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Physiology > CVR > Flashcards

CVR Flashcards

1
Q

Output is under what control?

A

Intrinsic.

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2
Q

Blood pressure in systemic circuit normally?

A

120/80.

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3
Q

Blood pressure in pulmonary circuit is?

A

28/8.

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4
Q

Average time of cardiac cycle assuming healthy is?

A

0.8 seconds.

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5
Q

Relaxation phase?

A

Diastole. (Fills blood).

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6
Q

Contraction phase?

A

Systole (Ejection of blood).

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7
Q

Pressure changes are brought by?

A

Conductive electrochemical changes within the myocardium that result in contraction of cardiac muscle.

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8
Q

PQRST- P wave is?

A

Atrial depolarisation.
Atria contract forcing blood flow to ventricles.

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9
Q

QRS complex is?

A

Ventricle depolarisation.
Ventricles contraction blood to lung and rest of body.

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10
Q

T wave?

A

Ventricles relax and prepare for next contraction.

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11
Q

Isovolumetric means?

A

All heart valves closed.
No blood in or out.

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12
Q

Wiggers diagram shows?

A

Relationship of pressure and volume over time.

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13
Q

In cardiac muscle what do intercalated discs do?

A

Link muscle cells together and contain desmosomes and gap junctions.
Allows action potentials to pass to adjacent cells.

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14
Q

What do desmosomes do?

A

Hold muscle cells together tightly.

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15
Q

What does a gap junction do?

A

Allows passage of action protections from one cell to next.
Allows cardiac muscle to function together as a syncytium.

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16
Q

3 major types of cardiac muscle?

A

Atrial.
Ventricular.
Specialised excitatory and conductive muscle fibers. (Conduction system).

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17
Q

Myocardial cells can spontaneously depolarise (eg SA node can make its own electrical impulse).

A
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18
Q

Spontaneous depolarisation generates a?

A

Pacemaker potential.

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19
Q

Synctium means?

A

Refers to multinucleated cell, but in heart it refers to functional unity.

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20
Q

Heart has?

A

2 synctiums.
Atrial synctium- Walls of two atria.
Ventricular- Walls of two ventricles.
Atria separated from ventricles by fibrous tissue that’s surrounds two AV valves.

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21
Q

What’s the importance of this fibrous tissue?

A

Lacks gap junctions and electrically isolated atria from ventricles.
Provides a border.

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22
Q

Resign potential is negative or positive?

A

Negative.

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23
Q

Which ions contribute to membrane potential?

A

Sodium.
Potassium.
Calcium.

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24
Q

What is the transmembrane potential?

A
  • This is the electrical difference between inside and outside the cell.
  • If there’s net moment of positive ions into a cell the TMP becomes more positive.
  • If there’s net movement outside, TMP become more negative.
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25
Q

Two main forces drive ions across cell membranes?

A
  • Chemical potential: Ion will move down conc gradient.
  • Electrical potential: Ion will move away from ions/molecules of charge.
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26
Q

Ionic movements or conductances occur the myocardial membrane?

A

In response to electrochemical gradient.
Controlled by selective ion permeability.

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27
Q

Cells of SAN depolarise over time with movement of insulin causing resting membrane potential to gradually decrease.

Cells of AVN are the same but more slowly.

A
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28
Q

Although SAN generates its own action potentials, it can be influenced by?

A

Sympathetic and parasympathetic nerves.

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29
Q

Excitation contraction coupling?

A

Represents process where electrical action potential leads to contraction of cardiac muscle cells.

Done by converting chem signal into mechanical energy via action of contractile proteins.

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30
Q

Crucial mediator that couples?

A

Calcium.
By circling in and out of myocytes cytosol.

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31
Q

Pacemaker potential?

A
  • At -60 funny channels open in SAN cell membrane.
  • Na enters through funny channel taking positive in cell.
  • Inside becomes less negative as compared to outside.
  • Calcium channels gated open, Ca enters.
  • Cells depolarise (pacemaker potential).
  • When threshold reached another type of Ca channel opens so Ca enters rapidly.
  • Results in rapid depolarisation, cardiac action potential.
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32
Q

Transient (temporary) type of channel?

A

T type calcium channel open briefly at low depolarisation at -50.

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33
Q

Long lasting calcium channel opens?

A

At threshold of -40. Full depolarisation.

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34
Q

Repolarisation?

A

Due to potassium.
Voltage gated.
Open at peak 10, potassium leaves cell.

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35
Q

Initial influx of Calcium into cells through?

A

L type channels. Insufficient to trigger contraction of myofibrils.
So signal amplified by CICR mechanism.

