min
57
What enhances cardiovascular function curve?
- Increased inotropy - Decreased HR - Reduced afterload
58
At zero CO, what is P(ra)?
8 mmHg
59
Hilum
Renal artery, renal vein and ureter together
60
Function of the glomerulus
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
Bowmann's capsule
Where the filtrate is collected
62
Glomerular filtration rate and the diameters of afferent and efferent arterioles
Diameter of afferent arteriole is directly proportional to the filtration rate Diameter of efferent arteriole is indirectly proportional to the filtration rate
63
Effect of higher pressure on glomerular filtration rate
Increases it
64
Proximal convulated tubule
Active resorption of glucose, Na+ and AA
65
Descending part of the Loop of Henle
Only permeable to water- major part of water resorption
66
Ascending part of Loop of Henle
Thick Salts are actively pumped out to make the medulla really salty so water can flow out with it Not permeable to water
67
Distal convulated tubule
More reabsorption | Ends with a lot of waste that is collected into the collecting duct
68
Collecting duct
Here, under the influence of ADH | More ADH, collecting duct is more porous and more water leaves- filtrate more concentrated
69
Three sites of drug regulation in the kidney
1) Glomerulus 2) Distal convulated tubule 3) Collecting duct
70
Two ways kidneys control BP
1) Cause arteries to constrict | 2) Blood volume
71
How does vasoconstriction occur in the kidneys
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
How do kidneys cause an increase in blood volume
Angiotensin II stimulates the adrenal gland to release ADH. ADH increases retention of salt and water in the distal tubule, increasing blood volume
73
Effect of angiotensin II on GFR
Increases it
74
Pre-capillary sphincter
A band of smooth muscle at the beginning of a capillary which causes blood flow in capillaries to constantly change route
75
Systemic vasoconstrictors
NA Serotonin Vasopressin Angiotensin II
76
Systemic vasodilators
Adrenaline ACh ANP
77
Local vasoconstrictors
Serotonin | Endothelin
78
Local vasodilators
NO Histamine Adenosine
79
Adenosine
Local vasodilator | Released in hypoxic conditions
80
Two types of hyperaemia
Active (increased metabolism) | Reactive (occlusion)
81
What happens to coronary pressure when aortic pressure is high
Low coronary pressure | During systole, everything is contracting and blood doesn't flow into coronary arteries
82
Functions of the conducting zone of the respiratory system
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
Functions of the pleura
Reduce friction Create suction Compartmentalisation
84
Boyle's Law
For air to go into the alveoli, their pressure must reduce below the atmospheric pressure- done through chest expansion
85
What is the normal pleural pressure
Always has to be negative (-5 cm/H2O) to suck lungs into the chest wall Expiration increases the pleural pressure close to 0
86
Definitions of spirometry
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
Dead space
Some inspired air doesn't contribute to gas exchange Made of anatomical dead space and alveolar dead space Hence, total dead space
88
Alveolar ventilation efficiency
Getting more air into the lungs is more effective in getting tissues more oxygenated when compared to increased the frequency
89
Elastic resistance and non-elastic resistance- name two viscous resistance factors
1) Viscous resistance | 2) Diameter of the tube
90
Compliance
How easily something can be stretched | *Ease with which the lungs expand
91
Elastance
Tendency to recoil to initial size after distention
92
What are residual volume and total lung capacity dependent on?
Chest wall
93
Function of Alveolar Type II cells
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
Low compliance
Stiff lung- cannot expand- fibrosis, TB, Pulmonary oedema
95
High compliance
Floppy lung due to loss of elastic tissue Extra work is needed to exhale Emphysema/COPD, Bronchitis
96
Histamine receptors
H1- increases secretions H2- increases viscosity **Mucosal oedema
97
Airway smooth muscle tone
Airways constrict with: - Increased ACh Airways dilate with: - Decreased ACh
98
Most common index of resistance
FEV1/FVC
99
On a flow volume chart- what is positive flow?
Expiration
100
Causes of restrictive lung disease
Parenchymal - Sarcoidosis - Pulmonary fibrosis - Pneumonia Extraparenchymal - Diaphragmatic problems - Myasthenia gravis - Lobectomy - Obesity - Ankylosing spondylitis
101
Restrictive lung disease
Reduced lung capacity Smaller lung volume Increased flow rate Increased FEV1/FVC
102
Obstructive lung disease
Increased resistance causing airway obstruction Reduced flow rate Larger lung volume Reduced FEV1/FVC
103
Diffusion rate is affected by four things
1) Surface area 2) Concentration gradient 3) Membrane thickness 4) Diffusion constant
104
How long does it take for gases to reach equilibrium
0.24 s
105
Limitations to pulmonary gas exchange
``` Low O2 conc Hypoventilation Diffusion limitations V/Q mismatching Right --> Left shunts ```
106
What is VA/Q at rest?
0.84
107
Dead space | Shunt
Dead space- Impaired perfusion (high VA/Q) | Shunt- Impaired ventilation (low VA/Q)
108
Autoregulation of arteriole and bronchiole diameter
O2- arteriole (high O2, arterioles dilate) CO2- bronchiole (high CO2 bronchioles dilate) **This is to match the mismatched V/Q
109
Regional differences in Va/Q
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
What is the V/Q ratio in pulmonary embolism
HIGH
111
O2 dissociation factors
More O2 unloaded: - High temp - High CO2 - High H+ (low pH) More O2 loaded - Low temp - Low CO2 - Low H+ (high pH)
112
Where does the dorsal respiratory group feed to?
Nucleus of tractus solitarius
113
Pneumotaxic centre
Limits inspiration | Controls the switch off point of inspiratory ramp
114
Hering Breur inflation reflex
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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