Theory Flashcards
(83 cards)
1
Q
Surfactant definition
A
Decreases surface tension of the alveolar fluid, decrease the tendency of alveoli to collapse
Increase lung compliance, ease WOB
2
Q
Atmospheric pressure
A
Pressure outside the body
3
Q
Intrapulmonary pressure
A
Inside the alveoli
4
Q
Process of inspiration
A
Inspirations muscles contract Cavity vol increases Intrapulmonary vol increases Intrapulmonary pressure decreases Air flows into lungs down its pressure gradient until it's 0 and equals atmospheric pressure
5
Q
Process of expiration
A
Inspiratory muscles relax Cavity vol decreases Elastic lungs recoil Decrease intrapulmonary vol Increase intrapulmonary pressure Air flows out of lungs down its pressure gradient
6
Q
Definition external respiration
A
Exchange of 02 and co2 between alveoli and blood
7
Q
Definition of internal respiration
A
Exchange of o2 and co2 between blood and tissues/cells
8
Q
Factors affecting diffusion (4)
A
- O2 concentration
- Altitude
- Loss of lung tissue
- PEEP,CPAP,BIPAP
9
Q
Regulation of ventilations
A
- Controller within CNS (medulla)
- Chemoreceptors central (brain stem)
- Peripheral chemoreceptors (aortic arch, carotid)
- Lung receptors (stretch receptors)
- Effectors ( muscle of ventilation that perform work on command by CNS)
10
Q
Different in Paed airways compared to adults
A
Large head Short neck High anterior larynx Narrow trachea Decreased dead space Increase chest wall compliance Increased vent-perfusion mismatch Smaller total lung capacity Increase oxygen consumption decreased resp reserve
11
Q
Tidal vol
A
Normal vol of air between inhalation and exhalation when extra effort is not applied (500ml)
12
Q
Vital capacity
A
Max amount of air a person can expel from the lungs after a max inhalation (4600/3100)
13
Q
Inspiratory reserve vol
A
Max vol that can be inhaled from the end-inspiratory level (3100/1900)
14
Q
Expiratory reserve vol
A
Max vol of air that can be exhaled from the end-expiratory position (1200/700)
15
Q
Inspiratory capacity
A
Sum of IRV and Vt (3800/2400)
16
Q
Total lung capacity
A
Vol in lungs at max inflation (VC+RV) (5800/4200)
17
Q
Functional residual capacity
A
Vol in lungs at end-expiratory position what’s left after (2300/1800)
18
Q
Residual vol
A
Vol that cannot be expelled or measured by spo2
19
Q
Dead space
A
Total vol of conducting airways from the nose or mouth down to the level of the terminal bronchioles. The dead space fills with inspired air at the end of each inspiration,but this air is exhaled (150mls)
area of no or little perfusion
20
Q
Mechanical ventilation advantages
A
Vent continues Increase oxygenation Decrease WOB/decrease fatigue Increase V/Q mismatch Pt able to talk/swallow Easy to start/finish
21
Q
Mechanical vent disadvantages
A
Non invasive Facial and nasal pressure injury/sores Gastric distension Dry mucous membrane and thick secretions Aspiration of gastric contents
22
Q
IPPV
A
Mechanical vent
Air is delivered into persons lungs under pressure and in short bursts to stimulate intake of breath
23
Q
PEEP
A
Pressure in lungs that exists after expiration
24
Q
CPAP
A
Positive
Alternative to PEEP
mild air pressure on continuous basis to keep the airways continuously open in a pt
Increase hydrostatic pressure within capillaries, overcome pressure balance
Increase pressure opening up more SA for gas exchange and flooding from occurring
25
Risks of intubation
Intubation of oesphagus/bronchus
Accidental extubation
Infection
Tracheal/laryngeal stenosis
26
Risks of mechanical ventilation
Increase airway pressure leads to barotrauma
Increased alveoli distension leads to volutrauma
Pneumothorax
Subcutaneous emphysema
27
Limitations of pulse oximetry
```
Low haemoglobin
Inadequate blood flow
Nail polish
Movement
Shock
Medication
Hypothermia
Dark skin pigments
Sensor application
```
28
What is Capnography
Detection of co2 in expired gas
Amount of light absorbed is proportional to the % of co2 in expired gas
Can measure resp output during CPR
can measure end tidal co2 in asthma,COPD,CHF
29
What is pulse oximetry
Indicates amount of oxygen bound to the haemoglobin in the blood
Oxygenated haemoglobin- infrared light
Deoxygenated haemoglobin- more red light
Comparing red to infrared calculates on sp02 reading
30
Oxygen dissociation curve
Proportion of haemoglobin in its saturated form against prevailing oxygen tension
Haemoglobin affinity for oxygen
How readily haemoglobin acquires and releases o2 molecules to surrounding fluid
31
Left shift of dissociation curve
Increase affinity of haemoglobin for o2
```
Decreased H+
Decreased 2/3 DPG
Decreased Paco2
Decreased temp
Increased pH
```
32
Right shift dissociation curve
Decreased affinity of haemoglobin for o2
```
Increased H+
Increased 2/3 DPG
Increased Paco2
Increased temp
Decreased pH
```
33
Airway pathway
```
Nose
Nasal cavity
Nasopharynx
Oropharynx
Laryngopharynx
Larynx
Trachea
Bronchi(bronchioles)
Alveoli
```
34
Definition V/Q mismatch
occurs when altered lung physiology or vent/perfusion dysfunction results in ineffective gas exchange
