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ALS > Block 2 > Flashcards

Block 2 Flashcards

1
Q

What is the SA node responsible for?

A

Action potentials of the heart

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2
Q

Where is the action potential conducted to?

A

Myocardiocytes through intercallated discs

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3
Q

Outline the mechanism of contraction? (9)

A
  • Action potential activates calcium channels in the T-tubules
  • This results in an influx of Ca2+ into the cell
  • Ca2+ binds to troponin which moves the troponin complex away from the actin binding site
  • Myosin head bins to the actin binding site forming cross bridges
  • myosin head pulls the actin filament towards the centre of the sarcomere contracting the muscle
  • myosin head binds with ATP when the cross bridges detach
  • ATP is hydrolysed and the myosin head uses this to form another cross bridge
  • sarcoplasmic reticulum removes Ca2+
  • this returns the troponin complex to its inhibiting position on the actin binding site
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4
Q

Describe the electrical pathway of the heart (5)

A
  • electrical impulses begin at the SAN
  • signals generated at the SAN spread across the atria causing the muscles to contract (only atria)
  • the signal stimulates the AVN and is delayed
  • the impulse then passes down the purkinje fibres which are spread throughout the ventricles
  • the impulses cause the ventricles to contract from the base up
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5
Q

What happens at atrial systole? (4)

A
  • atria contract and ventricles relax
  • tricuspid and mitral valves open
  • blood flows from the atria to the ventricles
  • lasts about 0.1 seconds
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6
Q

How to calculate blood pressure?

A

systolic/diastolic

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7
Q

Systolic

A

contraction of the heart

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8
Q

Diastolic

A

relaxation of the heart

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9
Q

What happens at ventricular systole? (4)

A
  • ventricles contract and atria relax
  • tricuspid and mitral valves close
  • aortic and pulmonary valves open
  • blood leaves the heart through the pulmonary artery and aorta
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10
Q

What happens during diastole? (4)

A
  • atria and ventricles are relaxed
  • aortic and pulmonary valves close
  • rebound of blood off closed aortic valves causes dicrotic wave on the aortic pressure curve
  • coronary arteries fill
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11
Q

What is isovolumetric relaxation?

A

the brief interval where all the valves are closed

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12
Q

What is the first heart sound?

A
  • ‘lub’ sound
  • closure of mitral and tricuspid valves
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13
Q

What is the second heart sound?

A
  • ‘dub’ sound
  • closure of aortic and pulmonary valves
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14
Q

What valves make up the semilunar valves? (2)

A
  • aortic valve
  • pulmonary valve
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15
Q

What valves make up the atrioventricular valves? (2)

A
  • mitral valve
  • tricuspid valve
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16
Q

Define cardiac output

A

Volume of blood ejected from the ventricles into the aorta/pulmonary trunk each minute

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17
Q

Define stroke volume

A

Volume of blood ejected by the ventricle after each contraction

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18
Q

Calculation for cardiac output

A

Stroke volume x heart rate

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19
Q

What are the 3 factors regulating stroke volume?

A
  1. preload - the degree of stretch before contraction
  2. contractility - the forcefulness of the contractions
  3. afterload - the pressure that must be exceeded for the ventricles to eject blood
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20
Q

What is the Frank-Starling law?

A

the more the heart fills with blood, the greater the force of contraction

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21
Q

What are the two main factors that determine end diastolic volume?

A
  1. the duration of ventricular diastole
  2. venous return
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22
Q

What is end diastolic volume?

A

the volume of blood in the right or left ventricle at the end of filling in diastole

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23
Q

What are positive inotropic agents?

A

Substances that increase contractility by promoting Ca2+ inflow during action potentials

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24
Q

What effect do parasympathetic fibres have on heart rate?

A

Decreases

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25
Q

How do parasympathetic fibres decrease HR? (4)

A
  • they reach the heart as branches from the right and left vagus nerves
  • they use Ach
  • they reduce force of contractions
  • they constrict coronary arteries
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26
Q

What effect do sympathetic fibres have on heart rate?

