5 курс / Пульмонология и фтизиатрия / Clinical_Manifestations_and_Assessment_of_Respiratory

Clinically, the most common oxygen saturation–based and content-based indices are (1) total oxygen delivery (DO2), (2) arterial-venous oxygen content difference (), (3) oxygen consumption (VO2), (4) oxygen extraction ratio (O2ER),

(5) mixed venous oxygen saturation (), and (6) pulmonary shunt fraction (QS/QT).9

Total Oxygen Delivery (DO2)10

Total oxygen delivery (DO2) is the amount of oxygen delivered to the peripheral tissue cells. The DO2 is calculated as follows:

where QT is total cardiac output (L/min),10 CaO2 is oxygen content of arterial blood (milliliters of oxygen per 100 mL of blood), and the factor 10 is used to convert the CaO2 to milliliters of oxygen per liter of blood.

For example, if the patient has a cardiac output of 3 L/min and a CaO2 of 10.5 mL/dL, the DO2 is 315 mL of oxygen per minute:

Normally, the DO2 is about 1000 mL of oxygen per minute. Box 6.1 provides factors that increase and decrease the DO2.

Clinically, the thermodilution method is used to measure the patient's cardiac output. A bolus of solution of known volume and temperature is injected into the right atrium, and the resultant change in blood temperature is detected by a thermistor previously placed in the pulmonary artery with a special catheter (see Chapter 7, Assessment of the Cardiovascular System, for more discussion on hemodynamics).

Box 6.1

Factors That Increase and Decrease the DO2

Factors That Increase the DO2

•Improvement of respiratory disease (e.g., reverse alveolar atelectasis or asthmatic episode)*

•Increased arterial oxygen saturation (e.g., increase FIO2)

•Increased hemoglobin concentration

•Increased cardiac output

Factors That Decrease the DO2

•Respiratory disease (e.g., asthmatic episode, pneumonia, emphysema)*

•Decreased arterial oxygen saturation (e.g., respiratory disease)

•Decreased hemoglobin concentration

•Decreased cardiac output

*See Table 6.3, page 89.

Arterial-Venous Oxygen Content Difference ()11

The arterial-venous oxygen content difference () is the difference between the CaO2 and the (CaO2 –

). Therefore if the patient's CaO2 is 15 mL/dL, the is 8 mL/dL, and the is 7 mL/dL:

Normally, the is about 5 mL/dL O2. The is useful in assessing the patient's cardiopulmonary status because oxygen changes in the mixed venous blood () often occur earlier than oxygen changes in arterial blood gas. Box 6.2 provides factors that increase and decrease the .

Box 6.2

Factors That Increase and Decrease the

Factors That Increase the

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•Decreased cardiac output

•Exercise

•Seizures

•Hyperthermia

Factors That Decrease the

•Increased cardiac output

•Skeletal muscle relaxation (e.g., induced by drugs)

•Peripheral shunting (e.g., sepsis)

•Certain poisons (e.g., cyanide)

•Hypothermia

Oxygen Consumption (V̇O2)12

Oxygen consumption (VO2), also known as oxygen uptake, is the amount of oxygen consumed by the peripheral tissue cells during a 1-minute period. The VO2 is calculated as follows:

where QT is the total cardiac output (L/min), is the arterial-venous oxygen content difference, and the factor 10 is used to convert the to mL O2/L.

Therefore if a patient has a cardiac output of 4 L/min and a of 6 mL/dL, the total amount of oxygen consumed by the tissue cells in 1 minute would be 240 mL:

Normally, the VO2 is about 250 mL of oxygen per minute. It is often reported as a function of body weight (i.e., mL/kg or mL/lb). Box 6.3 provides factors that increase and decrease the .

Box 6.3

Factors That Increase and Decrease the VO2

Factors That Increase the VO2

•Seizures

•Exercise

•Hyperthermia

•Increased body size

Factors That Decrease the VO2

•Skeletal muscle relaxation (e.g., induced by drugs)

•Peripheral shunting (e.g., sepsis)

•Certain poisons (e.g., cyanide)

•Hypothermia

•Decreased body size

Oxygen Extraction Ratio (O2ER)13

The oxygen extraction ratio (O2ER), also known as the oxygen coefficient ratio or oxygen utilization ratio, is the amount of oxygen consumed by the tissue cells divided by the total amount of oxygen delivered. The O2ER is calculated by dividing

the by the CaO2. Therefore if a patient has a CaO2 of 15 mL/dL and a of 10 mL/dL, the O2ER would be 33%:

Normally, the O2ER is about 25%. Box 6.4 provides factors that increase and decrease the O2ER.

