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MS 2 Sping > Resp Physiology Puri IL > Flashcards

Resp Physiology Puri IL Flashcards

1
Q
  1. Primary function of the lung
  2. Do conducting airways Perform gas exchange? When does gas exchange occur? What is last part of conducting airways called?
  3. Components of gas exchange airways (3) . Supplied and drained by what vessels?
  4. What is ANATOMICAL DEAD SPACE
A
  1. Primary function of lung
    - EXCHANGE O2 INTO THE BODY and REMOVE CO2 FROM THE BODY
    - key in acid base balance ( CO - H2CO3)
    - host defense / primary barrier (cilia remove foreign antigens)
    - synthesize ACE which convert angiotensin I to angiotensin II
  2. Gas exchange does not happen up until generation 17, and these (Gen 0-16) are called conducting airways. Terminal bronchiole is the last of conducting airways.
  3. Gas exchange airways or acinus is constituted by
    - respiratory bronchioles,
    - alveolar ducts and
    - alveoli.
    These are supplied by pulmonary artery and drained by pulmonary vein, back to the left atrium (systemic circulation).
  4. ANATOMICAL DEAD SPACE; volume of the conducting airways.
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2
Q

Lung volumes

TV 
FRC
IC 
IRV
ERV
RV
VC
TLC

***what lung volumes cannot be measured directly (3)

A
  • ** Lung volumes that cannot be measured directly: RV, TLC, FRC
  • *remember; IC = IRV + TV. And FRC = ERV + RV
  1. Tidal Volume (IC-IRV): air leaving/entering lung during single, quiet respiratory cycle
  2. Functional residual capacity (ERV + RV): volume in the lungs at the end of quiet expiration-neutral point.
  3. Inspiratory capacity (TV + IRV): max possible inspiration from the FRC.
  4. Inspiratory reserve volume (IC - TV): additional amount of air that can be inhaled after quiet inspiration.
  5. Expiratory reserve volume (FRC - RV): additional volume that can be expired after a normal expiration.
  6. Residual volume (FRC - ERV): amount of air in the lungs after maximal expiration.
  7. Vital capacity (ERV + IC): max. volume that can be inspired after max. expiration.
  8. Total lung capacity (IC + FRC): lung volume after max. possible inspiration.
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3
Q

Explain the opposing pull of the chest wall (thoracic cavity) and the lungs

** what is the net pressure governing the lungs ? What must the pressure be to keep lungs inflated?

**at FRC; what is PTP (transpumonary pressure) vs PIP ( intrapleural pressure)

A
  • Thoracic cavity is trying to explode while the lungs are trying to implode due to inward recoil of lungs and outward recoil of chest wall
  • The opposing pul lead to a relative vacuum in the intrapleural space with an intrapleural pressure of (-5cm H20). ***This balances the tendency of the lungs to collapse and keeps lungs inflated

Net pressure governing the volume of inner sphere = X-Y.
** where X = distending pressure of lungs (transpulmonary pressure), Y = collapsing pressure of intrapleural space.
The inner sphere (alveoli, lungs) will be in

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4
Q

PTP vs PA vs PIP

**formula and functions

A 
PTP = PA - PIP  OR
PIP = (-PTP) + PA 
PIP = static component (-PTP maintain current VL) + Dynamic component (PA cause airflow)

PIP
This is the pressure that isactively controlledby the body i.e. it can be changed by contraction or relaxation of the muscles of respiration. PIP is the sum of pressure within the alveoli (PA) and transpulmonary pressure (-PTP).

PTP
This is the static component of PIP i.e. changing PIP will change PTP; and, PTP overcomes lung recoil and changes lung volume.

