Physiology of Sedation Flashcards
breathing mechanics
- Diaphragm used for quiet breathing
- Inspiratory muscles contract
- Increase in thoracic volume
- Reduction in thoracic pressure
- Air pushed along pressure gradient
- Expiration is passive
- The intercostal and accessory muscles are used for more forceful breathing
contraction of diaphragm requires pressure on
abdominal cavity
air flow driven by
pressure gradients
intrapulmonary pressure during inspiration
less than atmospheric
intrapulmonary pressure during expiration
greater than atmospheric
intrapleural pressure during inspiration
falls during inspiration
intrapleural pressure during expiration
rises
TV
tidal volume
tidal volume represents
air moving in and out of lung during quiet breathing
force inspiration to maximum
air intake goes to IRV
IRV
inspiratory reserve volume
max inspiration
force expiration
ERV
ERV
expiratory reserve volume
forced breathe out
some of all reserve volumes
VC
vital capacity
sum of VC and RV =
TLC
total lung capacity
residual volume
RV
volume left in lung even after max expiration (ERV)
effect of posture on breathing
Movement facilitated in sitting position ?
Obesity can have an impact
FEV1
forced expiratory volume in 1 sec
COPD (restricted and obstructive types) affect on breathing
COPD reduces VC
Restrictive
- e.g. affecting thorax – obesity, fibrosis, pneumonia, TB, asbestosis
- VC and FEV similar, means small volumes are exchanged but occur at similar rate as normal pt
Obstructive
- e.g. emphysema, asthma, bronchitis
- Reduces VC and slows down expiration rate (lower FEV1
conductive zone in airway
trachea, bronchi, bronchiole terminals
no gas exchange = anatomical dead space
respiratory zone in airway
respiratory bronchiole, alveolar duct and sac
region of gas exchange
conducting zone and oral and nasal cavity are
DEAD SPACE
no gas exchange
150ml av
av tidal volume
450ml
av tidal volume is 450ml
so av breathe in takes in
300ml fresh air
as breathe in 150ml of dead space (conductive zone)
pulmonary gas exchange
Gas exchange occurs between the alveolar air and the pulmonary capillary blood
- In close contact
- 0.5-2 micrometers
Gases move across alveolar wall by diffusion
Diffusion is determined by partial pressure gradients (these are equivalent to conc gradients)
composition of air in atomsphere and alveoli
ventilation
amount of gasses passing into lungs
perfusion
amount of gasses travelling through pulmonary circulation
ventilation and perfusion
V:Q
- Match
- Upright person – vary in different parts of the lung
- V and Q are greater at the base of the lung, reduce as go up
- V:Q varies at different levels in the lung
- Differences are less marked in a subject lying flat
gas transport in blood
- Oxygen and CO2 transported in blood – erythrocytes (red blood corpuscles)
- Haemoglobin most imp in O2 transport
- Nitrous oxide does not bind to haemoglobin (carried in simple solution in blood)
haemoglobin structure
- Globular protein
- MW = 68,000
- 2 alpha & 2 beta protein chains
- 4 haeme groups:
- Porphyrin ring
- Iron atom
- Fe reversibly binds O2
- 200-300 Hb molecules / RBC
Affinity to oxygen changes at different partial pressures (binds to Fe)
(Fetus has Hb-F (fetal form) stronger bind to O2)
oxygen transport when breathing air
- Attached to haemoglobin 97%
- Dissolved in plasma 3%
oxygen transport when inc PO2 (e.g. breathing pure O2, hyperbaric O2_
- Little inc in O2 bound to haemoglobin
- Amount dissolved is increased in proportion to PO2
CO2 transport
Erythrocytes or plasma
- As
- Dissolved CO2 (10%)
- Combined to protein: carbamino compounds (20%)
- Bicarbonate ions (70%)
Bohr shifts on PO2
Physiological conditions affecting curve
- hypothermia as well as alkalosis will shift the curve to the left and increase haemoglobin affinity to oxygen
- easier to harvest oxygen in the lung but harder to give that oxygen away in the tissues.
- increase in temperature, acidosis, and increase in 2,3 DPG (diphosphoglycerate) shift the curve to the right reducing the affinity of haemoglobin to oxygen
- facilitate haemoglobin to give away oxygen when in the tissue.
- 2,3 DPG is an alternative by-product of glycolysis and is part of a feedback loop that can prevent tissue hypoxia.