Box 6.4

Factors That Increase and Decrease the O2 ER

Factors That Increase the O2ER

•Respiratory disease (e.g., asthmatic episode, pneumonia, emphysema)*

•Decreased cardiac output

•Periods of increased oxygen consumption

•Exercise

•Seizures

•Shivering

•Hyperthermia

•Anemia

•Decreased arterial oxygenation

Factors That Decrease the O2ER

•Improvement of respiratory disease (e.g., reverse alveolar atelectasis or asthmatic episode)*

•Increased cardiac output

•Skeletal muscle relaxation (e.g., induced by drugs)

•Peripheral shunting (e.g., sepsis, trauma)

•Certain poisons (e.g., cyanide)

•Hypothermia

•Increased hemoglobin

•Increased arterial oxygenation

*See Table 6.3, page 89.

Mixed Venous Oxygen Saturation ()14

When a patient has a normal arterial oxygen saturation (SaO2) and hemoglobin concentration, the mixed venous oxygen saturation () is often used as an early indicator of changes in the patient's , VO2, and O2ER, which are

measures of net tissue oxygenation. The can signal changes in the patient's , VO2, and O2ER earlier than arterial blood gases because the PaO2 and SaO2 levels are often normal during early tissue oxygenation changes. Normally,

the is about 75%. The can be measured directly by obtaining a venous blood sample from a pulmonary arterial catheter or derived as follows:

where the DO2 is the total oxygen delivery and the VO2 is the oxygen consumption. Thus if the patient has a normal DO2 of 1000 mL O2/min, and a normal VO2 of 250 mL O2/min, the is 0.75:

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Box 6.5 lists factors that increase and decrease the . Table 6.1 summarizes the way various clinical factors alter the patient's DO2, VO2, , O2ER, and .

Box 6.5

Factors That Increase and Decrease the

Factors That Increase the

•Improvement of respiratory disease (e.g., reverse alveolar atelectasis or asthmatic episode)*

•Increased cardiac output

•Increased concentration of oxygen (FIO2)

•Skeletal muscle relaxation (e.g., induced by drugs)

•Peripheral shunting (e.g., sepsis)

•Certain poisons (e.g., cyanide)

•Hypothermia

Factors That Decrease the

•Respiratory disease (e.g., asthmatic episode, pneumonia, emphysema)*

•Decreased cardiac output

•Decreased concentration of oxygen (FIO2)

•Periods of increased oxygen consumption

•Exercise

•Seizures

•Shivering

•Hyperthermia

*See Table 6.3, page 89.

TABLE 6.1

Clinical Factors That Affect Oxygen Transport Calculations*

Oxygen Transport Study		Equation	Factors That Increase Value	Factors That Decrease
				Value
Total oxygen delivery (DO2)			Increased blood	Decreased blood
			oxygenation	oxygenation
			Increased hemoglobin	Decreased hemoglobin
			Increased cardiac output	Decreased cardiac output
Arterial-venous oxygen content			Decreased cardiac output	Increased cardiac output
difference (	)		Increased O2 consumption	Skeletal muscle relaxation
			Exercise	Induced by drugs
			Seizures	Peripheral shunting
			Shivering	Sepsis
			Hyperthermia	Trauma
				Certain poisons
				Cyanide
				Hypothermia
Oxygen consumption (VO2)			Exercise	Skeletal muscle relaxation
			Seizures	induced by drugs
			Shivering	Peripheral shunting
			Hyperthermia	Sepsis
				Trauma
				Certain poisons
				Cyanide
				Hypothermia
Oxygen extraction ratio (O2ER)			Increased cardiac output	Decreased cardiac output
			Skeletal muscle relaxation	Increased O2 consumption
			induced by drugs	Exercise
			Peripheral shunting	Seizures
			Sepsis	Shivering
			Trauma	Hyperthermia
			Certain poisons	Anemia
			Cyanide	Decreased arterial
			Hypothermia	oxygenation
			Increased hemoglobin
			Increased arterial
			oxygenation
Mixed venous oxygen saturation (			Decreased cardiac output	Increased cardiac output
)			Increased O2 consumption	Skeletal muscle relaxation
			Exercise	induced by drugs
			Seizures	Peripheral shunting
			Shivering	Sepsis
			Hyperthermia	Trauma
				Certain poisons (cyanide)
				Hypothermia
Pulmonary shunt fraction (QS/QT)			See Table 6.3	N/A
*The availability of the oxygen saturation–based and content-based indices that require the venous oxygen content—the				, V̇O2, O2ER,	, and QṠ/QṪ—

may not be readily available because of the risk to benefit ratio associated with the insertion of the pulmonary arterial catheter needed to obtain mixed venous blood.