35
Respiratory failure causes
1. can be due to shunting which is caused by hypoxia due to an inability to maintain gas exchange (V/Q mismatch)
2. due to cardiac failure
36
Bipolar vs unipolar
Bi- 2 electrodes positive and negative each equally contributing to the tracing
Uni- one positive electrode and an indifferent connection which I'd achieved by connecting the electrodes from the 3 limb leads through resistances to the central terminal
37
Anaphylaxis CPG (ADULT)
```
Sudden onset of illness
and
two or more of RASH
Respiratory distress
Abdo symptoms
Skin/mucosal symptoms
Hypotension
```
OR
isolated hypotension
38
Anaphylaxis CPG (Paed)
Adrenaline 10mcg/kg repeat @5/60
high flow 02
treat bronchospasms per asthma guideline
upper airway oedema-nebulised adrenaline
MICA called early
Dex
Fluid
39
ss of Upper airway obstruction
- stridor
- hypoventilation
- chest retraction
- cyanosis/decreased sp02
- abdo protrusion
- increase use of accessory muscles
- decrease breath sounds
40
Definition of antibody
protein produced by the body in the presence of a specific antigen
41
Definition of antigen
any foreign substance that promotes an immune response
42
IgE and mast cell interactions (allergies)
person comes across allergen for first time
he or she makes large amounts of ragweed igE antibody
IgE molecules attach themselves to mast cells
The second time that person is exposed to their allergen
the igE primed mast cells release granules and powerful chemical mediators e.g histamine into the environment
these chemical mediators cause the characteristics symptoms of allergy
43
Definition of hypersensitivity
Objectively reproducible symptoms/signs initiated by exposure to a defined stimulus at a dose tolerated by a normal person
44
Definition of Allergy
type 1 hypersensitivity reaction characterised by excessive activation of mast cells and basophils by IgE
systemic inflammation
45
What does Adrenaline do for Anaphylaxis?
Increases peripheral vascular resistance (Increased BP, coronary artery perfusion)
decreased peripheral vasodilation
decreased angio-oedema
decreased urticaria
bronchodilation
Increased intracellular cAMP production in mast cells and basophils, decreased inflammation mediators
46
Electrical conduction through the heart
SA node- natural pacemaker of the heart, determines HR and activates both the left and right atrium
AV node- electrical gateway to ensure that all the blood is filling the ventricles before it contracts (slight delay)
AV bundle (bundle of his)
bundle branches
purkinje fibres
47
Vector
force and direction
48
P wave
```
Duration: 0.10 sec or less
upright in lead II
smooth rounded
SA node
Depolarisation of right/left ventricles
No more than 3mm
P wave is normal in leads I,II, aVf v5,v4,v6
P wave may be upright, disphasic, flat or inverted in leads III, aVL, v1,v2,v3
aVR- negative pwave is normal
```
49
PR interval
0.12-0.2 sec
begins with onset of P wave and ends with onset of QRS complex
shows onset of atrial depolarisation to onset of ventricular depolarisation
Prolonged- AV block or hypothyroidism
Shortened- pre excitation syndrome, AV junctional rhythm
50
QRS
0.12 sec or less
SA node/ AV junction
normal depolarisation of the right/left ventricles
narrow, sharply pointed
Leads I II V3 v4 v5 v6-- positive
Leads aVL, aVf can be positive, negative, or equiphasic
Lead aVR, NEGATIVE
51
T wave
```
0.10-0.25 or greater
less than 5mm
positive upright
repolarisation of ventricles
sharply/bluntly round, slightly assymetrical
```
Leads I,II,V2,v3, v4, v5,v6-positive
Leads aVR-inverted
leads aVL, aVF- can be positive,but may be inverted
Leads III, v1- varied
52
Small/Big squares of ECG
small: 0.04 sec
big: 0.2 sec
53
ST segment
begins at J point and ends at onset of T wave
represents early part of normal repolarisation
Duration: 0.20 sec or less depending on HR
normally flat or can be slightly elevated or depressed by less than 1mm
Depressed no more than 0.5mm
Elevated no more than 2mm
54
Definition of Angina
increased demand exceeding supply or supply being cut off
55
Causes of ST depression
Ischaemia= cellular starvation
56
Causes of ST elevation
Infarction= cell death
injury and/or permanent death
ischaemia has already done its thing
57
STEMI
St elevation occurs in conjunction to a MI
58
Non- STEMI
no ST elevation occurs in conjunction to a MI
59
Groups of leads
Septal- straddling the interventricular septum
V1 V2
Anterior- front face of the LV V3, V4
Lateral- side face of LV V5 V6
Inferior- floor of LV Lead II,III and AVF
AVR is special as it is the only lead looking at the right side of the heart(right atrium)
60
Sinus rhythm
P wave is generating QRS
normal P-R interval
appropriate width of QRS
regular
61
Sinus Brady
originates from SA node, rate is below 60
62
Sinus Tachy
Has the potential to be dangerous if you get incomplete filling, originates from SA node
63
SInus Arrythmia
only difference from normal sinus is irregularity, fit people can have their HR modified by their intrathoracic pressure or for no reason
