5 курс / Пульмонология и фтизиатрия / Clinical_Manifestations_and_Assessment_of_Respiratory
.pdf7.If the patient's CaO2 is 12 mL/dL and the 
is 7 mL/dL, what is the O2ER?
a.0.27
b.0.33
c.0.42
d.0.53
8.Clinically, the 
decreases in response to which of the following?
a.Increased cardiac output
b.Seizures
c.Peripheral shunting
d.Hypothermia
9.In the patient with severe emphysema, which of the following oxygenation indices are commonly seen?
1.Decreased 
2.Increased VO2
3.Decreased 
4.Increased O2ER
a.1 only
b.3 only
c.1 and 4 only
d.2 and 3 only
10.In the patient with pulmonary edema, which of the following oxygenation indices are commonly seen?
1.Increased O2ER
2.Decreased 
3.Increased VO2
4.Decreased VO2
a.2 only
b.4 only
c.1 and 2 only
d.1, 2, and 3 only
Case Study: Gunshot Victim (Questions 11 to 15)
A 37-year-old woman is on a volume-cycled mechanical ventilator on a day when the barometric pressure is 745 mm Hg. The patient is receiving an FIO2 of 0.50. The following clinical data are obtained:
Hb: 11 g/dL
PaO2: 60 mm Hg (SaO2 90%)
: 35 mm Hg (
65%) PaCO2: 38 mm Hg
Cardiac output: 6 L/min
11.Based on this information, calculate the patient's total oxygen delivery.
a.510 mL O2/min
b.740 mL O2/min
c.806 mL O2/min
d.930 mL O2/min
12.Based on this information, calculate the patient's arterial-venous oxygen content difference.
a.2.45 mL/dL O2
b.3.76 mL/dL O2
c.4.20 mL/dL O2
d.5.40 mL/dL O2
13.Based on this information, calculate the patient's intrapulmonary shunt fraction.
a.22%
b.26%
c.33%
d.37%
14.Based on this information, calculate the patient's oxygen consumption.
a.170 mL O2/min
b.200 mL O2/min
c.230 mL O2/min
d.280 mL O2/min
15.Based on this information, calculate the patient's oxygen extraction ratio.
a.16%
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b.24%
c.26%
d.28%
1Previously the quantity of oxygen in 100 mL of blood was written as volumes percent (vol%) of oxygen. Thus in this case, 0.3 vol%.
2Also abbreviated as grams percent of hemoglobin (g% Hb).
5For a more in depth discussion of the oxyhemoglobin dissociation curve, see Des Jardins. Cardiopulmonary Anatomy and Physiology–Essentials of Respiratory Care, 7th edition, Cengage Learning, Clifton Park, NY.
6See Appendix XV on the Evolve site for a representative example of a cardiopulmonary profile sheet used to monitor the oxygen transport status of the critically ill patient.
8The precise normal room air breathing PaO2/FIO2 ratio range is 380 to 476 (80 mm Hg/0.21 = 380; 100 mm Hg/0.21 = 476).
9The availability of the oxygen saturation–based and content-based indices that require the venous oxygen content—the
, VO2, O2ER, 
, and QS/QT—may not be readily available because of the high risk to benefit ratio associated
with the insertion of the pulmonary artery catheter needed to obtain venous blood. (See section on pulmonary artery catheter, page 97.)
10Important Clinical Note: It is important to understand that the formula used to calculate total oxygen delivery is one in which factors are multiplied 3 times (!) rather than added—in short, small decreases or increases in these factors have a marked influence on the final product. For example, consider the following: An elderly two-pack-per-day smoking gentlemen presents with dyspnea. His PaO2 is 65 mm Hg on room air. He is mildly anemic (Hb = 9.0 g/dL) and has an SpO2
of 90%. His carboxyhemoglobin level is (3.0%), which in turn makes the true SaO2 87% (90% − 3% = 87%). He is on a
beta-blocker for his hypertension, which reduces his cardiac output to 3.0 L/min. In addition, he has mild metabolic alkalosis (pH 7.48) from chronic diuretic therapy, which causes a leftward shift in his oxyhemoglobin dissociation curve. Inserting these figures into the total oxygen delivery calculation results in a markedly reduced oxygen delivery (oxygen transport) of about 321 mL of oxygen per minute. Couple this situation with fever and pain, which increase oxygen consumption, and we see real trouble ahead!
