Physiology Flashcards
What are the tissues/components that facilitate ventilation?
1) Chest Wall
- Skeleton (Ribs, sternum, clavicles)
- Muscles (Diaphragm, intercostal muscles)
2) Others (under certain conditions)
- Neck muscles (Scalene, Sternomastoids)
During quiet expiration, the chest cavity _____, thoracic volume (↑/↓). This (↑/↓) the pressure in the _____ and ______, allowing for air to flow out.
Chest cavity recoils (inspiratory muscles relax)
Thoracic volume ↓
Lung and pleural cavity ↑
During inspiration, inspiratory muscles: ___________contract, causing thoracic volume (↑/↓). This (↑/↓) the pressure in the _____ and ______, allowing for air to flow in.
Inspiratory muscles: diaphragm and EICM contract
Thoracic volume ↑
Lung and pleural cavity pressure ↓
Is quiet expiration an active or passive process?
Passive
Is inspiration an active or passive process?
Active
During stimulated ventilation, how are inspiratory and expiratory efforts strengthened?
Extra muscles are recruited in inspiration/expiration:
- neck
- Internal intercostal
- abdominal muscles
What are the changes to ventilation during excercise?
1) Extra muscles recruited (IICM, neck, abdominal)
2) ↑lung volume inhaled during inspiration/exhaled during expiration (↑TV)
3) ↑air drawn into lungs per unit time
What is the pressure in the pleural space?
Intrapleural pressure
Before inspiration, what are the intra-alveolar and intrapleural pressures?
Intra-alveolar=atmospheric @ sea level (760mmHg/ 0 relative pressure)
Intra-pleural<Intra-alveolar (757mmHg/ -3 relative)
Why is intrapleural pressure at rest subatmospheric?
Negative intrapleural pressure created by lung recoil against chest wall (tends to spring out)
What are the changes in the (i) intra-alveolar and (ii) intra-pleural pressure during ventilation?
Both negative relative pressure:
Intra-alveolar ↓ (759mmHg/ -1 relative)
Intra-pleural ↓ (754mmHg/ -6 relative)
What are the changes in the (i) intra-alveolar and (ii) intra-pleural pressure during quiet expiration?
Intra-alveolar ↑ (761mmHg/ 1 relative)
Intra-pleural ↑ back to normal (753mmHg/ -3 relative)
Why does intra-alveolar pressure increase to positive relative pressure during quiet expiration?
Due to the air taken in during inspiration
How does a pneumothorax (lung puncture → air entry) affect (i) intra-alveolar and (ii) intra-pleural pressure?
↑ Intrapleural pressure (to 0 relative)
No change to intra-alveolar (alr 0 relative)
How does pleural effusion, hemothorax, or a pneumothorax affect the pleural cavity?
Pleural cavity expands (air drawn in by negative relative pressure)
What are the 4 ventilation volumes in order of increasing volume?
1) RV (residual)
2) ERV (expiratory reserve)
3) TV (tidal)
4) IRV (inspiratory reserve)
What is Residual Volume (RV)?
Volume of air left after maximum expiration
What is Expiratory Reserve Volume (ERV)?
Volume of extra air expelled with maximum expiration (after passive expiration)
What is Inspiratory Reserve Volume (IRV)?
Volume of extra air entering with maximal inspiration (on top of TV)
What is Tidal Volume (TV)?
Volume of air entering @ each resting breath/volume expelled on passive expiration
How do the ventilation volumes in men compare to women?
Men on avg > Women
- men > muscular framework & chest wall
- > vol. during forceful inspiration/expiration
How does Tidal Volume change during exercise?
Resting VT < Exercising VT
- exercising recruits other lung volumes @ rest
(IRV increase, ERV decrease)
What are 5 factors that may impair the body’s ability to ventilate and thus ventilation volume?
1) Muscle power of chest wall
2) Skeletal deformities of chest wall
3) Resistance to air flow (lung pneumothorax, pleural effusion)
4) Stiffness in Lung (loss of elasticity)
5) Lung collapse
6) Restriction of diaphragm movement (eg. abdominal pain)
What is the term for increased ventilation?
Hyperventilation
What is the term for decreased ventilation?
Hypoventilation
What is the term for increased breathing rate/respiratory rate?
Tachypnoea
What is the term for distressful sensation of breathing?
Dyspnoea
How is Minute Ventilation measured?