A

increases

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27
Q

How do sympathetic fibres increase HR? (4)

A
  • they reach the heart through cardiac fibres from the sympathetic trunk
  • they use noradrenaline
  • they increase force of contractions
  • they cause vasoconstriction
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28
Q

What do increased levels of K+ and Na+ do to HR?

A

decrease heart rate and contractility

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29
Q

What does K+ do?

A

Block generation of action potentials

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30
Q

What does Na+ do?

A

Block Ca2+ inflow

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31
Q

What does the P wave represent?

A

atrial depolarisation

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32
Q

What does the PR interval represent?

A

time taken for the electrical impulses to travel from the SAN to the AVN

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33
Q

What does the PR segment represent?

A

conduction from AVN, down to the bundle of His and up the Purkinjee fibres

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34
Q

What does the Q wave represent?

A

initial ventricular depolarisation
- the impulse spreads from the Bundle of His

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35
Q

What does the QRS complex represent?

A

Ventricular depolarisation

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36
Q

What does the ST segment represent?

A

Time when the ventricles are depolarised during the plateau phase of action potential

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37
Q

What does the T wave represent?

A

repolarisation

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38
Q

What does the QT segment represent?

A

ventricular depolarisation to repolarisation

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39
Q

What does the U wave represent?

A

a small deflection following the T wave that shows repolarisation of papillary muscles or purkinje fibres

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40
Q

How many leads is an ECG measured using?

A
  • 3 or 12
  • only 10 electrodes
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41
Q

Physical factors that influence arterial pressure (4)

A
  • blood flow
  • resistance - higher the resistance, higher the pressure
  • volume of blood - the more blood present, the higher the rate of venous return = cardiac output increases
  • viscosity of blood - thicker the blood the higher the pressure
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42
Q

How to calculate blood pressure?

A

cardiac output x resistance

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43
Q

what are the three main types of sensory receptors in blood vessels?

A
  1. proprioceptors
  2. baroreceptors - aorta, internal carotid, large arteries in neck + chest
  3. chemoreceptors - carotid, aortic bodies
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44
Q

What happens at the carotid sinus reflex? (2)

A
  • blood pressure stretches the wall of the carotid sinus and stimulates baroreceptors
  • nerve impulses travel via the glossopharyngeal nerve to the brainstem from baroreceptor
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45
Q

What happens at the aortic reflex? (2)

A
  • blood pressure stretches the wall of the aorta and stimulates baroreceptors
  • nerve impulses travel via the vagus nerve
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46
Q

What happens to baroreceptors when blood pressure falls? (7)

A
  • receptors less stretched
  • slower rate of nerve impulses
  • decrease in parasympathetic
  • increase in sympathetic
  • more adrenaline and noradrenaline
  • cardiac output and resistance increases
  • blood pressure increases
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47
Q

Where is the carotid body located?

A

bifurcation of the carotid artery

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48
Q

Where is the aortic body located?

A

aortic arch

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49
Q

What do chemoreceptors detect?

A

changes in blood levels of O2, CO2 and H+

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50
Q

What stimulates chemoreceptors? (3)

A
  • hypoxia (<60)
  • acidosis
  • hypercapnia
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51
Q

How do chemoreceptors work? (4)

A
  • detect change in blood levels
  • stimulate chemoreceptors to send impulses to cardiovascular centre
  • CV centre can then increase or decrease blood pressure
  • chemoreceptors provide input to the respiratory centre in the brain centre to adjust breathing
52
Q

What does RAAS stand for?