11
may not be readily available because of the high risk to benefit ratio associated with the insertion of the pulmonary artery catheter needed to obtain venous blood. (See section on pulmonary artery catheter, page 97.)
12The determination of VO2 may not be readily available because of the high risk to benefit ratio associated with the
insertion of the pulmonary artery catheter needed to obtain venous blood. (See section on pulmonary artery catheter, page 97.)
13The determination of O2ER may not be readily available because of the high risk to benefit ratio associated with the
insertion of the pulmonary artery catheter needed to obtain venous blood. (See section on pulmonary artery catheter, page 97.)
14The determination of 
may not be readily available because of the high risk to benefit ratio associated with the insertion of the pulmonary artery catheter needed to obtain venous blood. (See section on pulmonary artery catheter, page 97.)
15The measurement of QS/QT may not be readily available because of the high risk to benefit ratio associated with the insertion of the pulmonary artery catheter needed to obtain venous blood. (See pulmonary artery catheter, page 97.)
16See Appendix VIII on the Evolve site.
17Note in Table 6.3 that virtually every respiratory disorder presented in this textbook causes the QS/QT to increase and the DO2 to decrease.
C H A P T E R 7
Assessment of the Cardiovascular
System
CHAPTER OUTLINE
The Electrocardiogram
Common Heart Arrhythmias
Sinus Bradycardia
Sinus Tachycardia
Sinus Arrhythmia
Atrial Flutter
Atrial Fibrillation
Premature Ventricular Contractions
Ventricular Tachycardia
Ventricular Fibrillation
Asystole (Cardiac Standstill)
Noninvasive Hemodynamic Monitoring Assessments
Heart Rate (Pulse), Cardiac Output, and Blood Pressure
Perfusion State
Invasive Cardiovascular Monitoring Assessments
Pulmonary Artery Catheter
Systemic Arterial Catheter
Central Venous Pressure Catheter
Cardiovascular (Hemodynamic) Monitoring in Respiratory Diseases
Self-Assessment Questions
CHAPTER OBJECTIVES
After reading this chapter, you will be able to:
•Describe the electrocardiogram pattern of a normal cardiac cycle.
•Evaluate and identify arrhythmias.
•Describe the noninvasive hemodynamic monitoring assessments.
•Evaluate the basic pathophysiologic mechanisms associated with an increased heart rate (pulse), cardiac output, and blood pressure and a decreased perfusion state.
•Describe invasive hemodynamic monitoring assessment methods.
•Describe how the hypoxemia, acidemia, or pulmonary vascular obstruction associated with respiratory disease alters the hemodynamic status.
•Define key terms and complete self-assessment questions at the end of the chapter and on Evolve.
KEY TERMS
Arterial Catheter (Systemic)
Asystole (Cardiac Standstill)
Atrial Fibrillation
Atrial Flutter
Atrial “Kick”
Bigeminy
Capillary Refill Test
Cardiac Arrest
Central Venous Catheter
Central Venous Pressure (CVP) Catheter
Coronary Angiography
Electrocardiograph (ECG) Patterns
Hemodynamics
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Invasive Hemodynamic Monitoring Assessments Noninvasive Hemodynamic Monitoring Assessments P Wave
Premature Ventricular Contraction (PVC) Pulmonary Artery Catheter (Swan-Ganz Catheter) Pulmonary Capillary Wedge Pressure (PWCP) Pulseless Electrical Activity (PEA)
QRS Complex Sinus Arrhythmia Sinus Bradycardia Sinus Tachycardia
Thermodilution Catheter T wave
Trigeminy
Ventricular Fibrillation
Ventricular Tachycardia
Because the transport of oxygen to the tissue cells and the delivery of carbon dioxide to the lungs are functions of the cardiovascular system, a basic knowledge and understanding of (1) normal electrocardiogram (ECG) patterns, (2) common heart arrhythmias, (3) noninvasive hemodynamic monitoring assessments, (4) invasive hemodynamic monitoring assessments, and (5) determinants of cardiac output are essential components of patient assessment.1
The Electrocardiogram
Because the respiratory care practitioner frequently works with critically ill patients who are on cardiac monitors, a basic understanding of normal and common abnormal electrocardiograph (ECG) patterns is important. An ECG monitors, both visually and on recording paper, the electrical activity of the heart.