TV x Respiratory rate (breaths/minute)
(~6L/min)
How does TV, RR and Minute Ventilation change during exercise?
All increase
What is the difference between physiologic and anatomic dead space?
Physiological: vol. of air breathed in that does not undergo gas exchange
- normally contributed by anatomic dead space (but not all and under all circumstances)
Anatomic: Air in airways up to respiratory bronchioles (just short of alveoli)
What is Alveolar Ventilation (VA) and how is it calculated?
Volume of air that reaches alveoli (L)/min
= (Tidal volume - Dead space) x Breaths per minute
What is the difference between minute ventilation and alveolar ventilation?
Minute ventilation: tidal volume of air breathed in/min
Alveolar ventilation: Air reaching alveoli/min (accounts for dead space)
In a pneumothorax, what are the ipsilateral changes to:
i) Intrapleural pressure
ii) Lung volume
iii) Ventilation volume
i) Intrapleural pressure increase
ii) Lung volume decrease
iii) Ventilation volume decrease
What are 5 factors affecting the rate of gas exchange at the alveoli?
a) Diffusion across alveolar-capillary barrier
1) Partial pressure of gases
2) Thickness of barrier
3) Surface area
4) solubility of gas
b) Blood flow
4) Perfusion of alveoli
5) Rate of blood flow through alveoli
How does the proportion of gas in a mixture affect diffusion?
Movement of gases from areas of high to low partial pressure
- partial pressure is proportional to % gas in mixture
(calculated by % x 760mmHg)
When does diffusion stop?
When gas partial pressures are equalised (no difference in partial pressures)
What are the epithelial barriers involved in gas exchange at alveoli?
1) Alveolar epithelium
2) Capillary endothelium
(basement membrane in between)
How does a pulmonary embolism affect gas exchange?
Blood flow ceases —> no gas exchange
True or false: Alveolar gases equilibrate at the same rates, depending on blood flow.
False
Different gases diffuse/equilibrate at different rates
What are the 3 components that attribute to functional surface area in the lungs?
1) Ventilation
2) Diffusion
3) Perfusion
How does kyphosis affect ventilation?
↓ ability to ventilate
What can cause ↓ alveolar ventilation (3)?
1) ↓ Tidal volume (eg. kyphosis, COPD, Emphysema
2) ↑ Dead space
3) ↓ RR
What type of breathing would have higher alveolar ventilation, Rapid shallow or Slow deep?
Slow and deep breathing
A foreign object is lodged in a small bronchiole, what will happen to the alveoli supplied by that bronchiole?
Collapse → ↓Alveolar ventilation/gas exchange
What can ↓ alveolar diffusion (3)?
1) ↓ diff in partial pressures (eg. high altitude)
2) Abnormal thickening of alveolar-capillary barrier (eg. fibrosis, oedema)
3) ↓ alveolar vol/functional alveoli (eg. pneumonia)
4) ↑↑/↓↓ blood flow (eg. fibrosis, embolism)
How are pack years calculated?
No. packs (20 sticks)/day x No. years smoking
What are 5 effects of cigarette smoke on the respiratory system?
1) Cumulative irritation of airways & lungs
2) ↑ Mucus secretion
3) ↓ cilliary function
4) Chronic inflammation of airways & lungs (eg. chronic bronchitis)
5) Lung cancer
Which circulation is of a higher pressure, pulmonary or systemic?
Systemic: 120/80
Pulmonary: 24/10
True or false: Physiologically, the lungs receive the whole of cardiac output at all times.
True.
Pulmonary circulation is a high flow system
True or false: Distribution of blood flow in the lungs is uniform as maintained by the successive branches of the pulmonary vessels.
False, it is not uniform.
What are 2 factors that influence the distribution of blood flow to the lungs?
1) Gravity (eg. posture)
2) Muscular tone of pulmonary arterioles (eg. distension, vasoconstriction)
Pulmonary circulation in foetus is a (high/low) pressure and (high/low) flow system while that after birth is (high/low) pressure and (high/low) flow system.
Foetus: High pressure, low flow
After birth: Low pressure, high flow
How does oxygenated blood come from in foetuses?
Placenta via umbilical vein (PO2 ~30mmHg)
What is the difference in pulmonary circulation in foetuses and at birth?
