RT 6, Ch 4, Ventilation

VA = CO2 elimination

CO2 elimination

VCO2

CO2 production; the amount of CO2 exhaled per minute

if RR increases, but VT decreases

Dead space increases; wasted ventilation goes up; VD/VT goes up

Determine whether hyperventilation or hypoventilation is present when reviewing the arterial carbon dioxide pressure (PaCO2).

If PaCO2 is above normal hypoventilation exists; if PaCO2 is below normal hyperventilation exists.

Describe how to predict the effects of minute ventilation changes on alveolar ventilation, dead space ventilation, and arterial carbon dioxide pressure (PaCO2).

If the frequency (respiratory rate), VT, and predicted VD are known, the initial VE and VA can be calculated using the following equations: VE = VT X f and VA = (VT - VD) X f or VA = (VT X f) - (VD X f). New values can be entered into the equation to predict the changes. This demonstrates the relationship between VE and respiratory rate. If VE stays the same while the respiratory rate increases (rapid, shallow breaths), the VT will decrease. If the VT decreases the VD will increase. If the VE remains the same and the respiratory rate decreases (slow, deep breaths), the VT will increase and the VD will decrease.To predict the new PaCO2, the following formula is used: PaCO2 X VA = K. Initial (PaCO2 x VA) = new (PaCO2 X VA) and then solve for the new PaCO2. This demonstrates the inverse relationship between PaCO2 and VA. If VA increases, PaCO2 decreases. If the VA decreases, PaCO2 increases.

what can cause pulmonary dead space?

a blood clot

Presence of a normal value indicates

a normal relationship

Bradypnea

abnormal decrease in breathing rate

Tachypnea

abnormal elevation of breathing rate

Hypercapnia

abnormal presence of excess amounts of CO2 in the blood (in arterial blood, PCO2 > 45 mm Hg

apnea

absence of breathing

Bohr

all Co2 in exhaled gas comes from the alveoli VA x FIO2

Capnogram

allows the PCO2 to be identified at the end of a tidal exhalation.

Alveolar dead space (VDA)

alveoli that are ventilated but are not perfused. The condition may exist when pulmonary circulation is obstructed, as by a thromboembolus

Physiological dead space (VE)

area in the respiratory system that includes the anatomic dead space together with the space in the alveoli occupied by air that does not contribute to the O2 - CO2 exchange

how are physiological normals measured?

at rest

compartments

atmosphere airways alveoli RBC

pulmonary embolism

blocked blood vessel

CO2 production does not change in

chronic lung disease

VDanat

conducting airway, ventilation without perfusion, no blood flow; anatomical dead space; the conducting airways from the mouth and nose down to and including the terminal bronchioles; no gas exchange occurs.

Anatomical dead space (VDanat)

conducting airways from the mouth and the nose down to and including terminal bronchioles.

what does shallow breathing increase?

deadspace, not enough VT going to alveoli, 20-40% must fill lungs plus inhaled air to adequately ventilate the alveoli

why is rapid respiratory rate not always abnormal?

depends on given metabolic demand e.g. exercise

capnometer

device

what normal activity causes a decrease in VD/VT?

during exercise

When does gas exchange occur?

during exhalation when capillaries less compressed

describe the relationship between VA and PaCO2

even a slight reduction in VA causes a sharp rise in PaCO2.

what are the two golden rules of fluid physics?

fluid follows path of least resistance fluid flows from highest to lowest concentration

what technique measure Vdanat?

fowler technique

bases of lungs

have more perfusion than ventilation; gravity dependent; when upright

In normal ventilatory pattern what is true?

if VE goes up, PaCO2 goes down If VE goes down, PaCO2 goes up VE responds to metabolic needs, no matter what activity VE matches CO2 production to maintain 35-45 mm Hg circulating in the blood

Hyperpnea

increased breathing but NOT hyperventilation

high VD/VT ratio

increased dead space; means that there is an increased requirement for ventilation for a given level of VCO2; can be elevated from either a reduction of VT or an actual increase in VD; cause a decrease in alveolar volume (VA) and hence in alveolar ventilation (VA).

rapid shallow breathing is always a signal of

increased work of breathing & potential respiratory failure

I:E ratio

inspiratory/expiratory ratio; respiratory cycle

CO2

maintains pH

What is a hazard of positive pressure?

may compress capillaries preventing gas exchange

which area of the lung has the best gas exchange?

middle of lung

VD/VT ratio and exercise

more VT & more RR

eupnea

normal breathing, ease of breathing

PaCO2 VE + PaCO2

physiologic adequacy of ventilation

Hypocapnia

presence of lower than normal amounts of CO2 in the blood (in arterial blood, PCO2 < 35 mm Hg

Capnography

process of obtaining a tracing of the proportion of CO2 in expired air using a capnograph

VDanat usually related to

pulmonary circulation defects

tachypnea

rapid breathing > 20 B/m

what happens when alveoli are inflated with O2 during inhalation?