A simple but helpful way to visualize the is to consider this oxygen index as reflecting the oxygen that is “left over” in the mixed venous blood after it has been used by the tissues in satisfying the metabolic needs of the body. This can be used as a good, quick estimate of the overall success of the gas exchange mechanism described in Chapter 3, The Pathophysiologic Basis for Common Clinical Manifestations.

Pulmonary Shunt Fraction (Q̇/Q̇)15

S T

Because pulmonary shunting and venous admixture are frequent complications in respiratory disorders, knowledge of the degree of shunting is desirable in developing patient care plans. The amount of intrapulmonary shunting can be calculated by using the classic shunt equation:

where QS is the cardiac output that is shunted, QT is the total cardiac output, CcO2 is the oxygen content of pulmonary

capillary blood, CaO2 is the oxygen content of arterial blood, and is the oxygen content of mixed venous blood.

To obtain the data necessary to calculate the patient's intrapulmonary shunt, the following information must be gathered:

•Barometric pressure

•PaO2

•SaO2 (arterial oxygen saturation)

•PaCO2

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•

• (mixed venous oxygen saturation)

•Hemoglobin concentration

•PAO2 (partial pressure of alveolar oxygen)16

•FIO2 (fractional concentration of inspired oxygen)

A clinical example of the shunt calculation follows:

Shunt Study Calculation in an Automobile Accident Victim

A 22-year-old man is on a volume-cycled mechanical ventilator on a day when the barometric pressure is 755 mm Hg. The patient is receiving an FIO2 of 0.60. The following clinical data are obtained:

•Hb: 15 g/dL

•PaO2: 65 mm Hg (SaO2: 90%)

•PaCO2: 56 mm Hg

•: 35 mm Hg (: 65%)

With this information the patient's PAO2, CcO2, CaO2, and

now can be calculated. (The clinician should

remember that PH2O represents alveolar water vapor pressure and is always 47 mm Hg.)

1.

2.

3.

4.

With this information the patient's intrapulmonary shunt fraction now can be calculated:

Therefore 36% of the patient's pulmonary blood flow is perfusing lung alveoli that are not being ventilated.

Table 6.2 shows the clinical significance of pulmonary shunting. Table 6.3 summarizes how specific respiratory diseases alter the oxygen saturation–based and content-based indices.17

TABLE 6.2

Clinical Significance of Pulmonary Shunting

Degree of Pulmonary Shunting	Clinical Significance
(%)
Below 10%	Normal lung status
10%–20%	Indicates a pulmonary abnormality but is not significant in terms of cardiopulmonary
	support
20%–30%	May be life threatening, possibly requiring cardiopulmonary support
Greater than 30%	Serious life-threatening condition, almost always requiring cardiopulmonary support

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TABLE 6.3

Oxygenation Index Changes Commonly Seen in Specific Respiratory Diseases

Respiratory Diseases	Oxygenation Indices
Pulmonary disorder	(75%)	DO2*		VO2		5 mL/dL		O2ER	QS/QT
		(1000 mL		(250 mL				(25%)	(<10%)
		O2/min)		O2/min)
Obstructive airway disease	↓	↓	~†		~		↑		↑
Chronic bronchitis
Emphysema
Asthma
Cystic fibrosis
Bronchiectasis
Loss of volume	↓	↓	~		~		↑		↑
Atelectasis
Infectious pulmonary diseases	↓	↓	~		~		↑		↑
Pneumonia
Tuberculosis
Pulmonary vascular diseases	↓	↓	~		↑‡		↑		↑
Pulmonary edema
Pulmonary embolism
Chest and pleural trauma	↓	↓			↑‡		↑		↑
Flail chest
Pneumothorax
Disorders of the pleura and chest	↓	↓	~		~		↑		↑
wall
Pleural disease (e.g.,
hemothorax)
Kyphoscoliosis
Lung cancer	↓	↓	~		~		↑		↑
Diffuse alveolar disease	↓	↓	~		~		↑		↑
Interstitial lung disease
Acute respiratory distress
syndrome
Neurorespiratory disorders	↓	↓	~		~		↑		↑
Sleep apnea
Amyotrophic lateral sclerosis
(ALS)
Newborn and childhood diseases	↓	↓	~		~		↑		↑
Meconium aspiration syndrome
Transient tachypnea of the
newborn
Respiratory distress syndrome
Pulmonary air leak syndrome
Respiratory syncytial virus
infection
Bronchopulmonary dysplasia
Congenital diaphragmatic hernia
Croup syndrome

*The DO2 may be normal in patients with an increased cardiac output, an increased hemoglobin level (polycythemia), or a combination of both. For example, a normal DO2 is often seen in patients with chronic obstructive pulmonary disease and polycythemia. When the DO2 is normal, the patient's O2ER is usually normal.