PA
Alveolar pressure is the driving force for air

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5
Q

Differentiate

Positive pressure ventilation vs Negative pressure ventilation (iron lung)

A

Positive Pressure Ventilation

- Mechanical ventilators e

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6
Q

Surfactant and pulmonary compliance

  1. what is the first and second variable that determine lung volume
  2. Compliance vs elastic recoil
    - explain compliance and how it changes with increase volume and calculation
  3. Lung recoil
    - how it change with increased volume
    - components (2 key determinants of compliance)

**How do disease affect lung compliance (2)

A
  1. Complianceis the second variable determining lung volume (first is PTP)
    - More stretchable lungs will achieve greater lung volume with the same PTP as the less stretchable lung.
    - A rubber band (more compliance) will cause greater stretch and lower recoil at PTP of 5
    - A steel spring (lower compliance) will cause lower stretch and greater recoil at PTP of 5.
  2. Compliance is the inverse of elastic recoil
    - Compliance is de
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7
Q

Summary of points

  1. What modulate PTP
  2. What governs lung volumes (2)
  3. Pathology of lung volumes (2)
  4. What dictate ease of flow ?
A
  1. PIP (intrapleural pressure) modulates PTP (transpulmonary pressure)
  2. PTP and COMPLIANCE govern lung volumes
  3. Increase lung volume by increasing PTP and reducing compliance
    A. Emphysema; increased compliance and higher lung volumes
    B. Restrictive pulmonary disease; decreased compliance and lung volumes
  4. None of these dictates the ease of airflow, which as always DEPEND ON RESISTANCE

**Compliance only governs lung volume not airflow

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8
Q

Summary point of lung compliance and hysteresis (during inspiration vs expiration)

A
  1. It takes greater pressure to in
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9
Q

Dynamics of airflow

Variables regulating air

A

Variables regulating air

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10
Q

What contribute the most vs the least to total airway resistance in healthy lungs

**What size bronchi has the greater resistance

A
  1. Central airways (>2mm)
    - resistance is greater than peripheral airways.
    - contribute approx 80% of total airway resistance (Same concept as arterioles and capillaries)
    - Generation 1-7. Number of parallel airways is proportionally small. Total cross sectional area is proportionally small

***Normally, GREATEST RESISTANCE IN MEDIUM SIZED BRONCHI

  1. Peripheral airways (<2mm)
    - resistance is low (only ~ 20% of lower airway resistance)
    - generations 8-23
    - number of parallel airways and total cross sectional area large
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11
Q

Airway resistance (Raw) modification (active vs passive mechanisms)

A

Active mechanisms

  1. ANS; vagus nerve - release ACh - M3 muscarinic receptor on bronchial smooth muscle - bronchoconstriction - increase RAW
    * *SNS has opposing effect (decrease RAW) via activation of beta 2 receptors (bronchodilation)
  2. Inflammatory mediators; histamine, leukotrienes cause bronchoconstriction and increase RAW
  3. Alveolar gases; decrease PAO2 cause bronchodilation and decreased RAW
    * *Chemical control of airways
    - bronchidilation will decrease RAW; SNS, b2 agonist, anticholinergics, NO, methylxanthines, Decreased PAO2, cromolyn sodium (prevent histamine release), montelukast (prevent LTD4)
    - bronchoconstriction will increase RAW; PNS, Ach, Histamine, Leukotrienes, adenosine, serotonin, thromboxanes A2, decreased PACO2

Passive mechanisms

  1. Physical airway wall or lumen changes; reduce airway radius and increase airway resistance and lung volume
    - Airway resistance increases as lung volume decreases (e.g expiration)
    - Radial traction decreases airway resistance during inspiration and high lung volumes
    - loss of mechanical tethering (loss of lateral traction) in emphysema will increase airway resistance
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12
Q

Summary of airway resistance

  • one of most powerful determinant of RAW
A

One of the most powerful determinants of R AW
is lung volume RAW is extremely high at residual volume (RV) but decreases steeply as VL increases.

