Pulmonary Physiology 4 Flashcards
SNS stimulation (via epi or norepi), histamine, alveolar hypoxia, alveolar hypercapnia, and decreased pH of venous blood all have what affect on PVR?
Increase PVR
Appear to exert much more control over pulmonary vasoconstriction than the SNS
Local mediators
What decreases PVR?
Upregulation of PNS tone, ACh, selective B2-adrenergic agonists, NO, and bradykinin
Shunts mixed venous blood from poorly ventilated sectors of the lung to those which are better ventilated
Hypoxic Vasoconstriction
Can result from alveolar hypoxia, atelectasis, or can be a local response that is controlled by vasoactive mediators
Hypoxic vasoconstriction
Decreased or absent air in all or parts of the lung
Atelectasis
Hypoxic vasoconstriction can be a local response controlled by vasoactive mediators such as
Histamine, catelcholamines, and certain prostaglandins
Hypoxia sets forth a cellular response, whereby outward K+ current is impeded in
Pulmonary vascular smooth muscle
This induces depolarization of vascular smooth muscle cells which causes subsequent
Ca2+ influx leading to contraction
In order for alveolar O2-CO2 exchange to meet metabolic demands, what must be matched?
Perfusion and ventilation
PaO2 and PaCO2 are dependent on
PAO2 and PACO2
PAO2 and PACO2 are influenced by the
V/Q ratio
An elevated V/Q (i.e. more ventilation than perfusion) in an alveolar capillary unit causes
Increased PAO2 and decreased PACO2
Elevated V/Q causes increased PAO2 and decreased PACO2. All other things equal, this would enable elevated
Oxygenation of blood
A lower V/Q will result in
- ) Decreased PAO2
- ) PACO2 close to that of mixed venous blood
- ) Reduced oxygenation of bloo
If severe enough, V/Q mismatching can result in the development of a
Shunt-like state
Approximately 2-5% of cardiac output returns to the left heart without encountering alveoli (via bronchial, pleural, or thesbian veins). This accounts for the
Normal anatomic shunt
Intrapulmonary shunts occur when there are V/Q mismatches. These include
Absolute shunts and shunt-like states
An ABSOLUTE shunt develops when there are
-no blood oxygenation occurs in these regions
Perfused but non-ventilated alveoli
In extreme cases, V/Q in non-ventilated regions equals
Zero
This can result from complete airway obstruction resulting in the equilibration of alveolar pressure with that of
Mixed venous blood
Result from alveolar-capillary units which have some degree of ventilation and perfusion that is below normal
Shunt-like states
Lead to a low V/Q
Shunt-like states
A High V/Q will form in regions with
Some ventilation but no perfusion
Non-perfused regions are referred to as
Alveolar dead space
In non-perfused but ventilated alveolar capillary units
- ) PAO2 is
- ) PACO2 is
- ) greater than 100 mmHg
2. ) 0
If sufficient shunting occurs, PaO2 and thus PaCO2 will be
Decreased
In the case of very poorly or non-ventilated alveoli, increasing FiO2 does not significantly impro the decreased
PaO2
What is better perfused and ventilated, the base of the lung or the apex?
Base
Blood pressure is greater at the lung base due to
Local mediators and gravity
Alveoli are smaller at the base of the lung, however, they are more
Compliant
Is the V/Q higher at the lung apex or the lung base?
Apex
Therefore, the apex has what characteristics?
Higher PAO2 and lower PACO2 than the base
In the apex of the lung, the:
- ) O2 content is
- ) CO2 content is
- ) Higher
2. ) Lower
However, more gas exchange occures in the
Base
Intravascular pressure is lower at the
Apex
Thus, the apex undergoes less recruitment and distension of blood vessels which leads to greater resistance to
Blood Flow
Although there is a more negative intrapleural pressure at the apex, the alveoli are
Larger and less compliant
This results in less ventilation in the apex than in the
Base
TO summarize, the V/Q ratio rises dramatically from the
Base to the apex
The major difference in the V/Q ratio between the base and the apex is due to their differences in
Perfusion (Q)
A healthy resting mean pulmonary arterial pressure is around
12-15 mmHg
Occurs when pulmonary blood pressure rises to levels that are inappropriate for a given cardiac output
Pulmonary HTN
A rare disease which occurs in the absence of other heart and lung pathologies.
-More prevalent in younger women than men
Idiopathic (primary) pulmonary HTN
Idiopathic (primary) pulmonary HTN usually leads to death within
2-8 years
rise from left-right intracardial shunts, increased PVR, occlusive/thromboembolic diseases, and elevated LAP
Secondary Pulmonary HTN
Cause a chronic increase in pulmonary blood flow
Left-right intracardial shunts
Burdened in the case of pulmonary HTN
Right Ventricle
Physical forces within the lumen and intersitium that will determine which direction fluid will move
Starling Forces
Shows how filtration is regulated by the relationships between hydrostatic and oncotic pressures in the capillaries and intersitium
Starling Equation
What are the four main Starling forces?