Fig. 7.1 illustrates the ECG pattern of a normal cardiac cycle. The P wave reflects depolarization of the atria. The QRS complex represents the depolarization of the ventricles, and the T wave represents ventricular repolarization.
FIGURE 7.1 Electrocardiographic pattern of a normal cardiac cycle.
In normal adults the heart rate is between 60 and 100 beats per minute (bpm). In normal infants the heart rate is 130 to 150 bpm. A number of methods can be used to calculate the heart rate. For example, when the rhythm is regular, the heart rate can be determined at a glance by counting the number of large boxes (on the electrocardiograph [ECG] strip) between two QRS complexes and then dividing this number into 300. Therefore if an ECG strip consistently shows four large boxes between each pair of QRS complexes, the heart rate is 75 bpm (300 ÷ 4 = 75). When the rhythm is irregular, the heart rate can be determined by counting the QRS complexes on a 6-second strip and multiplying by 10. The following heart arrhythmias are commonly seen and should be recognized by the respiratory care practitioner.
Common Heart Arrhythmias2
Sinus Bradycardia
In sinus bradycardia the heart rate is less than 60 bpm. Bradycardia means “slow heart.” Sinus bradycardia has a normal P-QRS-T pattern, and the rhythm is regular (Fig. 7.2). Healthy athletes often demonstrate this finding because of increased cardiac stroke volume and other poorly understood mechanisms. Common pathologic causes of sinus bradycardia include a weakened or damaged sinoatrial (SA) node, severe or chronic hypoxemia, increased intracranial pressure, obstructive sleep apnea, and certain drugs (most notably the beta-blockers). Sinus bradycardia may lead to decreased cardiac output and blood pressure. In severe cases, sinus bradycardia may lead to a decreased vascular perfusion state and tissue hypoxia. The patient may demonstrate a weak pulse, poor capillary refill, cold and clammy skin, and a depressed sensorium.
FIGURE 7.2 Sinus bradycardia at about 40 bpm. (From Aehlert, B. [2018]. ECGs made easy [6th ed.]. St. Louis, MO: Elsevier.)
Sinus Tachycardia
In sinus tachycardia the heart rate is greater than 100 bpm. Tachycardia means “fast heart.” Sinus tachycardia has a normal P-QRS-T pattern, and the rhythm is regular (Fig. 7.3). Sinus tachycardia is the normal physiologic response to stress and exercise. Common abnormal causes of sinus tachycardia include hypoxemia, severe anemia, hyperthermia, massive hemorrhage, pain, fear, anxiety, hyperthyroidism, and sympathomimetic or parasympatholytic drug administration.
FIGURE 7.3 Sinus tachycardia at about 125 bpm. (From Aehlert, B. [2018]. ECGs made easy [6th ed.]. St. Louis, MO: Elsevier.)
Sinus Arrhythmia
In sinus arrhythmia the heart rate varies by more than 10% from beat to beat. The P-QRS-T pattern is normal (Fig. 7.4), but the interval between groups of complexes (i.e., the R-R interval) varies. Sinus arrhythmia is a normal rhythm in children and young adults. The patient's pulse will often increase during inspiration and decrease during expiration. No treatment is required unless significant alteration occurs in the patient's arterial blood pressure.
FIGURE 7.4 Sinus arrhythmia at 63 to 81 bpm. (From Aehlert, B. [2018]. ECGs made easy [6th ed.]. St. Louis, MO: Elsevier.)