A

Renin-agiotensin-aldosterone system

53
Q

How does the RAAS system work? (4)

A
  • blood pressure and blood volume decrease
  • Juxtagomerular cells in the kidneys secrete renin (enzyme) into the blood stream
  • renin catalyses the conversion of angiotensinage to angiotensin 1
  • angiotensin 1 converted to angiotensin 2 by angiotensin converting enzyme (ACE) In the lungs
    = increase blood pressure
54
Q

How does angiotensin 2 increase blood pressure by? (3)

A
  • constricting the systemic atrioles
  • stimulating the adrenal cortex to secrete aldosterone
  • increases reabsorption of sodium ions and water by the kidneys
55
Q

How do adrenaline and noradrenaline increase blood pressure? (4)

A
  • released by adrenal medulla in response to sympathetic stimulation
  • increases cardiac output by increasing rate and force of contractions
  • vasoconstriction of atrioles and veins in skin and abdominal organs
  • vasodilaton of atrioles in cardiac and skeletal muscle
56
Q

What does antidiuretic hormone (ADH) do?

A

increase blood pressure

57
Q

How does ADH increase BP? (4)

A
  • produced by the hypothalamus
  • released from posterior pituitary gland in response to dehydration or decreased blood volume
  • it promotes water retention in the kidneys
  • it causes vasoconstriction
58
Q

What does atrial natriuretic peptide hormones do?

A

lower blood pressure

59
Q

How does atrial natriuretic peptide lower BP? (3)

A
  • released by cells in the atria
  • promotes loss of salt and water in urine
  • it causes vasodilation
60
Q

Describe the process of inspiration? (3)

A
  • contraction of the thoracic diaphragm flattens and increases superior-inferior dimensions
  • contraction of external intercostal muscles pushes sternum out (pump handle) and the lower ribs come up (bucket-handle) increases anterior posterior dimensions
  • sternocleidomastoid pulls the clavicles and the rib cage up - draws air into the lungs
61
Q

Describe the process of expiration? (2)

A
  • relaxing of the thoracic diaphragm (dome) - decreases the volume and increases pressure
  • relaxing external intercostal muscles and contraction of internal intercostal muscles lowers ribcage and sternum
62
Q

What is the purpose of the chloride shift?

A

ensures that no build up of electric charge takes place during gas exchange

63
Q

How does the chloride shift work? (2)

A
  • Cl- enters red blood cells in systemic capillaries
  • HCO3- leaves RBCs
64
Q

What happens in the reverse chloride shift? (2)

A
  • Cl- leaves red blood cells in pulmonary capillaries
  • HCO3- enters red blood cells
65
Q

What % is CO2 transported in the blood? (3)

A
  • bicarbonate - 70%
  • dissolved in plasma - 7%
  • bound to haemoglobin - 23%
66
Q

What does Co2 determine?

A

Ventilatory rate

67
Q

What structure in the brain is involved in respiration?

A

Brainstem
- medulla - rhythm, timing
- pons - speed, fine tuning of rate

68
Q

What is partial pressure?

A

a measure of the concentration of gas in a mixture of gasses

69
Q

What happens when ppO2 is high in the lungs?

A

O2 is loaded and binds to haemoglobin

70
Q

What happens when ppO2 is low in the tissues?

A

O2 is unloaded and haemoglobin releases some of the oxygen it is carrying

71
Q

What is the Haldane effect?

A
  • deoxygenated blood increases its ability to carry CO2
  • oxygenated blood has a reduced capacity for CO2
72
Q

What is the Bohr effect?

A

Hbs oxygen binding affinity is inversely related to both acidity and concentration of CO2

73
Q

Normal blood pH

A

7.35-7.45

74
Q

Factors that effect haemoglobin affinity (4)

A
  • acidity - shifts curve right, increases acidity enhances offloading of O2 by Hb
  • ppCO2 - shift curves right, Co2 also binds to Hb
  • Temperature - shift curve right, heat promotes release of O2
  • BP - shifts curve right, decreases affinity for O2
75
Q

How does the body compensate for acid-base imbalances? (2)

A
  • changing rate of ventilation
  • altering the concentration of Co2 in the blood
76
Q

How does the body respond to acidemia? (4)

A
  • increase breathing
  • expel CO2
  • less H+ in the blood
  • pH increases back to normal
77
Q

How does the body respond to alkalemia?