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36
Q

T tubules bring L type calcium into close contact with?

A

-Ryanodine receptors (specialised calcium receptors in the sarcoplasmic reticulum).
- When calcium enters through L type channels the ryanodine change conformation and cause larger release of Ca.

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37
Q

As actions potentials travel through heart muscle, they produce electrical currents which can be detected using electrodes on body surface.

A
  • ECG.
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38
Q

Trace varies depending on?

A
  • Direction of travel.
  • Whether cells are depolarising or repolarising.
  • Size of change in potential.
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39
Q

ECG evidences?

A
  • Depolarisation of atrial muscle. P wave.
  • Depolarisation of ventricular muscle. QRS complex.
  • Repolarisation of ventricular muscle. T wave.
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40
Q

Electrically charged particles generates an?

A

Electrical vector.

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41
Q

ECG therefore represents?

A

Electrical vectors of cardiac cycle.

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42
Q

We assume SA node fires at start of P wave and atrial contraction begins at peak of P wave.

Atrial depolarisation too minor to on ECG.

A
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43
Q

S in QRS?

A

Downward deflection and return to baseline- isoelectric point.

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44
Q

PR interval?

A
  • Measured from beginning of P wave to beginning of R portion.
  • PR starts with atrial depolarisation ends with ventricular depolarisation.
  • Assumed that impulses pass through AV node into ventricles.
  • Used to determine if impulse conduction from atria to ventricles is normal.
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45
Q

Prolonged PR interval may suggest?

A

AV node block is present.

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46
Q

PR segment?

A

Flat line between end of P and onset of QR, reflects slow impulse through AV node.

Serves as baseline/reference line of ECG.
Amplitude and deflection measured using PR segment.

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47
Q

Stroke volume=

A

End diastolic pressure - end systolic pressure.
So how much blood in ventricles when relaxed minus how much present after blood ejection.

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48
Q

Cardiac output=

A

Strike volume times heart rate.
mL/beat. Beats per minute.

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49
Q

What does stroke volume mean?

A

How much blood pumped by left ventricle in one contraction.

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50
Q

Cardiac output?

A

How much volume of blood heat pumps in one minute.

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51
Q

Preload means?

A

Extent of stretch of heart muscle.

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52
Q

Afterload means?

A

Pressure against which heart needs to pump.

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53
Q

Contractility?

A

Ability of muscle to produce a force.

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54
Q

3 facts to remember?

A
  1. More heart fills= more muscle stretched.
  2. Higher arterial pressure= lower stroke volume.
  3. More forcefully the muscle contracts= more blood expelled.
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55
Q

Venous return is increased during excessive due to?

A

Skeletal muscle pump.

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56
Q

If artery walls are stiff (eg due to aging)?

A

They stretch less when blood pumped, increasing pressure and afterload.

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57
Q

Inotropic agents such as Adrenalin and sympathetic nervous system?

A

Increase contractility.

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58
Q

Frank- Staling mechanism?

A
  • Force of contraction proportional to initial fibre length in diastole.
  • So increase in blood returning increases end diastolic volume which causes extra stretching so increase in next contraction.
    Heart pumps whatever volume it received within limits.
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59
Q

Physiological basis of Starlings Law?

A
  • Increased stretch increases sensitivity of contractile proteins to Ca.
  • Intracellular calcium required to generate 50% max tension lower than when muscle fibre stretched.
  • Optimal sarcomere length for max contraction. Length tension relationship.
  • Increased ventricular muscle stretch resists in increased actin and myosin overlap so more cross bridges.
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60
Q

Why is Frank- Starling important?

A
  • Allows heart to adapt pumping capacity to changes in venous return and to changes in arterial blood pressure.
  • Helps match output of right and left sides of heart.
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61
Q

Neural control of heart rate?

A

Neural control of heart rate is regulated by sympathetic and parasympathetic of ANS, both oppose each other to maintain cardiac homeostasis by regulating:
- HR.
- Conduction velocity.
- Force of contraction.
- Coronary blood flow.

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62
Q

Effects of ANS on heart are called?

A

Chronotrophic effects.

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63
Q

Positive chonotrophic effects?

A

-Increase heart rate.
-Most important sympathetic.
-Norepinephrine released by sympathetic nerve fibres activates Beta 1 receptors in SA node.
-Activation of Beta 1 produced increase in Na funny channels so less depolarisation required to reach threshold.
More action potentials.

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64
Q

Negative chronotrophic effects?

A

Decrease heart rate.
Acetylcholine released from parasympathetic.
Activates muscarinic receptors in SA node.
2 effects to decrease heart rate.