Atrial Flutter
In atrial flutter the normal P wave is absent and replaced by two or more regular sawtooth waves. The QRS complex is normal, and the ventricular rate may be regular or irregular, depending on the relationship of the atrial to the ventricular beats. Fig. 7.5 shows an atrial flutter with a regular rhythm with a 2 : 1 conduction ratio (i.e., two atrial beats for every one ventricular beat). The atrial rate is usually constant, between 250 and 350 bpm, whereas the ventricular rate is in the normal range or elevated. Causes of atrial flutter include hypoxemia, a damaged SA node, and congestive heart failure.
FIGURE 7.5 Atrial flutter. (From Aehlert, B. [2018]. ECGs made easy [6th ed.]. St. Louis, MO: Elsevier.)
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Atrial Fibrillation
In atrial fibrillation, the atrial contractions are disorganized and ineffective, and the normal P wave is absent (Fig. 7.6). The atrial rate ranges from 350 to 700 bpm. The QRS complex is normal, and the ventricular rate ranges from 100 to 200 bpm. Causes of atrial fibrillation include hypoxemia and a damaged SA node. Atrial fibrillation may reduce the cardiac output by 20% because of a loss of atrial filling (the so-called atrial kick). Atrial fibrillation is frequently seen in sleep apnea (see Chapter 32, Sleep Apnea).
FIGURE 7.6 Atrial fibrillation with a ventricular response of 63 to 100 bpm. (From Aehlert, B. [2018]. ECGs made easy [6th ed.]. St. Louis, MO: Elsevier.)
Premature Ventricular Contractions
A premature ventricular contraction (PVC) is not preceded by a P wave. The QRS complex is wide, bizarre, and unlike the normal QRS complex (Fig. 7.7). The regular heart rate is altered by the PVC. The heart rhythm may be very irregular when there are many PVCs. PVCs can occur at any rate. PVCs often occur in pairs. A PVC also may be seen after every normal heartbeat—an arrhythmia called bigeminal PVCs or bigeminy. A PVC also may be seen after every two normal heartbeats—an arrhythmia called trigeminal PVCs or trigeminy. Common causes of PVCs include intrinsic myocardial disease, hypoxemia, acidemia, hypokalemia, and congestive heart failure. PVCs also may be a sign of theophylline or alphastimulant or beta-agonist toxicity.
FIGURE 7.7 Sinus rhythm with premature ventricular complexes (PVCs). The fourth and sixth beats are very different in appearance from the normal conducted sinus beats. Beats 4 and 6 are PVCs. They are not preceded by P waves. (From Grauer,
K. [1998]. A practical guide to ECG interpretation [2nd ed.]. St. Louis, MO: Mosby.)
Ventricular Tachycardia
In ventricular tachycardia the P wave is generally indiscernible, and the QRS complex is wide and bizarre in appearance (Fig. 7.8). The T wave may not be separated from the QRS complex. The ventricular rate ranges from 150 to 250 bpm, and the rate is regular or slightly irregular. The patient's blood pressure is usually decreased during ventricular tachycardia. In fact, ventricular tachycardia may result in a lack of a palpable pulse and a blood pressure of zero. Clinically, the respiratory therapist should note that the treatment and management for ventricular tachycardia—with and without a pulse—is different, but both are medical emergencies.
FIGURE 7.8 Ventricular tachycardia. (From Aehlert, B. [2004]. ECG study cards. St. Louis, MO: Elsevier.)
Ventricular Fibrillation
Ventricular fibrillation is characterized by chaotic electrical activity and cardiac activity. The ventricles literally quiver out of control with no perfusion beat-producing rhythm (Fig. 7.9). During ventricular fibrillation, there is no cardiac output or blood pressure, and the patient will die in minutes without treatment. Ventricular fibrillation is treated with cardiopulmonary resuscitation (CPR) and electric shock (defibrillation). These actions often allow the normal heart rhythm to resume.
FIGURE 7.9 Ventricular fibrillation. (From Aehlert, B. [2018]. ECGs made easy [6th ed.]. St. Louis, MO: Elsevier.)