Foetus: (lungs collapsed)
- O2 blood from umbilical vein
- O2 blood R heart → L via Foramen Ovale
- O2 blood from Pulmonary artery → Aorta via Ductus Arteriosus → Systemic circulation
At birth:
- Lungs expand
- placenta lost, umbilical vein obliterated
- Foramen ovale closes
- Ductus arteriosus constricts
What are the 3 systems responsible for O2 delivery to tissues?
1) Respi
2) CVS
3) Blood
How is O2 transported in blood?
1) Hb (in RBC): ~99%
2) Dissolved: ~1%
How is CO2 transported in the blood?
1) HCO3-: ~70%
2) Carbamino compounds (eg. Hb): ~23%
3) Dissolved: ~7%
Gas with high solubility in fluid create a (higher/lower) gas pressure within fluid as compared to gas with lower solubility.
High solubility in fluid → ↑ dissolved gas in fluid → ↑ gas pressure in fluid
Is CO2 or O2 more soluble in blood?
CO2
What are 3 factors that affect the amount of O2 carried by Hb?
1) PO2 (↑PO2 → ↑HbO2 until saturation)
2) [Hb] (↑Hb → ↑HbO2)
3) Affinity of Hb for O2
- pH, temp, 2-3-diphosphoglycerate
What is the HbO2 dissociation curve?
Shows sigmoid curve of [O2] for Hb/Blood PO2
(@pH7.4, 37°C, pCO2 40mmHg)
Describe the shape of the HbO2 dissociation curve.
1) Steep lower part
- When blood pO2 <60mmHg, → severe ↓ %HbO2 → ↓↓O2 Ss in blood for tissues (>prop.Δ)
2) Plateau
- When 60< blood pO2 <100mmHg, → minimal ↓%HbO2 → sufficient O2 supply in blood for tissues (<prop.Δ)
How does increasing affinity of Hb for O2 affect the HbO2 dissociation curve and what is the significance?
↑affinity → ↑O2 capacity → leftward shift
↑O2 binding at the same pO2
What are 3 factors that decrease the affinity of Hb for O2?
1) ↑temp
2) ↓pH (↑pCO2/H+)
- eg. exercise
3) ↑2,3 -DPG in RBC
- eg. chronic hypoxia
In these blood samples:
1) no RBC
2) RBCs with no Hb
3) RBCs with Hb
Which would have the highest arterial pO2?
Which would have the highest total O2 content?
All same pO2 (all same dissolved O2)
3 has highest O2 content (has both dissolved and HbO2)
In anaemia, [Hb] or [RBC] ↓. Assuming the respiratory system is normal:
i) arterial PO2 (↑/↓)
ii) %HbO2 saturation (↑/↓)
iii) blood O2 content/ concentration (↑/↓)
iv) O2 delivery to tissues (↑/↓)
i) arterial PO2: same
ii) %HbO2 saturation: same
iii) blood O2 content/ concentration: ↓
iv) O2 delivery to tissues: ↓
The transport of ______ maintains electrical neutrality as HCO3- is moved across plasma membranes into the blood/tissues.
Cl-
In respiratory compensation for acid-base disorders, ↑ventilation → ↑______ and thus ↓_________.
↑ventilation → ↑CO2 eliminated/↑pH and thus ↓pCO2
What is the relationship between pCO2 and VA (alveolar ventilation)?
Inverse:
pCO2 ∝ 1/VA
(↑pCO2 → ↓VA)
The CO2 dissociation curve is much _______________ compared to the O2 dissociation curve.
Steeper and more linear
- ↑pO2 → slower ↑O2 content until saturation
- as long as pCO2↓ → CO2 content↓
What is the difference between hypoxia and hypoxemia?
Hypoxemia: ↓arterial pO2
Tissue hypoxia: ↓tissue pO2
What is the term for ↑arterial pCO2?
Hypercapnia/hypercarbia
What is the hypercapnic drive?
↑ventilation in response to high arterial pCO2/pH
→ ↑CO2 excretion and H+ loss
→ ↓pCO2 and ↑pH
What are the different sensors involved in the regulation of ventilation?
1) Central chemoreceptors in medulla
- #1 pCO2
2) Peripheral chemoreceptors in carotid/aortic bodies
- #1 pO2
- also pCO2, H+ (pH)
In the brainstem respiratory center, 2 main tissues control ventilation in different ways:
Pons: __________________
Medulla: ________________
Pons: Modify rate and depth of ventilation
Medulla: rhythmic discharge of neurons (automatic ventilation)
What are 3 sensors that transmit to the brainstem respiratory center?
