From O’Toole M, editor: Miller-Keane encyclopedia and dictionary of medicine, nursing, and allied health, revised revision, Philadelphia, 2005, Saunders.

2. Cardiac impulse travels to the AV node, bundle of His, and the Purkinje fibers, which are represented on the ECG as the PR interval.

3. Cardiac impulse reaches muscles in the ventricles, causing ventricular depolarization (contraction), which is represented on the ECG as the QRS complex.

4. Ventricular repolarization is represented on the ECG as the ST segment and T wave.

I. Basic Steps to ECG Interpretation

1. Calculate heart rate

a. As mentioned, most ECG paper has 3-s intervals marked off at the top of the paper. Count the number of R waves in a 6-s period and multiply by 10 to obtain the number of beats/minute.

b. Normal rate: 60 to 100 beats/min

c. Bradycardia: less than 60 beats/min

d. Tachycardia: more than 100 beats/min

2. Determine regularity of the rhythm

a. Using calipers, measure the distance between a pair of R waves. Leave the calipers at that distance, and measure the next pair of R waves to determine whether the distance is the same.

b. Continue measuring the distance between successive pairs of R waves to determine whether it is constant. If the distances remain constant, the rhythm is regular.

3. Observe P waves and PR interval

a. Make sure that there is a P wave before every QRS complex and that they are of the same shape.

b. Using calipers, measure several PR intervals to determine whether they are consistent.

c. As stated earlier, the normal PR interval is 0.12 to 0.20 s. If the PR interval is longer than 0.20 s, first-degree heart block is present.

4. Determine length of the QRS complex

a. Remember, the QRS complex represents the time it takes for ventricular depolarization to occur. The normal QRS complex takes 0.06 to 0.12 s; any longer duration would indicate heart block.

Exam Note

If all the above observations are within normal limits, the ECG shows normal sinus rhythm.

J. Cardiac Arrhythmias: most often encountered by RCPs

1. Sinus bradycardia

FIGURE 9-9 Sinus bradycardia.

From Davis D: Differential diagnosis of arrhythmias, ed 2, Philadelphia, 1997, Saunders.

a. Rate: less than 60 beats/min

b. Rhythm: regular

c. Wave pattern abnormalities: none

d. Cause: stimulation of vagus nerve (e.g., during tracheal suctioning), hypothermia, increased ICP; sinus bradycardia may be normal in well-conditioned athletes.

e. Treatment: If accompanied by shortness of breath, hypotension, or abnormal beats, atropine is used; a pacemaker may also be indicated.

2. Sinus tachycardia

FIGURE 9-10 Sinus tachycardia.

From Davis D: Differential diagnosis of arrhythmias, ed 2, Philadelphia, 1997, Saunders.

a. Rate: 100 to 160 beats/min

b. Rhythm: regular

c. Wave pattern abnormalities: none

d. Cause: hypoxemia, increased sympathetic nervous system stimulation (e.g., fear, anxiety), medication

e. Treatment: stop underlying cause; administration of digitalis or beta blockers

3. Sinus arrhythmia

FIGURE 9-11 Sinus arrhythmia.

From Davis D: Differential diagnosis of arrhythmias, ed 2, Philadelphia, 1997, Saunders.

a. Rate: 60 to 100 beats/min

b. Rhythm: irregular

c. Wave pattern abnormalities: R to R cycles vary more than 0.16 s. In Figure 9-11, note how the distance between the R wave of the QRS complex varies and is inconsistent.

d. Cause: none; normal in young, healthy individuals; heart rate may increase during inspiration and decrease during expiration.

e. Treatment: none necessary

4. Premature Atrial Contraction

FIGURE 9-12 Premature atrial contraction (PAC).

From Davis D: Differential diagnosis of arrhythmias, ed 2, Philadelphia, 1997, Saunders.

a. Rate: 60 to 100 beats/min. Less than 6 PACs per minute is considered a minor arrhythmia; more than 6 PACs per minute is considered major arrhythmia.

b. Rhythm: regular, except for PAC

c. Wave pattern abnormalities: the premature P wave looks different than the sinus P wave; the PAC occurs sooner than the next beat would be expected.

d. Cause: atrial irritability caused by organic heart disease, CNS disturbances, sympathomimetic drugs, tobacco, caffeine

e. Treatment: if more than 6 PACs per minute, lidocaine may be used

5. Premature Ventricular Contraction

FIGURE 9-13 Premature ventricular contraction (PVC).

From Davis D: Differential diagnosis of arrhythmias, ed 2, Philadelphia, 1997, Saunders.

a. Rate: 60 to 100 beats/min; less than 6 PVCs per minute is considered minor and more than 6 PVCs per minute is considered major.

b. Rhythm: regular, except for PVCs

Exam Note

When every other beat is a PVC, the arrhythmia is termed bigeminy, which is considered a dangerous arrhythmia.

c. Wave pattern abnormalities: the shape of the QRS complex is abnormal and wider than 0.12 s.

d. Cause: ventricular irritability caused by hypoxia, acid–base disturbances, electrolyte abnormalities, excessive dose of digitalis, CHF, myocardial inflammation, coronary artery disease

e. Treatment: lidocaine IV or other antiarrhythmia drugs, such as procainamide or propranolol if more than 6 PVCs per minute

6. Atrial fibrillation

FIGURE 9-14 Atrial fibrillation.