Rate 60-100
64
Sinus Pause
missed beat, comes back in the same place each time
65
Sinus Arrest
Long pause comes back in any place
66
SVT
occurs above the ventricles which means that the abnormal heart rhythm occurs at or above the AV node
>100bpm at rest
P waves may or may not be visible, if they are visible they will have abnormal morphology
QRS normal
is a regular rhythm
67
Ventricular tachycardia
>0.12
68
Atrial FIbrillation
P wave is absent(atrial kick is lost,irregular)
AV conduction random, multiple, simultaneous chaotic waves of depolarisation
multiple re-entry in atria
no organised atrial contraction
QRS -narrow but IRREGULAR
HR- 100-180
irregulaly irregular
69
Atrial Flutter
P-R interval may be normal
determined by saw tooth appearance in leads II, III aVf
rate is too slow or too fast
2:1
Atrial rate is 240-360
QRS usually normal and REGULAR
70
1st Degree Block
rate of underlying rhythm,regularity of rhythm
delayed through AV node
PR interval- >0.20 sec
QRS is normal
71
2nd degree block Type I- Wenckebach
```
irregular
P-R interval keeps getting longer until dropped beat occurs
QRS is usually normal
progressive delay through AV node
ratio is always one off 5:4 4:3 3:2
```
72
PVCs
P waves may be present or absent
QRS complex is wide and bizzare
Identical PVCs- uniform
different QRS complex-multiform
Single site- unifocal
2 or more sites-mulitfocal
73
2nd degree block Type II
Dropped beat but PR interval is long
occasional beat not conducted
Damage to AV node
QRS is irregular
74
3rd degree block
p waves occur independently of the QRS
no PR intervals
QRS is usually abnormal
although they are firing at different rates they are still regular within their own rhythm
ventricles wait and then fire by themselves, no conduction of impulse from the atria to ventricles NO ASSOCIATION BETWEEN P WAVES(SA NODE) AND QRS COMPLEX (AV NODE)
75
Idioventricular Rhythm
```
originates in ventricles
looks like slow VT
Regular rhythm
no discernable P waves
QRS>0.12
rate above 60 and below 100 is accelerated idioventricular rhythm
```
76
Causes of ischaemia,injury,infarction
```
coronary thrombosis
coronary artery spasm
decreased coronary artery blood flow
increased myocardial workload
hypoxaemia
toxic exposure
```
77
Difference between pacemaker and an internal defibrillator
Pacemaker restores the natural rhythm of the heart when it detects an abnormal change. e.g when the heart is going too slow the pacemaker sends an electrical impulse to increase heart rate (when it senses a normal HR it wont fire)
An internal defib has pacemaker properties as well as defib properties. If it detects an arrhythmia such as VT or VF it can shock the heart back into normal rhythm (can be quite painful)
78
what are Vectors
vectors show the strength/ direction of electrical impulse for cardiac cell per cardiac cycle
if 2 vectors are going the same way you add them together
if they are going towards each other it equals 0
if they are going opposite ways to each other its an average
79
Difference between STEMI and non- STEMI
A STEMI is a full thickness myocardial infarction meaning that the cells the whole way through the heart wall are dying, it is also associated with ST elevation on an ECG
a non- STEMI means that it is a partial thickness myocardial infarct this means that the cells are dying the whole way through the cell wall it may only be half way. It also explains why on an ECG during these types of infarct that there may or may not necessarily be big changes.
80
how a myocardial infarct occurs
plaque starts to build up inside an artery
eventually the plaque rupture causing thrombosis to occur( lots of blood cells coagulate to form a clot)
decreased blood flow to descending artery
decreased o2, increase in pain from oxygen starvation,signals sent to brain
thrombus increases in size
increased adrenaline causes heart to race as body is trying to compensate for that loss in o2
cells slow down and stop beating altogether,heart tries to compensate by working harder
cells begin to weaken, tear and release toxins (troponin into the blood stream
cells burst and die
81
definition of ischaemia
restricted blood supply
82
V/Q mismatch
perfusion in the capillaries compared to ventilation in the lungs
where there is an increase in V/Q mismatch= increase in ventilation, decrease in perfusion- increase in oxygenation because of good ventilations but there is not enough blood being pumped
where there is a decrease in V/Q mismatch= there is a decrease in ventilation and increase in perfusion- it means that there is more blood so less is getting oxygenated as there is a decrease in ventilation as there is more of it to oxygenate.
83
Anaphylaxis
APC cell displays the antigen
T helper cell comes along, then displays the antigen
it attracts B cells who bind with the T cell
IgE antibodies are produced
These antibodies bind to mast and basophils
next time an immune response occurs due to the antigen, increase in immune response
Quick degranulation, histamine and other inflammatory mediators are released