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65
Q

Sympathetic?

A

Increase heart rate.
Increases rate of sodium and calcium.
More frequent cardiac potentials.

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66
Q

Parasympathetic?

A

Decreases rate of influx.
Takes longer to reach threshold for action potential.

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67
Q

Reduced heart rate= increase blood pressure so baroreceptors (carotid artery).

A
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68
Q

Increase heart rate and stroke volume= increased PCO2 and decreased PO2 so chemoreceptors (carotid body).

A
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69
Q

BP=

A

Cardiac output times the resistance the blood encounters as it moves through arterial system.

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70
Q

Elastic tissue in blood vessel walls is stretched when blood is pushed into vessels.

A
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71
Q

Windkessel vessels?

A

Elastic arteries.
Heart is pumping blood intermittently. However blood flow in aorta is continuous.

72
Q

Why elastic arteries are called Windkessels vessels?

A

Because of so much elastic tissue.

73
Q

Pulsatile flow appears to maintain optimal function of tissues via?

A

Distinct effects on gene transcription.

74
Q

Blood pressure regulated by?

A

Baroreceptor.
Nerve root endings in carotid sinuses and aortic arch.

75
Q

As arterial pressure rises rate of firing of these neurons increases causing?

A

Decrease in heart rate and arterial pressure.

Primary mechanism for blood pressure in acute setting. Acts as buffer in changes to volume.

If blood pressure remains high it can reset or down.

76
Q

Long term blood pressure maintained by?

A

Renin- angiotensin.

77
Q

Vasoconstriction?

A

Contraction of smooth muscle.
Causes narrowing.
Caused by sympathetic nerve activity and hormone angiotensin 2.
Increases resistance blood vessels to blood flow.

78
Q

Vasodilation?

A

Relaxation.
Causes widening.
Caused by withdrawal of sympathetic activity and chemicals like lactic acid.
Decreases resistance of blood vessels to blood flow.

79
Q

Arterioles play major role in control of blood flow to organs or tissues.
Control of blood flow to organs.

A
80
Q

Arterial pressure is the product of?

A

Peripheral resistance.
Affected by conditions.
BP generally rises with age.
Uncertain why because hypertension is common as it increases with age.

81
Q

Main age related changes?

A

Increased stiffness of large arteries due to arteriosclerotic lesions and calcification.
Deceased baroreceptor sensitivity.
Increased responsiveness to sympathetic nervous system activity.
Alteration in RAA system relationships.

82
Q

Hypertension is?

A

A heterogenous disorder with patients have different causes.

83
Q

Secondary hypertension?

A

Has an identifiable cause.
Among most common causes are kidney disease.
Anatomic consideration- Coarction: narrowing of aorta or chronic changes in vascular structure.

84
Q

Effects of hypertension on body?

A
  • Stroke due to brain haemorrhage.
  • Damage to eye capillaries.
  • Oedema.
  • Left ventricular hypertrophy. Heart muscle stiffens and enlarged. Reduced pumping ability- failure.
  • Damage to kidney vessels. Renal failure.
  • Injury to artery walls.
85
Q

Risk factors of essential hypertension?

A

Modifiable?
Excess salt.
Obesity.
Alcohol.
Inactivity.
Smoking.

Non modifiable?
Age.
Race.
Genetic factors.

86
Q

Risk factors of Secondary hypertension?

A

Renal disease.
Excess aldosterone.
Phaechromoocytoma.
Other disorders.

87
Q

What is aldosterone?

A

A hormone produced by adrenal glands that help regulate blood pressure by promoting sodium and water holding in kidneys.
Increases blood pressure.

88
Q

Atherosclerosis development?

A
  1. Injury to vascular endothelium. (By inflammation or physical stress).
  2. Lipoprotein deposition-
  3. Inflammatory reaction-
  4. Cap formation-
89
Q

What’s respiration?

A

Exchange of gases between atmosphere, blood and cells.

90
Q

Combination of 3 processes needed for respiration to occur?

A
  • Ventilation.
  • External pulmonary respiration.
  • Internal tissue respiration.
91
Q

CV assists respiratory system by transporting gases.

A
92
Q

At rest a normal human breathes?

A

12-15 times a minute.
500mls of air per breath.
Or 6-8 litres a minute are inspired and expired.

93
Q

This air mixes with gas in alveoli and by simple diffusion oxygen enters blood in pulmonary capillaries while carbon dioxide enters the alveoli.

A
94
Q

Functionally components of respiratory system are divided in 2 zones?

A

Conducting zone.
Respiratory zone.

95
Q

Anatomical dead space?