One reason for this eff

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13
Q
  1. When is intrapleural pressure positive
  2. Effort dependence - inspiration s expiration
  3. Emphysema vs pulmonary fibrosis
A
  1. PIP positive ONLY DURING FORCEFUL EXPIRATION
    • Inspiration is effort dependent
    • expiration is effort dependent to a point and become effort dependent once you meet pressure point. Effort independence reached sooner if lung volume is lower.
3. 
A. emphysema; shift pressure point lower which decrease airflow
- TLC increase
- FVC decreased
- FEV1 severe decrease 
- FEV1/FVC; decrease 
B. pulmonary fibrosis; shift pressure point higher which increase airflow 
- TLC decrease
- FVC decrease
- FEV1 decrease 
FEV1/FVC N or increased
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14
Q

Summarize respiratory gas laws

A
  1. Gases flow down their partial pressure gradient, just like ions flow down their conc gradient
  2. Dalton’s law ; total pressure e= sum of individual pressures. PB = 760 = 160 O2 + 600 N2 + 0 CO2
  3. Boyle’s law ; P1V1 = P2V2
    * *At contestant temp, pressure is inversely proportional to volume
  4. Henry’s law; amount of gas that dissolves in liquid is equal to partial pressure of the gas in equilibrium.
    * *PaO2 = PAO2 = 100mmHg
  5. Water vapor is different
    - partial pressure of water vapor increases with temp but is independent of atmospheric pressure.
    - water vapor will decrease partial pressure of other gases.
    - partial pressure of O2 go from 160 to 150 at sea level (760 - 47) x .21
  6. Gas in solution also exert partial pressure. At equilibrium, the partial pressure of a gas in solution is equal to the partial pressure of gas in the gaseous phase
  7. When in solution, only dissolved gas exerts partial pressure. Not the one bound to proteins, like hemoglobin ***
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15
Q

Total vs alveolar ventilation

A
  1. Total ventilation or minute ventilation
    Ve= Tidal volume x RR = 500 x 12 = 6L/min.
  2. Alveolar ventilation VA
    VA= (total ventilation - dead space) x RR = (500-350) x 12 = 4.2L/min

**Increasing tidal volume will increase both total and alveolar ventilation

**if dead space VD ? Anatomical dead space (1mL/pound); this indicates presence of physiologic dead space (volume of airways not engaging in gas exchange) e.g PE - ventilation but no perfusion

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16
Q

Fick’s law (diffusion of gases)

**factors affecting rate of gas diffusion (4)

A

Gas flow across a barrier is proportional to diffusing capacity and concentration gradient (Fick’s law)

factors affecting rate of gas diffusion

  1. Thickness of alveolar capillary membrane
  2. Surface area of the membrane
  3. Diffusion coefficient (solubility) of gas in substance of membrane and intervening fluid layers
  4. Partial pressure difference of the gas between the two sides of the membrane.
    * *everything subject to change except diffusion coefficient

VGAs (flow of gas) = Area x change in P x diffusion coefficient / thickness of A-C membrane

  • emphysema; decrease area - decreases Vgas
  • fibrosis; increase thickness - decrease Vgas

**exercise, into, furosemide, supplemental oxygen all increase flow of gas.

17
Q

Perfusion vs diffusion limitation

A

PERFUSION LIMITED across A-C membrane

  • Both O2 and CO2
  • This means that the Pa = PA, by the time blood leaves the capillary around the alveoli. This is because of good solubility of these gases, high pressure gradient across the A-C membrane, and not too high hemoglobin binding

DIFFUSION LIMITED ; CO
- PACO is not equal to PaCO. Due to lower gas solubility, low pressure gradient across the A-C membrane, too high hemoglobin binding (preventing CO from going into solution)

***If PAgas = Pagas; the gas is perfusion limited
If PAgas is not equal to Pagas; the gas is diffusion limited

18
Q

Factors that shift HbO2 curve right vs left

A

CADET shift right ; ** Hb has reduced affinity for oxygen

  1. Increased CO2
  2. Increased acid (decreased pH)
  3. Increase 2,3 - DPG
  4. Increased temperature
    * *Chronic hypoxia; high altitude, COPD due to increase 2,3 DPG
    * *Hb kansas- an abnormal hemoglobin in which glutamic acid replaces alanine at position 76 of the beta chain; P50 70-75 mmHg

Factors that shift curve left

  • decreased temp
  • increased pH
  • decreased PCO2
  • *Top 3 called both effect - left ward shift of the curve caused by increased pH and decrease CO2
  • HbFl don’t bind 2,3 - DPG
  • CO; extreme leftward shift of COHb - increase Hb affinity for CO