restricts and compresses surrounding capillaries

Hypopnea

shallow low breathing.

bradypnea

slow breathing < 12 B/m

How to fix Vdanat?

take a deep breath positive pressure increase VT

capnography

test

Minute ventilation

total lung ventilation per minute, the product of tidal volume and respiration rate. It is measured by expired gas collection for a period of 1 to 3 minutes; normal rate is 5 to 10 L/min

hypopnea

usually neurological, < normal VT

Hypoventilation

ventilation less than necessary to meet metabolic needs; signified by PCO2 greater than 45 mm Hg in the arterial blood; rise in blood PCO2 due to inadequate ventilation

dead space

ventilation without perfusion

Dead-space ventilation (VD)

volume of air that is inhaled that does not take part in gas exchange.

when is VE abnormal?

when Ve changes but CO2 is not in normal range, depending on the patient's normal (CO2)

VD/VT =

(PaCO2 - PeCO2)/PaCO2 where PeCO2 is the mean expired carbon dioxide pressure, which is obtained from an expired air sample that is collected over a few minutes time. Normal PeCO2 is approximately 28 mm Hg. Thus 40--28/40 = 0.30.

VD/VT should equal

60%- 80%, VE = VA

Determine what the dead space ventilation would be if the VT were 600 mL, the RR was 10 BPM, the PaCO2 was 40 mm Hg, and the VCO2 was 200m l/min.

= (200 mL/min x 0.863)/40 mm Hg = 4.315 L/min = f x VT = 10/min x 600 mL = 6000 mL/min = 6000 mL/min - 4315 mL/min = 1685 mL/min

hyperpnea

> normal VT

how much gas is Vdanat?

1/3

normal VD

1/3

what is the deadspace constant?

150 ml

Vdanat

1ml/lb

how much gas reaches alveoli?

2/3

How much air participates in gas exchange?

2/3 or 60 - 65%

normal resting CO2 production

200 ml/min

what is an average VE?

4 - 6 L/min

normal resting VA

4-5 L/min

what is an average adults VE and PaCO2?

4-6 l/min maintains 40 mmHg

normal PCO2

40 mmHg (35-45 mmHg)

A 55-year-old woman is admitted to the hospital in obvious respiratory distress. Her increased rate and depth of breathing have raised her minute ventilation to 15 L/min. Arterial blood gases show a normal PaCO2 of 40 mm Hg. It seems odd that this woman, with a minute ventilation this great, has a normal PaCO2. What is the explanation for this?

A normal PaCO2 associated with high minute ventilation indicates that much of this patient's ventilation is not in contact with blood flow. Dead space is the term used to describe alveoli that have normal ventilation but no blood flow through their capillaries. Any factor that decreases perfusion increases alveolar dead space. Increased alveolar dead space decreases alveolar ventilation if minute ventilation stays the same. Pulmonary embolism and shock are conditions that cause increased alveolar dead space. VD/VT increases as a larger percentage of the VT becomes dead space. In conditions producing dead space, the body tries to maintain a normal PaCO2 by increasing the minute ventilation. This increased minute ventilation does not mean alveolar ventilation increases because much of the minute ventilation is directed toward dead space units. A physiological consequence of increased dead space as the increased work of breathing required to maintain a normal PaCO2. Patients with obstructive lung disease have impaired ventilatory capacity and may be unable to accommodate the increased demand for minute ventilation created by conditions that produce dead space. Increased dead space may precipitate ventilatory failure in these patients.

Describe why the PO2 of the tracheal gas is less than that of the inspired atmospheric gas.

According to Dalton's law, O2 exerts a partial pressure proportional to its fractional concentration of air. Once air is inspired it is heated and humidified in the body and creates water vapor. The water vapor escapes the lungs and reduces the partial pressure of inspired O2 to 149 mmHg as it travels from the upper airway down into the trachea..

Explain the effect on alveolar ventilation if dead-space ventilation increases, but minute ventilation stays the same.

Alveolar ventilation will decrease because VE-VD equals (VA) alveolar ventilation.

Describe what the above affect would have on gas exchange between the blood and the air

Bringing in more CO2 free gas can cause less of the CO2 rich alveolar to exhale because when we exhale we bring in more air that needs to be exhaled therefore CO2 will not be exhaled properly.

State the physiological explanation for a patient whose total minute ventilation is 18 L/min (normal is 5 - 8 L/min), but the PaCO2 is normal at 40 mm Hg

It explains that this person's ventilation is not in contact with blood flow, because deadspace is used to describe alveoli with no perfussion and only ventilation through the capillaries. A patient with blood clots or decreased cardiac output can experience high minute ventilation with a normal PaCO2

Discuss how minute ventilation, alveolar ventilation, and dead-space ventilation are inter-related.

Minute ventilation is the volume of air entering or leaving the lung each minute, which includes alveolar ventilation and dead space ventilation. To get the true minute ventilation the dead space ventilation (VD) and the alveolar ventilation (VA), must be added together (VE = VDanat + VA).