Asystole (Cardiac Standstill)
Asystole (cardiac standstill) is the complete absence of electrical and mechanical activity. As a result, the cardiac output stops and the blood pressure falls to zero. The ECG tracing appears as a flat line and indicates severe damage to the heart's electrical conduction system (Fig. 7.10). Occasionally, periods of disorganized electrical and mechanical activity may be generated during long periods of asystole; this is referred to as an agonal rhythm or a dying heart. Defibrillation is not effective for this rhythm—CPR and Advanced Cardiovascular Life Support (ACLS) medications are required.
FIGURE 7.10 Asystole. (From Aehlert, B. [2018]. ECGs made easy [6th ed.]. St. Louis, MO: Elsevier.)
Noninvasive Hemodynamic Monitoring Assessments
Hemodynamics describes forces that influence the circulation of blood. The general hemodynamic status of the patient can be monitored noninvasively at the bedside by assessing the heart rate (via an ECG monitor, auscultation, or pulse), blood pressure, and perfusion state. During the acute stages of respiratory disease, the patient frequently demonstrates the hemodynamic changes described in the following paragraphs.
The most common causes of cardiac arrest are ventricular fibrillation, asystole, and pulseless electrical activity (PEA)–also called electrical mechanical dissociation. Advanced Cardiac Life Support (ACLS) and Pediatric Advanced Life Support (PALS) guidelines for cardiac arrest appear in Chapter 33 and Chapter 34. The role of the Respiratory Therapist in these conditions should focus on airway management. Recent literature suggests that the survival and neurological sequelae of cardiac standstill are basically equal whether intubation or bag-mask ventilation is used. The provision of an adequate airway, ventilation, oxygenation, chest compressions and defibrillation are more important than administration of medications and take precedence over initiating an intravenous line or injecting pharmacologic agents. Doses of medication may be administered via an endotracheal tube, but are 2.0-2.5 times the intravenous dose.
Heart Rate (Pulse), Cardiac Output, and Blood Pressure
Abnormal heart rate, pulse, and blood pressure findings frequently develop during the acute stages of pulmonary disease. Tachycardia can result from the indirect response of the heart to hypoxic stimulation of the peripheral chemoreceptors, primarily the carotid bodies. When the carotid bodies are stimulated, reflex signals are sent to the respiratory muscles, which in turn activate the pulmonary reflex; this triggers tachycardia and an increased cardiac output and blood pressure. The increased cardiac output is a compensatory mechanism that at least partially counteracts the hypoxemia produced by the pulmonary shunting in respiratory disorders.
Other causes of increased heart rate, cardiac output, and blood pressure include severe anemia, high fever, anxiety, and hyperthyroidism. When the heart rate increases beyond 150 to 175 bpm, cardiac output and blood pressure begin to decline (Starling's relationship). Bradycardia (reduced heart rate), reduced cardiac output, and hypotension may be seen in acute myocardial infarction. Most severe cardiac arrhythmias result in measurable hypotension.
Perfusion State
The perfusion of the body state can be evaluated by examining the patient's skin color, capillary refill, and sensorium. Under normal conditions the patient's nail beds and oral mucosa are pink. If these areas appear cyanotic or mottled, poor perfusion and tissue hypoxia are likely to be present. When the nail beds are compressed to expel blood, they should refill and turn pink within 2 seconds when the pressure is released (capillary refill test). If the nail beds remain white, perfusion is inadequate. Under normal conditions the patient's skin should be dry and warm. When the skin is diaphoretic (wet), cool, or clammy, local perfusion is inadequate. Finally, when the patient is disoriented as to person, place, and time, a decreased perfusion state and cerebral hypoxia may be present.
Invasive Cardiovascular Monitoring Assessments
Invasive monitoring is used in the assessment and treatment of critically ill patients. Invasive cardiovascular monitoring includes the measurement of (1) intracardiac pressures and flows via a pulmonary artery catheter, (2) arterial pressure via an arterial catheter (systemic), (3) central venous pressure via a central venous catheter and (4) coronary artery pathology (e.g., the use of the procedure coronary angiography in severe arteriosclerotic heart disease and angina pectoris). Monitoring of these parameters provides rapid and precise measurements (assessment data) of the patient's cardiovascular function, which in turn are used to down-regulate or up-regulate the patient's treatment plan in a timely manner.