A

Refers to part of the airway that is not involved in gas exchange (conducting zone). Average 150ml.

96
Q

Alveolar dead space?

A

This refers to alveoli that are ventilated but not perfused.

97
Q

Functions of conducting zone (including nose/mouth/pharynx).

A

Transports air to lungs.
Warms humidified and cleans air.
Mucus traps small particles.
Voice production in larynx as air passes over vocal folds.

98
Q

Upper airway- Nose to vocal cords.
Lower airway- Trachea and bronchial structures to alveolus.

A
99
Q

Main stem bronchi beach into?

A

Liber bronchi.
3 on right.
2 on left.

100
Q

Right and left main stem bronchi penetrate?

A

The lung parenchyma (tissue of lung).

101
Q

Nasal breathing is preferential as?

A
  • Nose filters particulate matter and plays role in lung defense.
  • Nose humidifies inspired air as a result of large surface area created by nasal septum and turbinates.
    Higher resistance than mouth.
102
Q

What is surface tension?

A

Attraction between molecules at a gas or liquid interface that pulls molecules together.

103
Q

What does surfactant do?

A

Reduced surface tension.
Essential to allow expansion of alveoli.

104
Q

In spherical structures like alveoli surface tension increases pressure, smaller the alveolus greater the pressure.

A
105
Q

Neonatal respiratory distress syndrome (RDS) related to surfactant deficiency.

A
106
Q

Primary principle of ventilation?

A

Air moves down pressure gradient.
High to low pressure.
To achieve inspiration higher pressure outside body.

107
Q

Boyles law?

A
  • As volume increases, pressure decreases.
  • As volume decreases, pressure increases.
    Remember C1V1= C2V2.
108
Q

During inspiration?

A

Thoracic cavity expands.
External intercostal and diaphragm contracts.
Increased volume.

109
Q

During expiration?

A

Thoracic cavity reduces.
External intercostal and diaphragm relax.
Lung volume decreases.

110
Q

Mechanics of breathing?

A
  • Inspiration active= Expiration at passive rest.
111
Q

Diaphragm most important muscle of inspiration. Supplied by?

A

Phrenic nerves that originate at C3,4,5.

112
Q

During exercise expiration is?

A

Active and abdominal muscles contract.

113
Q

Ventilation at rest- when diaphragm is relaxed, alveolar pressure is equal to?

A

Atmospheric pressure and there is no air flow.

114
Q

Transpulmomary pressure?

A

760-756=4

115
Q

Interpleural pressure?

A

756.

116
Q

Inter alveolar pressure?

A

760.

117
Q

Pulmonary pressure?

A

Pleural sac- -4. Force due negative pressure.
Lung- 0. Functional residual capacity.

118
Q

A person normally inhales and exhales 500. This is?

A

Tidal volume.

119
Q

A person cannot exhale around 1200. This is?

A

Residual volume.

120
Q

If person inhales and inhales more forcefully, this is called?

A

Inspiration reserve.

121
Q

Transpleural pressure?

A

Pressure difference across lungs, difference between pressure at airway opening and pressure on visceral pleural surface.

122
Q

Alveoli must remain open to?

A

Participate in gas exchange.
Alveoli are interconnected with elastic tissue so if one inflated alveoli helps to expand adjacent alveoli.

123
Q

Factors affecting gas exchange?

A

Surface area.
Diffusion gradient.
Diffusion distance.

124
Q

Distance of diffusion?

A

Increased if fluid in lungs (like in pneumonia).
Or mucus in lungs (cystic fibrosis).
Normally short- 0.2-0.4.

125
Q

Lung compliance?

A

The ease which lungs can expand.
Defined as change in v divided by change p.
Reduced during conditions like pulmonary fibrosis (lung tissue stiffer.

126
Q

Elasticity?

A

Lung contain elastic tissue that’s stretches on inhalation.
During exhalation elastic tissue recoils.
Disorders cause loss of elasticity (emphysema).

127
Q

Type 2 cuboidal cell- occupies only ?

A

7% of alveolar surface.

128
Q

Lung has two separate circulations?

A
  • Pulmonary circulation- Deoxygenated to oxygenated.
  • Bronchial circulation- Arises from aorta and nourishes lung parenchyma.
129
Q

During external respiration oxygen diffuses?

A

From alveoli to capillaries.

130
Q

During internal respiration oxygen diffuses?

A

From capillaries to tissues.

131
Q

Perfusion?

A

Blood flow reaching alveoli.

132
Q

Ventilation?

A

Amount of gas reaching alveoli.

133
Q

Ventilation and perfusion need to be matched for efficient gas exchange.
However regional differences due to gravity and air.