A
  • decrease breathing
  • more H+
  • pH decreases back to normal
78
Q

Define ventilation (V)

A

air that reaches the alveoli

79
Q

Define perfusion (Q)

A

blood that reaches the alveoli

80
Q

What is a normal V/Q ratio?

A

0.8

81
Q

What happens when there is a low V/Q ratio? (3)

A
  • occurs when the airway is blocked
  • decreases arterial ppO2
  • excretion of Co2 is also impaired
82
Q

What happens when there is an increases V/Q ratio?

A
  • physiological dead space
  • occurs when artery is blocked
  • decreases alveolar ppCo2
    increases alveolar ppO2
83
Q

What V/Q ratio is respiratory acidosis?

A

low V/Q

84
Q

What happens during respiratory acidosis? (3)

A
  • lungs retain Co2
  • increases HCO3-
  • decreases pH
85
Q

How does the body compensate respiratory acidosis? (2)

A
  • kidneys retain HCO3-
  • excrete H+
86
Q

What V/Q ratio is respiratory alkalosis?

A

high V/Q

87
Q

What happens during respiratory alkalosis? (3)

A
  • lungs loose excess Co2
  • decreases HCO3-
  • increases pH
88
Q

How does the body compensate respiratory alkalosis? (2)

A
  • kidneys retain H+
  • excrete HCO3-
89
Q

What are atrial fibrillations?

A

fluttering contractions of atrial fibres so that atrial pumping ceases all together

90
Q

What happens during atrial fibrillation?

A
  • the ventricles may speed up, resulting in rapid heart beat
  • on the ECG of AF there are no clearly defined P waves and irregularly spaced QRS complexes
91
Q

What are extrasystole?

A
  • premature cardiac contraction that is independent of the normal rhythm
  • arises in response to an impulse outside the SA node
92
Q

What is heart failure?

A

the heart is unable to pump blood around the body properly

93
Q

Conditions that lead to heart failure? (4)

A
  • coronary heart disease (atherosclerosis)
  • high BP
  • arrhythmias (atrial fibrillation)
  • congenital heart disease
94
Q

How does the body compensate (and overcompensate) for heart failure? (8)

A
  • activate sympathetic nervous system (adrenaline and noradrenaline)
  • cause the heart to beat harder and faster
  • if the receptors are overused, this results in a down relegation
  • increase the amount of salt and water retained by the kidneys
  • increases the volume of blood, increases preload so stronger contractions
  • after a while contractions weaken
  • ventricular hypertrophy - enlargement of muscular walls of the ventricles, more forceful contraction
  • eventually walls become stiff
95
Q

What is digoxin-cardiac glycoside?

A
  • cardiac slowing and reduced rate of conduction through AV node
  • increased force of contractions
  • disturbance or rhythm increased ectopic pacemaker activity
96
Q

What is the mechanism of digoxin-cardiac glycoside? (3)

A
  • inhibits Na+, K+, ATPase membrane pump, resulting in increased intracellular Na+
  • sodium calcium exchanger tries to force out the sodium and in doing so pumps in more calcium
  • strengthens contractions - heart is able to pump more blood with each beat
97
Q

How does adrenaline increase HR?