1) Brain above pons
- voluntary and involuntary control → integration w activities eg. speech, emotion
2) Chemoreceptors
- medullary
- carotid (glossopharyngeal)
- aortic (vagal)
3) Lung stretch receptors
- ↑stretch → ↓inspiration
4) Lung C-fibre receptors
- irritation (eg. J fibres in pulmonary edema) → ↑ventilation
5) joint/muscle proprioceptors (eg. in exercise)
- movement → ↑stimulates ventilation
↑arterial pCO2 is a potent stimulator of ventilation. When _____< pCO2 <_______ (normal: _____________), ↑pCO2 → proportionate ↑ ventilation.
45<pCO2<70mmHg
(normal 38-45mmHg)
↓arterial pO2 stimulates ventilation when <__________ (normal: ___________________)
pO2 <60mmHg
(normal: 80-100mmHg)
How can one increase the length of breath holding?
Hyperventilate prior
- ↑pO2 ↓pCO2
Why is the ventilatory drive less sensitive to chronic ↑pCO2 vs acute ↑pCO2?
Acute: CO2 diffuses across BBB → CSF (ECF in brain) → medullary chemoreceptor → ↑ventilation
Chronic: Buffers! → ↓free H+ → ECF in brain < acidic → ↓stimulation of medullary chemoreceptors
In a COPD patient, arterial pCO2 is chronically ↑ and arterial pO2 is usually low.
What is the patient’s main drive to ↑ventilation?
Hypoxic drive:
↓arterial pO2
(pO2 sensitivity unchanged in chronic hypercapnia)
Why is giving 100% supplemental O2 to a COPD patient ill advised?
Since main drive to ventilation is arterial pO2 rather than pCO2 (chronic ↓stimulation of central chemoreceptors)
↑pO2 → ↓RR and ventilation → ↑↑pCO2
(unless px is really hypoxic)
During exercise, Hb has (↑/↓) affinity for O2.
↓ affinity
- ↑release of O2 for muscles
- via ↑temp ↓pH (↑pCO2, ↑H+)
What is compliance in of the lungs and chest wall?
How easily they can stretch and expand.
Compliance= ΔV/ΔP
(change in volume/change in airway pressure)
↓compliance: ↓__________and ↑ _______________
↓compliance: ↓stretchability and ↑ work of breathing
Elastic recoil of the lungs is due to _______________.
Elastic fibres in the lung tissue.
What are 3 factors that may ↓lung compliance?
1) Lack of surfactant (#1)
2) Fibrosis
3) Oedema of alveolar walls (CHF)
4) Kyphosis
how does surfactant ↑lung compliance?
↓alveolar surface tension → ↓pressure needed to overcome attracting forces and collapse → ↑compliance
Why do smaller alveoli have tendency to collapse?
Pressure ∝ Surface tension/radius
smaller → ↓r → surface tension → ↑P within alveoli
→ tendency to empty into bigger alveoli w ↓P →collapse
- need to generate >subatmospheric P to keep small alveoli open
Surfactant produced by ________________ and is composed of a mixture of ____________________.
Type 2 pneumocytes
Mixture of phospholipids, lipids and proteins
What are 3 factors that can ↑ airway resistance?
By narrowing:
1) Bronchoconstriction
2) Mucus accumulation
3) ↓lung volume (↓pathways for airflow)
Irritants (eg. smoke and cold air) can cause bronchoconstriction, mediated by _________ nerves.
This can be countered via administration of ____ adrenergic agonists that act as sympathetic mediators.
Vagus (parasympathetic)
Countered via ß2 adrenergic agonists
What is infant respiratory distress syndrome in new born premature babies?
Lack of surfactant in premature babies born <28-32 weeks
What causes ↑ airway resistance in asthma (3)?
1) Mucus accumulation
2) Airway swelling
3) Bronchoconstriction
What can be done to ↓airway resistance in asthma (pharmacologically)?
1) Bronchodilation (ß-agonists)
2) Anti-inflammatory drugs (steroids)
What is FEV1?
forced expiratory volume of air exhaled in 1 sec after full inspiration
What is FVC?
forced vital capacity – total volume expired forcefully after full inspiration
How is FEV1/FVC affected in restrictive lung diseases?
FEV1/FVC ≥ 0.7-0.8
- restrictive → ↓lung compliance
→ ↓total air exhaled
→ FEV1 and FVC ↓
How is FEV1/FVC affected in obstructive lung diseases?