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Pulmonary Artery Catheter
Right-heart catheterization assists in the diagnosis and management of heart valve problems, congestive heart failure, and pulmonary hypertension. The pulmonary artery catheter (Swan-Ganz catheter) is a balloon-tipped, flow-directed catheter that is inserted at the patient's bedside; the respiratory therapist monitors the pressure waveform as the catheter, with the balloon inflated, is guided by blood flow through the right atrium and right ventricle into the pulmonary artery (Fig. 7.11).
FIGURE 7.11 Insertion of the pulmonary catheter (shown in blue in the illustration). The preferred insertion site is the right internal jugular (IJ) vein. Other possible sites are the basilic, brachial, femoral, subclavian, or internal insertion sites. As the catheter advances, pressure readings and waveforms are monitored to determine the catheter's position as it moves through the
right atrium (RA), right ventricle (RV), mean pulmonary artery (
), and finally into a pulmonary capillary wedge pressure (PCWP) position. Immediately after a PCWP reading, the balloon is deflated to allow blood to flow past the tip of the catheter. When the balloon is deflated, the catheter continuously monitors the pulmonary artery pressure.
The pulmonary artery catheter is used to directly measure the (1) right atrial pressure (via the proximal port), (2) pulmonary artery pressure (via the distal port), (3) left atrial pressure (indirectly via the pulmonary capillary wedge pressure [PCWP]), (4) cardiac output via the thermodilution technique,3 and (5) oxygenation levels in the central
venous blood to be used for oxygen transport studies ( |
, VO2, O2ER, |
, and Qs/QT) (see Chapter 6, |
Assessment of Oxygenation).
The insertion of a pulmonary catheter is not without risks and can be life-threatening. For example, it can lead to arrhythmias, rupture of the pulmonary artery, thrombosis, infection, pneumothorax, and bleeding. Because of the high risk to benefit ratio associated with the insertion of the pulmonary artery catheter, its use is reserved for only the most critically ill patients.
Systemic Arterial Catheter
The systemic arterial catheter (referred to as an a-line) is the most commonly used mode of invasive hemodynamic monitoring. It is generally inserted in the radial artery for patient comfort and convenient access. The indwelling arterial catheter allows (1) continuous and precise measurements of systolic, diastolic, and mean blood pressure; (2) accurate information regarding fluctuations in blood pressure; and (3) guidance in the decision to up-regulate or down-regulate therapy—for example, in hypotension or hypertension. The arterial catheter is also useful in patients who require frequent or repeated arterial blood gas samples (e.g., the patient being mechanically ventilated). The blood samples are readily available, and the patient is not subjected to the pain of repeated arterial punctures.
Central Venous Pressure Catheter
The central venous pressure (CVP) catheter readily measures the CVP and the right ventricular filling pressure. It serves as an excellent monitor of right ventricular function. An increased CVP reading is commonly seen in patients who
(1) have left ventricular heart failure (e.g., pulmonary edema), (2) are receiving excessively high positive-pressure mechanical breaths, (3) have cor pulmonale, or (4) have a severe flail chest, pneumothorax, or pleural effusion.
Table 7.1 summarizes the hemodynamic parameters that can be measured directly. Table 7.2 lists the hemodynamic parameters that can be calculated from results obtained from these direct measurements.