†~ Unchanged.

‡The increased is associated with a decreased cardiac output.

Hypoxemia Versus Hypoxia

Hypoxemia refers to an abnormally low arterial oxygen tension (PaO2) and is frequently associated with hypoxia, which is

an inadequate level of tissue oxygenation (see the following discussion). Although the presence of hypoxemia strongly suggests tissue hypoxia, it does not necessarily mean the absolute existence of tissue hypoxia. For example, the reduced level of oxygen in the arterial blood may be offset by an increased cardiac output or an increased hemoglobin level. However, in sick patients, these compensatory mechanisms often are not available. A good example would be an anemic patient on beta-adrenergic blockers such as propranolol or an elderly patient with reduced cardiac function.

Hypoxemia is commonly classified as mild hypoxemia, moderate hypoxemia, or severe hypoxemia (Table 6.4). Clinically, the presence of mild hypoxemia generally stimulates the oxygen peripheral chemoreceptors to increase the

patient's breathing rate and heart rate (see Fig. 3.5).

TABLE 6.4

Hypoxemia Severity Classifications*

Classification	PaO2 (mm Hg) (Rule of Thumb)
Normal	80–100
Mild hypoxemia	60–80
Moderate hypoxemia	40–60
Severe hypoxemia	<40

*The hypoxemia classifications provided in this table are generally accepted in clinical practice. Minor variations of these values are found in the literature. As a general rule of thumb, however, the hypoxemia classifications and PaO2 range(s) presented in this table are useful guidelines.

Hypoxia refers to low or inadequate oxygen for aerobic cellular metabolism. Hypoxia is characterized by tachycardia, hypertension, peripheral vasoconstriction, dizziness, and mental confusion. Table 6.5 provides an overview of the four main types of hypoxia. When hypoxia exists, alternative anaerobic mechanisms are activated in the tissues that produce dangerous metabolites, such as lactic acid, as waste products. Lactic acid is a nonvolatile acid and causes the pH to decrease.

TABLE 6.5

Types of Hypoxia

Hypoxia	Descriptions	Common Causes
Hypoxic hypoxia (also called	Inadequate oxygen at the tissue cell caused by low	Low PAO2 caused by:
hypoxemic hypoxia)	arterial oxygen tension (PaO2)	Hypoventilation
		High altitude
		Diffusion impairment
		Interstitial fibrosis
		Interstitial lung
		disease
		Interstitial pulmonary
		edema
		Pneumoconiosis
		Ventilation-perfusion
		mismatch
		Pulmonary shunting
Anemic hypoxia	PaO2 is normal, but the oxygen-carrying capacity and	Decreased hemoglobin
	thus the oxygen content of the blood is inadequate	concentration
		Anemia
		Hemorrhage
		Abnormal hemoglobin
		Carboxyhemoglobin
		Methemoglobin
Circulatory hypoxia (also called	Blood flow to the tissue cells is inadequate; therefore	Hypotension
stagnant or hypoperfusion	adequate oxygen is not available to meet tissue	Slow flow or stagnant
hypoxia)	needs	(pooling) of peripheral
		blood
		Arterial-venous shunts
Histotoxic hypoxia	Impaired ability of the tissue cells to metabolize	Cyanide poisoning
	oxygen

Pathophysiologic Conditions Associated With Chronic Hypoxia

Cor Pulmonale

Cor pulmonale is the term used to denote pulmonary arterial hypertension, right ventricular hypertrophy, increased right ventricular work, and ultimately right ventricular failure. The three major mechanisms involved in producing cor pulmonale in chronic pulmonary disease are (1) the increased viscosity of the blood associated with polycythemia, (2) the increased pulmonary vascular resistance caused by hypoxic vasoconstriction, and (3) the obliteration of the pulmonary capillary bed, particularly in emphysema. Items 1 and 2 are discussed in greater depth in the following paragraphs.