**Total carrying capacity is still the same (1 molecule of oxygen bind to 4 Hb). Only thing that can change this is CO.

19
Q

Discuss PaO2, SaO2, CaO2 in COPD vs anemia

**remember; CaO2 = [Hb] x 1.34 x SaO2

A

COPD
- severe diffusion impairment - lower PaO2 and thus lower SaO2 (e.g 80%). Therefor CaO2 will be decrease
CaO2 = 15 x 1.34 x .8 = 16 (Normal is 20)

Anemia
- lower Hb concentration (e.g 7) but normal PaO2. Thus SaO2 is NORMAL
CaO2 = 7 x 1.34 x 0.98 = 9.1

20
Q

Carbamino Hemoglobin (The haldene effect)

A
  • Deoxygenated Hb binds CO2 more readily than oxygenated Hb - known as the haldene effect
  • As a result, CO2 content is higher in venous than arterial blood
21
Q

Highlights of pulmonary circulation

A
  • *low pressure, high flow, low resistance, highly distensibe and compressible, thin walled, less smooth muscle.
  • *lowest PVR is at the FRC
  1. Pulmonary blood
22
Q

Passive vs active determinants of PVR

A

Passive determinants of PVR (5)

  1. Pulmonary artery pressure
  2. Pulmonary blood flow (right CO)
  3. Lung volume
  4. Positive pressure ventilation
  5. Gravity

Active determinant of PVR
1. PAO2 i.e hypoxic vasoconstriction
A. Decreased PAO2 - precapillary pulmonary vasoconstruction - increase PVR
B. Conditions
I) High altitude; decreased barometric pressure - decreased PIO2 - decreased PAO2
II) Hypoxemia caused by hypoventilation, shunting and V/Q mismatch
III) Fetal circulation (PO2 only about 25 mHg)

23
Q

Causes of pulmonary edema (6)

A
  1. Increased capillary hydrostatic pressure e,g CHF
  2. Decreased colloid osmotic pressure e,g nephrotic syndrome
  3. Increased capillary permeability (increased Kf) e.g ARDS
  4. Decreased interstitial pressure e.g rapid evacuation of pneumothorax
  5. Lymphatic insufficiency
  6. Unknown etiology; HAPE (high altitude pulmonary edema), head injury, heroic overdose

**IF THE UNVENTILATED ALVEOLI CONTINUE TO BE PERFUSED SERVER RIGHT TO LEFT SHUNT ENSUES.
**AT TIMES, pulmonary edema is the only presentation of an underlying diastolic dysfunction
Arterial gases:- hypoxemia (low PaO2) is seen early. This causes re

24
Q

Treatment of pulmonary edema

Cardiogenic vs non Cardiogenic

A

Cardiogenic

  1. IV morphine ; ease back pressures on lungs and relieve PE. Vasodilation caused will reduce cardiac afterload and improve CO
  2. Phlebotomy; remove 100-500mL of blood. When pt is not in shock and when drugs and supportive care are not immediately available
  3. Nitrate; dilate veins and reduce cardiac preload
  4. IV loop diuretics ; prompt diuresis and symptom relief
  5. Low dose dopamine ; improve renal flow and is an inotropic agent

Non Cardiogenic PE

  1. Intubate and positive pressure ventilation are the KEY
  2. Treat cause of lung injury
  3. Steroids (long used) is not beneficial
  4. Surfactant
  5. Prostaglandins, NO, IL1 antagonist are being tested
25
Q

Asthma

  1. Hallmark mechanism?
  2. Pathology of asthma (3)
  3. Pathophysiology of asthma (4)
A
  1. Hallmark of asthma is IgE mediated mast cell activation, with acute mediator release (histamine, Leukotrienes, platelet activating factor)
    * **Type 2 immune responses in lower airway are the abnormality - result in airway hyperresponsiveness, airflow obstruction and mucus secretion