IHS
why need to give pt 100% O2 until all N20 diffused out
- As if straight normal air sudden drop in maintenance oxygen with the slowly diffusing N2O, would increase shift towards N2O
here it is 50:50 but room air O2 is just 21%
breathing control
Breathing automatic process controlled by ‘voluntary’ (Skeletal) type muscles
- But not autonomic process
- Rhythm generated by respiratory centres in the brainstem
- can be modified by signals from various ‘sensory’ receptors
breathing rhythm can be increased by
- conscious cerebral cortex
- peripheral (arterial) chemoreceptors – reduction PO2, inc PCO2
- central chemoreceptors – dec in pH, inc PCO2 (CSF)
inc in breathing rhythm causes
- lung stretch receptors detect and inflation and reduce resp centre rhythms
increase in physical activity causes
inc in resp centre and breathing rhythm
hypoxia
reduction in O2 delivery to tissues
hypoxic, anaemia, stagnant (ishaemic) or cytotoxic
how does the partial pressure of oxygen and carbon dioxide affects breathing?
low oxygen concentration, small variations of carbon dioxide have greater effect in pulmonary ventilation, when compared to higher concentrations of oxygen and vice versa.
PCO2 and PO2 respiratory control of breathing are intertwined; a change in one will affect the respiratory response of the other.
hypoxic hypoxia due to
less O2 reaching alveoli or less O2 diffusion into blood
anaemic hypoxia due to
reduction of O2 transport due to low Hb or ability of Hb to funtion as carrier (e.g. due to CO poisoning)
stagnant (ishaemic) hypoxia due to
reduction in transport due to reduced flow
cytotoxic hypoxia
reduction in o2 utilisation by cells
cyanosis
Blue colour of skin and/or mucous membranes
Due to >5gm de-oxygenated Hb/dl of blood (deoxyhaemoglobin)
- 1/3 of ‘normal’ (so 5 not 15gm Hb)
2 main forms
- Central
- Affects whole body, evident in oral tissues
- Generally due to dec O2 delivery to blood, hypoxic hypoxia
- Low atmospheric PO2
- Dec airflow in airways (obstruction)
- Dec O2 diffusion into blood
- Dec pulmonary blood flow
- ‘shunting’ (‘venous’ blood à arteries)
- Peripheral
- Due to dec O2 delivery to a localised and ‘peripheral’ part of body
- Often due to red blood flow to tissues – stagnant hypoxia
- Peripheral vascular diseases e.g. atherosclerosis
Pulse oximeter providing early warning of falling PaO2
Alarm set higher than evidence of cyanosis
central cyanosis
- Affects whole body, evident in oral tissues
- Generally due to dec O2 delivery to blood, hypoxic hypoxia
- Low atmospheric PO2
- Dec airflow in airways (obstruction)
- Dec O2 diffusion into blood
- Dec pulmonary blood flow
- ‘shunting’ (‘venous’ blood à arteries)
peripheral cyanosis
- Due to dec O2 delivery to a localised and ‘peripheral’ part of body
- Often due to red blood flow to tissues – stagnant hypoxia
- Peripheral vascular diseases e.g. atherosclerosis
pulmonary circulation volume %
20%
short to lungs
systemic circulation volume %
80%
to body
heart structure
4 chambers:
- -right atrium
- -right ventricle
- -left atrium
- -left ventricle
4 main valves:
- -tricuspid
- -pulmonary
- -mitral (bicuspid)
- -aortic
coronary vessels
Arterial blood supply to the myocardium is via the right & left coronary arteries and their branches
Venous drainage is mostly via coronary veins into the right atrium
heart conducting system
Conducting system of heart
Electric signal
Not all chambers sim
Atrium first then ventricles
Sino-atrial SA node – pacemaker, define cardiac rhythm
- Initiate contraction
Atrio-ventricular AV node next
- atria contract, fill ventricle
Then down to apex of heart
- right and left bundle of His
heart innervation
Both Parasym and sym nervous system
Parasympathetic (vagus):
- Actions on SAN, AVN
- Via muscarinic cholinergic receptors
- Negative chronotropic and dromotropic effect
- slow down pacemaker and inc delay, reducing conduction velocity
Sympathetic :
- Actions on SAN, AVN, myocytes
- Via b-1 adrenoreceptors
- Positive chronotropic and dromotropic effect and Positive inotropic effect
- E.g noradrenaline, inc HR conduction velocity and contractility
cardiac cycle
- Ventricular systole:
- Isovolumetric contraction
- Ejection phase
- Ventricular diastole:
- Isovolumetric relaxation
- Passive filling
- Active filling (Atrial systole)
- Pressure changes and timing
- Volumes
- Mechanical events (valves)
- Electrical events (ECG)
ECG
electrocardiogram
