Pulmonary Physiology 4 Flashcards by Joel Glotfelty

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

How well did you know this?

Not at all

Perfectly

Appear to exert much more control over pulmonary vasoconstriction than the SNS

Local mediators

How well did you know this?

Not at all

Perfectly

What decreases PVR?

Upregulation of PNS tone, ACh, selective B2-adrenergic agonists, NO, and bradykinin

How well did you know this?

Not at all

Perfectly

Shunts mixed venous blood from poorly ventilated sectors of the lung to those which are better ventilated

Hypoxic Vasoconstriction

How well did you know this?

Not at all

Perfectly

Can result from alveolar hypoxia, atelectasis, or can be a local response that is controlled by vasoactive mediators

Hypoxic vasoconstriction

How well did you know this?

Not at all

Perfectly

Decreased or absent air in all or parts of the lung

Atelectasis

How well did you know this?

Not at all

Perfectly

Hypoxic vasoconstriction can be a local response controlled by vasoactive mediators such as

Histamine, catelcholamines, and certain prostaglandins

How well did you know this?

Not at all

Perfectly

Hypoxia sets forth a cellular response, whereby outward K+ current is impeded in

Pulmonary vascular smooth muscle

How well did you know this?

Not at all

Perfectly

This induces depolarization of vascular smooth muscle cells which causes subsequent

Ca2+ influx leading to contraction

How well did you know this?

Not at all

Perfectly

In order for alveolar O2-CO2 exchange to meet metabolic demands, what must be matched?

Perfusion and ventilation

How well did you know this?

Not at all

Perfectly

PaO2 and PaCO2 are dependent on

PAO2 and PACO2

How well did you know this?

Not at all

Perfectly

PAO2 and PACO2 are influenced by the

V/Q ratio

How well did you know this?

Not at all

Perfectly

An elevated V/Q (i.e. more ventilation than perfusion) in an alveolar capillary unit causes

Increased PAO2 and decreased PACO2

How well did you know this?

Not at all

Perfectly

Elevated V/Q causes increased PAO2 and decreased PACO2. All other things equal, this would enable elevated

Oxygenation of blood

How well did you know this?

Not at all

Perfectly

A lower V/Q will result in

) Decreased PAO2
) PACO2 close to that of mixed venous blood
) Reduced oxygenation of bloo

How well did you know this?

Not at all

Perfectly

If severe enough, V/Q mismatching can result in the development of a

Shunt-like state

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Intrapulmonary shunts occur when there are V/Q mismatches. These include

Absolute shunts and shunt-like states

How well did you know this?

Not at all

Perfectly

An ABSOLUTE shunt develops when there are

-no blood oxygenation occurs in these regions

Perfused but non-ventilated alveoli

How well did you know this?

Not at all

Perfectly

In extreme cases, V/Q in non-ventilated regions equals

Zero

How well did you know this?

Not at all

Perfectly

This can result from complete airway obstruction resulting in the equilibration of alveolar pressure with that of

Mixed venous blood

How well did you know this?

Not at all

Perfectly

Result from alveolar-capillary units which have some degree of ventilation and perfusion that is below normal

Shunt-like states

How well did you know this?

Not at all

Perfectly

Lead to a low V/Q

Shunt-like states

How well did you know this?

Not at all

Perfectly

A High V/Q will form in regions with

Some ventilation but no perfusion

How well did you know this?

Not at all

Perfectly

Non-perfused regions are referred to as

Alveolar dead space

In non-perfused but ventilated alveolar capillary units 1. ) PAO2 is 2. ) PACO2 is

1. ) 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: 1. ) O2 content is 2. ) CO2 content is

1. ) 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?

1. ) Capillary pressure (Pc) 2. ) Interstitial fluid pressure (Pi) 3. ) Plasma colloid osmotic pressure (Or Oncotic pressure PIc) 4. ) 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?

2. ) Pc is high 2. ) Pi is negative 3. ) PIc is robust 4. ) 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?

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)