TABLE 7.1
Hemodynamic Values Measured Directly
Hemodynamic Value |
Abbreviation |
Normal |
|
|
Range |
Central venous pressure |
CVP |
0–8 mm Hg |
Right atrial pressure |
RAP |
0–8 mm Hg |
Mean pulmonary artery pressure |
|
10– |
|
|
20 mm Hg |
Pulmonary capillary wedge pressure (also called pulmonary artery wedge, pulmonary |
PCWP |
4–12 mm Hg |
artery occlusion) |
PAW |
|
|
PAO |
|
Cardiac output |
CO |
4–6 L/min |
TABLE 7.2
Hemodynamic Values Calculated From Direct Hemodynamic Measurements
Hemodynamic Value |
Abbreviation |
Normal Range |
Stroke volume |
SV |
40–80 mL |
Stroke volume index |
SVI |
40 ± mL/beat/m2 |
Cardiac index |
CI |
3.0 ± 0.5 L/min/m2 |
Right ventricular stroke work index |
RVSWI |
7–12 g/m2 |
Left ventricular stroke work index |
LVSWI |
40–60 g/m2 |
Pulmonary vascular resistance |
PVR |
50–150 dynes × s × cm–5 |
Systemic vascular resistance |
SVR |
800–1500 dynes × s × cm–5 |
Cardiovascular (Hemodynamic) Monitoring in Respiratory Diseases
Because respiratory disorders can have a profound effect on the cardiopulmonary system, the data generated by the previously described invasive cardiovascular monitors can be used in the assessment and treatment of these patients. For example, respiratory diseases associated with severe or chronic hypoxemia, acidemia, or pulmonary vascular obstruction can increase the pulmonary vascular resistance (PVR) significantly. An increased PVR, in turn, can lead to a variety of secondary hemodynamic changes such as increased CVP, right atrial pressure (RAP), mean pulmonary artery pressure (
), right ventricular stroke work index (RVSWI), and decreased cardiac output (CO), stroke volume (SV), stroke volume index (SVI), cardiac index (CI), and left ventricular stroke work index (LVSWI). Table 7.3 lists common hemodynamic changes seen in pulmonary diseases discussed in this volume.
TABLE 7.3
Hemodynamic Changes Commonly Seen in Respiratory Diseases
Disorder |
Cardiovascular Indices |
|
|
|
|
|
|
|
||||
CVP RAP |
|
PCWP CO SV SVI CI |
RVSWI LVSWI PVR SVR |
|||||||||
|
|
|||||||||||
|
|
|
|
|
|
|
|
|
|
|
|
|
Chronic obstructive pulmonary disease (COPD) |
↑ |
↑ |
↑↑ |
~ |
~ |
~ |
~ |
~ |
↑ |
~ |
↑ |
~ |
Chronic bronchitis |
|
|
|
|
|
|
|
|
|
|
|
|
Emphysema |
|
|
|
|
|
|
|
|
|
|
|
|
Cystic fibrosis |
|
|
|
|
|
|
|
|
|
|
|
|
Bronchiectasis |
|
|
|
|
|
|
|
|
|
|
|
|
Pulmonary edema (cardiogenic) |
~ |
↑ |
↑ |
↑↑ |
↓ |
↓ |
↓ |
↓ |
↑ |
↓ |
↑ |
↓ |
Pulmonary embolism |
↑ |
↑ |
↑↑ |
↓ |
↓ |
↓ |
↓ |
↓ |
↑ |
↓ |
↑ |
~ |
Acute respiratory distress syndrome (ARDS)— |
~↑ |
~↑ |
~↑ |
~ |
~ |
~ |
~ |
~ |
~↑ |
~ |
~↑ |
~ |
severe |
|
|
|
|
|
|
|
|
|
|
|
|
Lung collapse |
↑ |
↑ |
↑ |
↓ |
↓ |
↓ |
↓ |
↓ |
↑ |
↓ |
↑ |
↓ |
Flail chest |
|
|
|
|
|
|
|
|
|
|
|
|
Pneumothorax |
|
|
|
|
|
|
|
|
|
|
|
|
Pleural disease (e.g., hemothorax) |
|
|
|
|
|
|
|
|
|
|
|
|
Kyphoscoliosis |
↑ |
↑ |
↑ |
~ |
~ |
~ |
~ |
~ |
↑ |
~ |
↑ |
~ |
Pneumoconiosis |
↑ |
↑ |
↑↑ |
~ |
~ |
~ |
~ |
~ |
↑ |
~ |
↑ |
~ |
Chronic interstitial lung diseases |
↑ |
↑ |
↑↑ |
~ |
~ |
~ |
~ |
~ |
↑ |
~ |
↑ |
~ |
Cancer of the lung (tumor mass) |
↑ |
↑ |
↑ |
↓ |
↓ |
↓ |
↓ |
↓ |
↑ |
~ |
↑ |
~ |
Hypovolemia |
↓↓ |
↓ |
↓ |
↓ |
↓ |
↓ |
↓ |
↓ |
↓ |
↓ |
~ |
↑ |
Hypervolemia (burns) |
↑↑ |
↑ |
↑ |
↑ |
↑ |
↑ |
↑ |
↑ |
↑ |
↑ |
~ |
~ |
Right-heart failure (cor pulmonale) |
↑↑ |
↑↑ |
↓ |
↓ |
~ |
~ |
~ |
~ |
~ |
~ |
~ |
~ |
~, Unchanged; CI, cardiac index; CO, cardiac output; CVP, central venous pressure; LVSWI, left ventricular stroke work index; 
, mean pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; PVR, pulmonary vascular resistance; RAP, right atrial pressure; RVSWI, right ventricular stroke work index; SV, stroke volume; SVI, stroke volume index; SVR, systemic vascular resistance.