- ) Capillary pressure (Pc)
- ) Interstitial fluid pressure (Pi)
- ) Plasma colloid osmotic pressure (Or Oncotic pressure PIc)
- ) Interstitial colloid osmotic pressure (PIi)
Colloid osmotic pressure is caused by the concentration of proteins, namely
Albumin
High colloid osmotic pressure tends to draw fluid
IN to the cappilaries (results in increased reabsorption of H2O)
At the entrance to the capillary network (arterial feed), forces cause a net outward movement of fluid. This net outward movement is known as
Filtration
Wht are the characteristics of the forces in the arterial feed of the capillaries?
- ) Pc is high
- ) Pi is negative
- ) PIc is robust
- ) PIi is modest
Occurs primarily at the arterial feed of a capillary network
Filtration
At the venous end of the capillary network, what is the characteristic of the starling forces?
PIc is larger than the other 3 and so reabsorption occurs
When considering the mean net force of the capillary network, a general trend favors
Filtration
This concept of net filtration over absorption is referred to as the
Starling equilibrium
Designed to drain away the fluid accumulation that would occur due to the net filtration which occurs in the capillary beds
Lymphatic system
The capillary endothelium is much more permeable to fluid when compared to the
Alveolar membrane
First occurs in the interstitium and can migrate to the alveoli if severe enough
Pulmonary edema
The presence of edema increases the diffusion barrier for O2-CO2 exchange between the
Pulmonary capillaries and alveoli
Pathologic changes in 1) capillary membrane permeability, 2) capillary hydrostatic pressure, 3) interstitial hydrostatic pressure, 4) blood protein content, and 5) lymphatic vessel structure/function all an lead to
Pulmonary edema
Can result from one or more pathologies inducing left heart failure; mitral and aortic valve insufficiencies
Cardiogenic pulmonary edema
The reduction of PaO2
Hypoxemia
The cellular manifestation of low O2 tensiondue to hypoxemia
Hypoxia
Decreased atmospheric pressure, decreased inspired fraction of O2, alveolar hypoventilation, V/Q mismatch, shunts, and diffusion impairments all are pathologic mechanisms that can lead to
Hypoxemia
Recall that in healthy lungs, complete equilibration of gas tensions between ventilated alveoli and capillary blood occurs during
Capillary transit time
In the event of reduced alveolar ventilation (decreased atmospheric pressure, decreased FiO2, or alveolar hypoventilation), the A-a gradient is preserved since
Both PaO2 and PAO2 are low
Whereas, the cardiopulmonary causes of hypoxemia (V/Q mismatch, shunt, and diffusion impairment) each result in abnormal
A-a gradients
Two very common causes of hypoxemia due to V/Q mismatch
COPD and Asthma
With increased altitude, we see a drop in
Ambient PO2
The ensuing drop in PaO2 triggers activation of the
Peripheral hypoxic drive
Activation of the peripheral hypoxic drive raises both
Tidal volume and respiratory rate
Increased minute ventilation lowers PaCO2, resulting in a
Respiratory Alkalosis
Hypocapnia in turn dampens the
Central ventilatory drive
Over days, renal compensation drives the excretion of HCO3- in
Urine
This moves the pH toward normal and allows the central ventilatory drive to once again turn up the ventilatory rate, thereby increasing
PAO2
People who live in high altitude environments undergo a
Hypoxic desensitization phenomenon
Finally, increased production of erythropoietin stimulates polycythemia. This enables
Increased O2 delivery to tissues
Increased cardiac output is coupled to rise in
Tidal volume and alveolar ventilation
During intense exercise, minute ventilation can increase from around 5-6 L/min to upwards of
150 L/min
The limiting factor to the level of exercise a healthy individual can sustain is
Cardiac function (NOT pulmonary function)
With intense exercise, increased alveolar ventilation results in
Lower PACO2 with increased PAO2
This lower PACO2 and increased PAO2 results in
Raised PaO2, reduced PACO2
This elevated tissue O2 uptake increases the
Arteriovenous O2 difference (PaO2-PvO2)
With increased tidal volume, the work of breathing required to overcome elastic recoil of both lungs and chest wall is
Elevated
More turbulent airflow and increased dynamic compression of airways also contribute to the increased work of breathing during
Exercise
While exerciosing, with increased exercise intensity, there is a linear increase in
Pulse rate and systolic BP
Why does diastolic blood pressure stay stable or maybe even drop during exercise?
Production of vasodilators in skeletal muscle
The increase in cardiac output is relatively greater than the fall in TPR, thus there is a slight increase in
MAP
Does mean pulmonary BP rise significantly during intense exercise?
No
During intense exercise, increased perfusion of previously under-perfused alveolar-capillary units raises
DLCO (thereby elevating V/Q)
Control of the cardiorespiratory response during exercise is complex. Important control mechanisms include
CNS, arterial baroreceptors, arterial chemoreceptors, central venous chemoreceptors, muscle mechanoreceptors, and muscle chemoreceptors
Mediated largely through neurons known as class IV unmyelinated C fibers
Muscle chemoreceptors
During intensive exercise, the act of increased respiratory rate may contribute substantially to the generation of
Lactic acid
Lactic acid accumulation in muscles causes the release of endorphins in the CNS, which blunts the
Respiratory response
Blunting the respiratory response limits unnecesary
O2 utilization and lactate production
Part of a two-fold mechanism that increases venous return during exercise
SNS-induced vasoconstriction (especially in splanchnic beds)