FEV1/FVC < 0.8
- obstructive → ↑airway resistance
→ ↓total air exhaled + slow exhalation → ↓↓FEV1 (compared to restrictive)
but also can’t exhale completely → FVC↓
How is asthma treatment monitored?
Spirometry
In what px is “barrel chest” seen?
COPD px
airways narrowed → air trapped during expiration
→hyperinflation of lungs and chest “barrel chest”
What is the oxygen cascade?
O2 transfer from air to tissues:
1) Air: pO2 ~ 150-160 mmHg
2) Alveolus: pO2 ~ 100 mmHg
3) Arterial: pO2 ~97 mmHg (some incomplete diffusion)
4) Tissues: <40 mmHg
(O2 taken up for metabolism)
How does the oxygen cascade shift at high altitudes?
Everything ↓
- pO2 in air ↓ but % loss via incomplete diffusion etc. same
What are 3 symptoms of acute mountain sickness?
Hypoxia and Alkalosis:
1) Fatigue and dizziness
2) Nausea
3) Headache
4) Palpitations
5) Tachypnea
What are 3 physiological mechanism for acclimatisations to sustained low pO2?
1) ↑2-3, DPG in RBC
→ ↓Hb affinity for O2 → ↑O2 released to tissues
2) ↑EPO by kidney
→ RBC → ↑O2 carrying capacity
3) ↓H+ excretion and HCO3- reabsorption (by type B intercalated cells
What is an alveolar shunt?
Alveolus is not ventilation but perfused
→ De-O2 blood returns to systemic circulation without passing through ventilation alveoli (no gas exchange)
What is the normal V/Q ratio?
1
When is V/Q >1?
Alveolar dead space
- V>Q (ventilation but air does not undergo gas exchange)
- have ventilation, no perfusion
When is V/Q <1?
Shunting
- V<Q
- no ventilation
What are 2 conditions that may result in V/Q >1?
1) Pulmonary embolism
2) Poor cardiac output
What are 2 conditions that may result in V/Q <1?
1) Atelectasis (collapsed alveoli)
2) Alveolar edema (CHF, inflammation eg. pneumonia)
How can the effects of a shunt be physiologically reduced?
Hypoxic vasoconstriction
- local response to low alveolar pO2
→ arteriolar smooth muscle contract →redirect blood to better ventilated regions
What are 2 types of shunts that can cause V/Q <1?
1) Shunt A (pulmonary)
- alveoli no ventilated but perfused
2) Shunt B (vascular)
a) normal: bronchial capillaries drain directly to pulmonary veins and left heart, mixing with pulmonary capillaries
b) abnomral connections between R and L heart (eg. ASD, VSD)
What is the effect of shunts on arterial pO2?
↓arterial pO2
What are 2 factors that may blunt ventilatory responses?
1) Altered/↓ responses to pCO2 in arterial blood
- desensitisation of central chemoreceptors
2) Depression of respiratory control centres in the brain
- sedatives/narcotics (opioids)
- anaesthetics/alcohol
What is CO2 narcosis?
Usually ↑pCO2 → ↑ventilation but severely ↑↑pCO2 → depresses CNS → ↓ventilation
What is CO poisoning?
CO binds to Hb with >200x affinity than O2
→ prevents Hb from carrying O2
→ “cherry-pink” appearance
What is cyanosis?
Blue discoloration of tissues due to lack of O2
- excess de-O2 Hb (>5g/dL) in blood
True or false.
The absence of cyanosis in a patient is enough to assume SaO2 is normal.
False
Cyanosis usually corresponds with O2 saturation (SaO2) of about 70-80%
→ small drop in SaO2 may not be reflected as cyanosis
What is the treatment for CO poisoning?
100% O2 at high atm pressure (hyperbaric O2 therapy)
What is N2 narcosis?
Breathing compressed air during diving
→ pN2 affects CNS: “anaesthetic”
→ euphoria, loss of coordination, coma
What are 4 poisonous gases?
1) CO2
2) CO
3) N2
4) O2
What can O2 be toxic?
Generation of free radicals (eg. H2O2, superoxides)
- 80-100% O2 administered for many hours → irritation of airways
- 100% O2 administered @ high (4-6 atm) pressures → CNS toxicity (muscle twitching, convulsions)
What are 3 indications of hyperbaric O2 therapy?
1) Decompression sickness
2) CO poisoning
3) Healing of bad wounds, acute ischaemic injury