Other noninvasive methods used to assess cardiac pathophysiology include cardiac ultrasound and echocardiography, which are discussed in Chapter 8, Radiologic Examination of the Chest.
Self-Assessment Questions
1.In which of the following arrhythmias is there no cardiac output or blood pressure?
a.Ventricular flutter
b.Arial fibrillation
c.Premature ventricular contractions
d.Ventricular fibrillation
2.The general hemodynamic status of the patient can be monitored noninvasively at the patient's bedside by assessing which of the following?
1. Perfusion state
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2.Heart rate
3.Pulse rate
4.Blood pressure
a.4 only
b.2 and 3 only
c.2, 3, and 4 only
d.1, 2, 3, and 4
3.Cardiac output and blood pressure begin to decline when the heart rate increases beyond which of the following?
a.125 to 150 bpm
b.150 to 175 bpm
c.175 to 200 bpm
d.200 to 250 bpm
4.An increased central venous pressure reading is commonly seen in the patient who:
1.Has a severe pneumothorax
2.Is receiving high positive-pressure breaths
3.Has cor pulmonale
4.Is in left-sided heart failure
a.3 only
b.4 only
c.2, 3, and 4 only
d.1, 2, 3, and 4
5.What is the normal range of the mean pulmonary artery pressure?
a.0 to 5 mm Hg
b.5 to 10 mm Hg
c.10 to 20 mm Hg
d.20 to 30 mm Hg
6.What is the normal range for the pulmonary capillary wedge pressure?
a.0 to 4 mm Hg
b.4 to 12 mm Hg
c.12 to 20 mm Hg
d.20 to 25 mm Hg
7.The hemodynamic indices in patients with chronic obstructive pulmonary disease commonly show which of the following?
1.Increased central venous pressure
2.Decreased right atrial pressure
3.Increased mean pulmonary artery pressure
4.Decreased pulmonary capillary wedge pressure
5.Increased cardiac output
a.3 only
b.1 and 3 only
c.2 and 4 only
d.3, 4, and 5 only
8.The hemodynamic indices in patients with pulmonary edema commonly show which of the following? 1. Decreased central venous pressure
2. Increased right atrial pressure
3.Decreased mean pulmonary artery pressure
4.Increased pulmonary capillary wedge pressure
5.Decreased cardiac output
a.1 and 3 only
b.2, 3, and 5 only
c.2, 4, and 5 only
d.1, 2, 4, and 5
9.Atrial flutter is defined as a constant atrial rate of:
a.100 to 150 bpm
b.150 to 250 bpm
c.250 to 350 bpm
d.350 to 450 bpm
10.In sinus arrhythmia, the heart rate varies by more than:
a.5%
b.10%
c.15%
d.20%
1See Appendix XV on the Evolve site for an example of a cardiopulmonary profile sheet used to monitor the hemodynamic status of the critically ill patient.