P-wave: atrial depolarisation
QRS-wave: ventricular depolarisation
T-wave: ventricular repolarisation
coronary blood flow
- Coronary BF is greatest during ventricular diastole
- Coronary arteries are compressed during systole
- Coronary blood flow is decreased by:
- Increased heart rate
- Low aortic diastolic BP
BP = CO x TPR
- BP = Mean arterial Blood Pressure
- CO = Cardiac Output
- TPR = Total Peripheral resistance
CO =
Stroke Volume x Heart Rate
factors for stroke volume
end diastolic volume (preload)
- venous return
- HR
ventricular contractility
after load (TPR)
heart rate determined by
SA node
venous return
- Blood returning to right atrium
- ‘Push’ forces:
- momentum (from systole)
- muscle pump (limb muscles; venous valves)
- ‘Pull’ forces:
- Thoracic ‘pump’ (negative intrathoracic pressure)
pre-load (Stroke volume)
- The tension in the heart wall as a result of filling
- Determined by end-diastolic volume
- Starling’s law of heart
- increase EDV then increase stroke volume
- Length-tension relationship (overlap of actin and myosin filaments)
contractility impact on SV
compared to a normal contractility for instance by increasing the inotropic activity and thus increasing force and contraction of the cardiac muscle, the heart will increase its end diastolic volume for the same stroke volume. It becomes more efficient pumping blood.
However, in heart failure and diseases that limit contractility the opposite is true and the heart becomes less efficient pumping blood
after load (stroke volume)
- Force that heart must develop to pump blood against the arterial BP and peripheral resistance
- After-load is increased in patients with hypertension:
- Increased cardiac ‘work-load’
- Can affect coronary blood flow
blood pressure
typical value
dependent on
In systemic circulation the ideal 120/80 drops at the arterioles level until reaches below 35mm mercury at the venules and the difference between systolic and diastolic disappears
- depends on level you measure at what normal readings should be
The systolic and diastolic pressure from the pulmonary circulation is much lower
7 pulses
Arterial
- External carotid artery
- Facial artery
- Superficial temporal artery
- Radial artery
- Accessibility
- Continuous monitoring
Jugular venous pulse
blood flow
Blood flow to an organ is determined by various factors – Poiseuille’s Law
- Delta P = pressure difference
- Radius – large impact
- Small change in it – big change in flow
local blood flow is determined by
arteriolar radius
arteriolar radius determined by (3)
local factors - O2, CO2, pH, temp, vascoactive agents
sympathetic nerves (alpha and beta effects)
hormones - adreanline, ADH, angiotensin II
total peripheral resistance
TPR = the combined resistance of systemic vessels
BP = CO x TPR
changes can occur in vascular beds but TPR and MAP stay the same
how
No change in TPR so no change in arterial blood pressure
- Dilation in some vascular beds can occur without changing the mean arterial BP
- there is ‘compensatory’ vasoconstriction in other vascular beds
postural effects on blood vessels
Standing
- Additional hydrostatic pressure due to gravity = 80 mmHg
- Veins are more compliant than arteries
Veins distend = ‘venous pooling’ =Reduced venous return
hypovolemia
when loose blood – dec intravascular volume
reduce – SV, CO, MAP
Inc HR and inc TPR by vasoconstriction
2 most commonly used cannulation sites
cubital fossa of forearm
dorsum of hand
4 adv of dorsum of hand as cannulation site
- access
- no nearby arteries
- no nearby nerves
- no joints
4 disadv of dorsum of hand for cannulation
- small veins
- susceptible to cold/anxiety
- mobile veins
- more painful
cubital fossa of forearm cannulation site
Mainly use CEPHALIC VEIN, BASILIC VEIN & MEDIAN CUBITAL VEIN
- cannulate lateral to biceps tendon
Larger veins more predictably sited
Better tethered to underlying connective tissue
3 adv of cubital fossa as cannulation site
- Big well tethered veins
- Less painful
- Less venoconstriction
4 disadv of cubital fossa cannulation site
- Access
- Potential nerve damage
- Potential intra arterial injection
- Joint immobilisation
veins in cubital fossa
used
- median cepahlic (or cubital) vein
- cephalic vein
- basilic vein
other structures
- brachial artery
- median basilic vein
Cannulate lateral to biceps tendon
veins in dorsum of hand
basilic vein
cephalic vein
dorsal venous network