Polycythemia

When pulmonary disorders produce chronic hypoxia, the renal cells release higher than normal amounts of the hormone erythropoietin, which in turn stimulates the bone marrow to increase red blood cell production. Red blood cell production is known as erythropoiesis. An increased level of red blood cells is called polycythemia. The polycythemia that results from hypoxia is an adaptive mechanism that increases the oxygen-carrying capacity of the blood.

Unfortunately, the advantage of the increased oxygen-carrying capacity in polycythemia is at least partially offset by the increased viscosity of the blood when the hematocrit reaches 50% to 60%. Because of the increased viscosity of the blood, a greater driving pressure is needed to maintain a given flow.

Hypoxic Vasoconstriction of the Lungs

Hypoxic vasoconstriction of the pulmonary vascular system (hypoxic vasoconstriction of the lungs) commonly develops in response to the decreased PAO2 that occurs in chronic respiratory disorders. The decreased PAO2 causes the smooth

muscles of the pulmonary arterioles to constrict. The exact mechanism of this phenomenon is unclear. However, the PAO2 (and not the PaO2) is known to chiefly control this response.

The early effect of hypoxic vasoconstriction is to direct blood away from the hypoxic regions of the lungs and thereby offset the shunt effect. However, when the number of hypoxic regions becomes significant, such as during the advanced stages of emphysema or chronic bronchitis, a generalized pulmonary vasoconstriction develops, causing the pulmonary

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vascular resistance to increase substantially. Increased pulmonary vascular resistance leads to pulmonary hypertension, increased work of the right side of the heart, right ventricular hypertrophy, and cor pulmonale.

The cor pulmonale associated with chronic respiratory disorders may develop from the combined effects of polycythemia and pulmonary arterial vasoconstriction. Both of these conditions occur as a result of chronic hypoxia. Clinically, cor pulmonale leads to the accumulation of venous blood in the large veins. This condition causes (1) the neck veins to become distended (see Fig. 3.25), (2) the extremities to show signs of peripheral edema and pitting edema (see Fig. 3.24), and (3) the liver to become enlarged and tender.

True Hypoxia—Can It Be Measured?

Our understanding of oxygen transport and cellular utilization of oxygen may be on the threshold of greatly increased depth and scientific sophistication. In the past decade, a number of cell-permeable phosphorescence-based probes for imaging of intracellular oxygen tension (icO2) have been developed. These probes are 1/600th of the diameter of a human hair. Once placed they can aid in the analysis of true tissue hypoxia and gradients across the cellular, nuclear, and mitochondrial membranes and can evaluate oxygenation responses to pharmacologic and oxygen therapy manipulations with high cellular component resolution. That is, you will be able to analyze tissue oxygen at the mitochondrial level. The technology of the probes themselves, called nanostraws, is remarkable and too complex to describe in detail here. The operational performance of this technology is still being evaluated in individual cell and tissue models, but it is clear that the next edition of this volume may well describe oxygen-related physiology at the “end-user level,” where it counts—that is, in the powerhouse of the cell, the mitochondria themselves!

Self-Assessment Questions

1. A 46-year-old woman with severe asthma arrives in the emergency department with the following clinical data: Hb: 11 g/dL

PaO2: 46 mm Hg SaO2: 70%

Based on these clinical data, what is the patient's CaO2?

a.6.75 mL/dL O2

b.10.50 mL/dL O2

c.12.30 mL/dL O2

d.15.25 mL/dL O2

2.If the patient has a cardiac output of 6 L/min and a CaO2 of 12 mL/dL, what is the DO2?

a.210 mL O2/min

b.345 mL O2/min

c.540 mL O2/min

d.720 mL O2/min

3.If the patient's CaO2 is 11 mL/dL and the is 7 mL/dL, what is the ?

a.4 mL/dL O2

b.7 mL/dL O2

c.11 mL/dL O2

d.15 mL/dL O2

4.Clinically, the patient's increases in response to which of the following?

1.Hypothermia

2.Decreased cardiac output

3.Seizures

4.Cyanide poisoning

a.2 only

b.4 only

c.2 and 3 only

d.1 and 4 only

5.If a patient has a cardiac output of 6 L/min and a of 4 mL/dL, what is the VO2?

a.160 mL O2/min

b.180 mL O2/min

c.200 mL O2/min

d.240 mL O2/min

6.Clinically, the VO2 decreases in response to which of the following?

1.Exercise

2.Hyperthermia

3.Body size

4.Peripheral shunting a. 2 only

b. 4 only

c.1 and 3 only

d.2, 3, and 4 only