A mechanical ventilator is delivering 10 breaths per minute to your patient. The VT is 700 mL, and this patient's estimated VDanat is 160 mL. Arterial blood gas results reveal a PaCO2 of 40 mm Hg. What happens to VA and PaCO2 if the respiratory rate is increased to 16 breaths per minute but the VE remains constant?

More air enters in the Alveoli and VA increases. VE is an unreliable indicator for VA. The PaCO2 will decrease.

You are called to assess a patient who seems to be hyperventilating. Your patient's respiratory rate is 30 breaths per minute. You measure the patient's arterial blood gases and find the PaCO2 is normal. Is this patient hyperventilating?

No the patient is not hyperventilating because their PaCO2 is normal the only time you can say a patient is hyperventilation is if their PaCO2 was below normal.

ventilation determines

PCO2 in lungs and arterial

in absence of lung disease

PaCO2 = PACO2

each increase of VE by 2X results in

PaCO2 decreasing by 2X (approx. 10 mmHgx2)

If VE increases

PaCO2 should decrease

if VE decreases

PaCO2 should increase

in healthy individuals VA changes with

RR X TV

calculate timing of breaths

RR/60 = timed breath

Explain how the ventilatory pattern affects dead space-to-tidal volume ratio, and subsequently, alveolar ventilation and arterial carbon dioxide pressure (PaCO2).

Respiratory pattern affects VD/VT: Identical VE values can yield different VA and PaCO2 values depending on the rate and depth of breathing. If VE stays the same while the respiratory rate increases (rapid and shallow), the VT and VA will decrease while the VD and PCO2 will increase. If VE stays the same while the respiratory rate decreases (slow, deep breathing), the VT and VA will increase and the VD and PCO2 will decrease.

Discuss the effect that the taking of a deep breath would have on the VD and VA.

Taking a deep breath increase the VD because the person is taking in more air which causes the lungs to expand more increasing the surface area, it also increases VA because there is more air available for gas exchange.

The lungs of a patient in the intensive care unit are mechanically ventilated with the following settings: f = 12/min and VT = 500 mL You also have the following information about your patient: VD = 150 ml PaCO2 = 40 mm Hg. Approximately 1 hour later, the patient seems to be agitated and is triggering the ventilator at a rate of 24/min (VT is still 500 mL). Estimate the patient's new PaCO2.

The PaCO2 will be reduced by half, since the VA has increased 2X. VA and PaCO2 are inversely related: VA=VE-VD VA=(500mL x12)- (150 mL x 12) VA=600 mL/min-1800 mL/min VA=4200 mL/min VA= (500 mL x 24) -(150 x 24) VA=12,00 mL/min - 3600 mL/min VA= 8400 mL/min 40 x 40 x 4200/8400 168000/8400= 20 mmHg

Discuss the theoretical basis for the measurement and calculation of dead space and alveolar Ventilation.

The anatomical dead space does not change unless parts of the lungs are removed. No gas exchange takes place in the conducting airways. In normal adult lungs, dead space is approximately 1 mL per pound of ideal body weight. The dead space in the alveoli refers to ventilation that does not participate in gas exchange because there is no blood flow and mixes with the next inhalation in a conical fashion. To measure the total physiologic dead space, the anatomical dead space and alveolar dead space are added together: VD=VDanat + VDA. The most accurate way to measure dead space is to calculate the VD/VT ratio using the following equation: (PACO2-PeCO2)/PACO2. A capnometer can measure the exhaled PCO2 which equals the PACO2 which equals PETCO2. Plugging this value into the equation gives you the VD/VT ratio.

Alveolar ventilation (VA)

The exchange of gas between the alveoli and the external environment

VE =

VA + VD = (driven by CO2 production) and VT x f = (total ventilation)

Because of deadspace...

VA always < VE

Discuss the rationale that underlies the calculation of anatomical dead space, alveolar ventilation, and physiological and anatomical dead space-to-tidal volume ratios.

VA can be calculated if the fraction of VT that is dead space (VD/VT) is known. Shallow tidal volumes increase VD/VT because conducting airway volume (VDanat) remains constant. Deep breaths decrease VD/VT for the same reason, causing a larger percentage of the inspired volume to reach the alveoli.

what is hypoventilation?

VA decreases and PCO2 exceeds rate @ which lungs are removing it

Explain why alveolar ventilation affects arterial carbon dioxide pressure (PaCO2).

VA determines arterial PCO2 because it controls alveolar PCO2. PACO2 is inversely related to VA; if VA is cut in half, PACO2 doubles. If VA doubles, PACO2 is cut in half.

triangular relationship between

VE, pH, CO2

VA=

VT - VD (volume of fresh gas reaching alveoli

VT =

VT -VD

first 150 ml of gas exhaled comes from?

Vdanat @ end of exhalation