A
134
Q

Normal ventilation perfusion ratio is?

A

0.8.
Apices= more ventilation.
Bases= more perfusion.

135
Q

Due to gravity blood flow is?

A

Greater at base than apex of lungs.

136
Q

Ventilation increase from top to bottom of lungs.
Effect of gravity means intraoleural pressure greater at base.
Less difference between pressure in atmosphere and in lungs.
Means between breaths they are not as expanded as alveoli at apex. So greater capacity to expand during inhalation.

A
137
Q

Alveoli at base therefore get?

A

A greater proportion of tidal volume.

138
Q

More ventilation less perfusion. Pulmonary arteries will?

A

Dilate.

139
Q

More perfusion less ventilation. Pulmonary arteries will?

A

Constrict.

140
Q

Factors that decrease V-Q ratio?

A

Chronic bronchitis.
Asthma.
Fluid build up in lungs (pulmonary oedema).
Pulmonary fibrosis (decreases compliance).

141
Q

These factors mean?

A

Gas exchange is limited.

142
Q

Factors that increase V-Q ratio?

A
  • Pulmonary embolism. (Blood clot in lungs).
  • COPD.
143
Q

This means that?

A

There is plenty of air but oxygen is not getting into the blood.

144
Q

Normal automatic pressure vessel of breathing originates in impulses and comes from?

A

Brainstem.

145
Q

Cortex can override these if?

A

Voluntary control is desired.

146
Q

Eupnea?

A

Normal breathing.

147
Q

Apnea?

A

No breathing.

148
Q

Dyspnea?

A

Laboured breathing.

149
Q

Tachypnea?

A

Rapid breathing.

150
Q

Costal breathing?

A

Breathing by ribs movement only.

151
Q

Diaphragmatic breathing?

A

Breathing by diaphragmatic movement only.

152
Q

The three sensors?

A
  • Perioheral chemoreceptors.
  • Central chemoreceptors.
  • Pulmonary mechanoreceptors.
153
Q

Respiratory control centre?

A

Medulla, pons. Next spinal cord.

154
Q

Effectors?

A

Respiratory muscles.
Diaphragm.

155
Q

Respiration is controlled by?

A

Central co2 divide sensors and,
Peripheral co2 and oxygen chemoreceptors.

156
Q

Hypercapnia?

A

Slight increase in PCO2, thus H+.
Stimulates central and peripheral (carotid) chemoreceptors.

157
Q

Hypoxia?

A

Oxygen deficiency at tissue level.
Caused by low Po2 in arterial blood due to high altitude, obstruction of fluid.
Stimulated peripheral (carotid chemoreceptors).

158
Q

Lung receptors?

A

Pulmonary stretch receptors (slowly adapting) lie within airway smooth muscle.
Discharge in response to distension in lung.
Impulses travel in vagus nerve via large myelinated fibres.
….
Hering- Breuer.

159
Q

Hering- Breuer inflation reflex?

A

Provided self regulatory negative feedback mechanism.
Inflation inhibits further inspiratory muscle activity.
Deflation initiates inspiritory activity.

160
Q

Peripheral chemoreceptors?

A

Located in carotid and aortic body.
Respond to decreased arterial Po2 and increased PCo2 and H+.
Rapidly responding.

161
Q

Central chemoreceptors?

A

Located near ventral surface of medulla.
Sensitive to PCO2.
Respond to change of PH of ECF/CSF when CO2 diffuses out of cerebral capillaries.

162
Q

Rhythm created by?

A

Pre-Botzinger complex.

163
Q

Which then excites?

A

Dorsal respiratory group neurones (inspiratory).

164
Q

Firing leads to?

A

Firing in bursts.
Leads to contraction of inspiratory muscles- inspiration.

165
Q

When firing stops?

A

Passive expiration.

166
Q

Pre botzinger complex?

A

Collection of pace maker cells at upper end of dorsal respiratory group.
Synaptic connection with DRG.
Function- Discharges rhythmic respiratory signals.

167
Q

Pins and medulla generate?

A

A normal cyclic pattern of respiration.

168
Q

This pattern is altered by?

A

Homeostatic and adaptive reflexes.

169
Q

Central control is modified by?

A

Peripheral chemoreceptors.

170
Q

Increase frequency and depth of breathing.
Increased pco2.
Chemoreceptors.

A
171
Q

During quiet breathing?

A
172
Q

During forceful breathing?

A
173
Q

Stimuli

A
174
Q

Stimuki

A
175
Q

Stimumi

A
176
Q

Stimuli

A
177
Q

Other influences on control of breathing?

A

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Physiology (2 decks)

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