Pathology of asthma

  1. Airway mucus is qualitatively abnormal. Increase eosinophils
  2. Subepithelial fibrosis
  3. Airway smooth muscle cells undergo hypertrophy and hyperplasia in some severe types

Pathophysiology

  1. Increased airway resistance
  2. V/Q mismatch ; ventilation of respiratory units becomes non uniform and contribute to hypoxemia
  3. Increased work of breathing
  4. Even mild hypercapnia should be viewed as an ominous sign during a severe asthma
26
Q

Effect of bronchodilator vs histamine and methacholine on asthma pt

A

Bronchial hyperresponsiveness—is de

27
Q

Management of asthma (12 yrs of age)

A
  1. Intermittent asthma
    A. SABA as needed e.g albuterol (DOA - 4 hrs)
  2. Persistent asthma (more than 3 times a week)
    A. Inhaled steroids +/-
    B. cromolyn, LTRA (montelukast/zirfulukast) or theophylline
  3. Persistent asthma step 2
    A. Inhaled steroids +- LABA +-
    B. LTRA (increase risk of asthma related death) or zileuton or ipratropium bromide if needed
  4. Persistent asthma step 3
    A. Oral CS + LABA + omalizumab (monoclonal antibody against IgE)
28
Q

Emphysema

  1. Mechanism
  2. Hallmark
A
    • Alveolar wall is destroyed as a result of imbalance of proteases (elastase) and antiprotease (alpha 1 antitrypsin)
    • **Congenital deficiency of alpha 1 antitrypsin dramatically accelerate this damage
    • Endothelial dysfunction and eventual destruction of pulmonary vessels will cause increase in pulmonary vascular resistance and pulmonary hypertension.

**Increased TLC and RV in patients with COPD. Increase RV/TLC is characteristic of emphysema

29
Q

Chemical control of breathing

**Peripheral chemoreceptors; exposed to arterial blood

Vs

**central chemoreceptors

A

Chemical stimuli
A) Peripheral chemoreceptors
1) Decrease PaO2 (not total arterial O2 content); <60mmHg
2) Increase PaCO2
3) decrease pH (carotid chemoreceptors only)

B. Central chemoreceptors (located in the VLM and retrotrapezoid nucleus RTN); not stimulated by hypoxemia

1) Increase PaCO2
2) Not stimulated by decreased PO2
* *Central chemoreceptors are comprised of neurons activated and inhibited by pH
- neurons activated by pH release serotonin and ACTIVATE the respiratory centers
- neurons inhibited by pH release GABA, which is inhibitory to the respiratory centers. **Thus activating the activator and inhibiting the inhibitor.

30
Q

SIDS vs Ondine’s curse (Congenital central hypoventilation syndrome)

A

SIDS (sudden infant death syndrome)–Many infants who have died of sudden infant death syndrome (SIDS) have a de

31
Q

Summary of respiratory drive

A
  1. Hypoxic (↓PaO2) ventilatory drive–primarily
    mediated by peripheral chemoreceptors–is accentuated by hypercapnia (respiratory acidosis). This is due to synergistic activation of BOTH central and peripheral chemoreceptors and increased sensitivity of peripheral chemoreceptors to O2 during hypercapnia.
  2. Hypercapnic (↑PaCO2) ventilatory drive–primarily mediated by central chemoreceptors- -is accentuated by hypoxia and metabolic acidosis–similar reasons as above.
  3. Opiates and BZDs reduce or abolish (depending on dose) ventilatory drive to hypoxia and hypercapnia
32
Q

Regional distribution of V/Q

A

V/Q is greater at the apex and lowest at the base. This is because blood flow is slower at the apex than the base.

  • Ventilation is highest at base and lowest at the top
  • Perfusion is highest at the base and lowest at the top
33
Q

Anaerobic threshold

Signs of increase in altitude

A

The point (owlets point) where lactate begin to increase linearly (e.g during exercise).

**Point is higher with trained athletes

High altitude adaptations
- recall, PACO2 will not be affected till the ventilation changes

Signs of increase in altitude

  • Amnesia, dizziness, anorexia
  • loss of consciousness and death

MS 2 Sping (3 decks)

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