A

direct stimulation of cardiac muscle increases the strength of ventricular contractions

98
Q

Mechanism of adrenaline (3)

A
  • non-selective agonist of all adrenergic receptors to produce ‘fight-or-flight’
  • acts via membrane receptors which trigger a second messenger response
  • action on the B-receptor increases the heart rate and contractility of the heart
99
Q

tidal volume

A

amount of air inspired and expired during a normal breath

100
Q

inspiratory reserve volume

A

air that can be inhaled after a normal breath

101
Q

expiratory reserve volume

A

air that can be exhaled after a normal breath

102
Q

residual volume

A

amount of air left after max exhale - lungs are never empty

103
Q

inspiratory capacity

A

max inhilation

104
Q

functional residual capacity

A

amount of air left after normal exhalation

105
Q

vital capacity

A

max inhale + exhale

106
Q

total lung capacity

A

total amount of air the lungs can hold

107
Q

FEV1

A

forced expiratory volume in 1 second

107
Q

FVC

A

forced vital capacity - total forced expiratory

108
Q

high FEV1/FVC

A

lungs are stiff and unable to bend e.g. fibrosis

109
Q

What are the characteristics of a low FEV1/FVC? (2)

A
  • resistance in lungs
  • difficult for patient to get air out e.g. COPD, asthma
110
Q

What is respiratory failure?

A

inadequate gas exchange, arterial O2, Co2 cant be kept of normal levels

111
Q

What is type 1 respiratory failure?

A
  • V/Q is high
  • low levels of O2 in blood (hypoxeamia) without increased level of Co2 due to…
  • high altitude,
  • V/Q mismatch (pulmonary embolism)
  • diffusion problems (pneumonia)
  • shunt
112
Q

What is type 2 respiratory failure?

A
  • V/Q is low
  • low level of oxygen in the blood (hypoxemia) with increased levels of CO2 (hypercapnia) due to…
  • inadequate alveolar ventilation
  • decrease surface area
  • reduced breathing efforts
  • increased airway resistance (COPD, asthma)
113
Q

Why do we cough?

A

to remove foreign material or mucus from the lungs and upper respiratory tract

114
Q

what is a productive cough?

A

produces sputum

115
Q

what nerve is associated with the cough?

A

vagus

116
Q

where are cough receptors located? (4)

A
  • trachea
  • pharynx
  • carnia of trachea
  • less abundant in distal airways
117
Q

what is the mechanism of cough? (5)

A
  • diaphragm and external intercostal muscles conteact
  • air rushed into lungs
  • glottis closes and vocal cords contract to shut larynx
  • abdominal muscles contract to increase air pressure in the lungs
  • vocal cords relax and glottis opens forcing air out
118
Q

Where does the signal of a cough travel?

A
  • impulses travel via laryngeal nerve to the medulla
  • efferent pathway travels from the cerebral cortex and medulla via the vagus and superior laryngeal nerves to the glottis, external intercostals, diaphragm and other major inspiratory and expiratory muscles
119
Q

what is the first stage of an action potential? (4)

A
  • neurotransmitters bind to the receptors on dendrites
  • ligand gated ion channels open
  • allows ions to move down conc gradient (K+ out of cell, Na+ and Cl- into cell)
  • when net influx is +ve ions (excitatory) charge will reach -55mV
120
Q

what is the second stage of an action potential?

A
  • when -55mV threshold value is reached, voltage gated Na+ open down the axon hillock
121
Q

what is the third stage of an action potential?

A
  • As the Na+ rushes in, causes nearby Na+ channels to open
  • chain reaction that happens all the way down the axon
  • neuron has ‘fired’
122
Q

what is the fourth stage of an action potential?

A
  • depolarisation process ends when Na channels stop allowing Na+ in
  • they become inactive
123
Q

what is the fifth stage of an action potential?

A
  • voltage-gated K+ channels are slow to respond and only open once Na channels have become inactive
  • K+ channels now open
  • K+ travels down the gradient and out of the cell (depolarisation)
124
Q

what is the sixth stage of an action potential?

A
  • during depolarisation, sodium-potassium pump kicks in and moves 3 Na out of the cell for every 2 K
  • “absolute refractory period”
  • purpose is to stop AP from happening too close to each other
  • stays in one direction
125
Q

what is the seventh stage of an action potential?

A
  • neuron becomes hyperpolarised
126
Q

what is the last stage of an action potential?

A

-K channels close
- neuron returns to its resting potential

ALS (10 decks)

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