From Davis D: Differential diagnosis of arrhythmias, ed 2, Philadelphia, 1997, Saunders.

a. Rate: variable; atrial rate greater than 350 beats/min

b. Rhythm: irregular

c. Wave pattern abnormalities: P waves cannot be distinguished and have an uneven baseline; PR interval is also indistinguishable.

d. Cause: hypoxia, arteriosclerotic heart disease, mitral stenosis, valvular heart disease

e. Treatment: cardioversion, propranolol, digitalis

Exam Note

Atrial fibrillation is considered to be a major arrhythmia, whereby the atria fail to pump blood adequately to the ventricles, which results in a significant decrease in cardiac output.

7. Atrial flutter

FIGURE 9-15 Atrial flutter.

From Davis D: Differential diagnosis of arrhythmias, ed 2, Philadelphia, 1997, Saunders.

a. Rate: atrial, 200 to 400 beats/min; ventricular, 60 to 150 beats/min

b. Rhythm: regular or irregular

c. Wave pattern abnormalities: P waves have a characteristic sawtooth pattern and thus are often referred to as “F” waves

d. Cause: hypoxia, arteriosclerotic heart disease, MI, rheumatic heart disease

e. Treatment: cardioversion, carotid artery massage, procainamide, digitalis, tranquilizers

Atrial flutter is an arrhythmia that results in blockade of atrial impulses in what is called a 2 : 1, 3 : 1, or 4 : 1 block. In a 2 : 1 block, there are two atrial impulses for each ventricular beat, and there are three or four impulses to each ventricular beat in a 3 : 1 or 4 : 1 block, respectively.

8. Ventricular tachycardia (lethal)

FIGURE 9-16 Ventricular tachycardia (lethal).

From Davis D: Differential diagnosis of arrhythmias, ed 2, Philadelphia, 1997, Saunders.

a. Rate: 140 to 200 beats/min

b. Rhythm: regular

c. Wave pattern abnormalities: P waves and PR intervals are absent or hidden in the QRS complex; each QRS is wider than normal and is a run of three or more PVCs.

d. Cause: arteriosclerotic heart disease, coronary artery disease, myocardial ischemia, mitral valve prolapse, hypertensive heart disease

e. Treatment: lidocaine, defibrillation, CPR

9. Ventricular fibrillation (lethal)

FIGURE 9-17 Ventricular fibrillation (lethal).

From Davis D: Differential diagnosis of arrhythmias, ed 2, Philadelphia, 1997, Saunders.

a. Rate: cannot be determined

b. Rhythm: cannot be determined

c. Wave pattern abnormalities: no distinguishable waves

d. Cause: coronary artery disease, hypertensive heart disease, acute MI, digitalis overdose

e. Treatment: defibrillation, CPR. If this arrhythmia is not reversed, death soon results because there is essentially no blood being pumped out of the heart.

10. First-degree heart block

FIGURE 9-18 First-degree heart block.

From Davis D: Differential diagnosis of arrhythmias, ed 2, Philadelphia, 1997, Saunders.

a. Rate: 60 to 100 beats/min

b. Rhythm: regular

c. Wave pattern abnormalities: PR interval longer than 0.20 s

d. Cause: complication of digoxin or beta blockers, ischemia of the AV node

e. Treatment: atropine, isoproterenol

11. Second-degree heart block

FIGURE 9-19 Second-degree heart block. Electrocardiographic (ECG) tracing showing the widened QRS complex.

From Levitsky MG, Cairo JN, Hall SM: Introduction to respiratory care, Philadelphia, 1990, Saunders.

a. Rate: 60 to 100 beats/min

b. Rhythm: regular or irregular

c. Wave pattern abnormalities: the QRS complex is normal but may be preceded by two to four P waves.

d. Cause: myocardial ischemia; may be a progression from first-degree block

e. Treatment: isoproterenol, atropine; pacemaker

12. Third-degree heart block

FIGURE 9-20 Third-degree heart block. Electrocardiographic (ECG) tracing showing the widened QRS complex.

From Levitsky MG, Cairo JN, Hall SM: Introduction to respiratory care, Philadelphia, 1990, Saunders.

a. Rate: atrial rate, normal; ventricular rate, less than 40 beat s/min

b. Rhythm: Atrial and ventricular rhythm are regular but are independent of each other.

c. Wave pattern abnormalities: PR interval cannot be determined; QRS complex may be normal or widened.

d. Cause: myocardial ischemia, AV node damage

e. Treatment: pacemaker

13. Pulseless Electrical Activity (PEA)

a. A condition in which there is dissociation between the electrical and mechanical activity of the heart. The ECG pattern that appears on the oscilloscope (or ECG monitor) does not reflect the actual mechanical activity of the heart.

b. For example, the ECG may show regular QRS complexes, but the patient has no pulse. Certainly, the tracing should be ignored and chest compressions started.

c. Although PEA is not common, it is often associated with cardiac trauma, tension pneumothorax, severe electrolyte disturbances, and severe acid–base imbalances.

K. Electric Cardiac Pacemakers

FIGURE 9-21 Electric cardiac pacemaker.

1. Electric pacemakers are devices used to replace the heart’s natural pacemaker (SA node); they control the contractions of the heart by a series of rhythmic electrical discharges.

2. External pacemaker: The electrodes that deliver the discharges are placed on the outside of the chest.

3. Internal pacemaker: The electrodes are placed inside the chest wall.

4. The transvenous pacemaker, a temporary internal pacer, is introduced into a peripheral vein and, with the use of fluoroscopy and ECG monitoring, is advanced through the superior vena cava and right atrium and positioned in the right ventricle.

Indications for the temporary transvenous pacemaker are second- and third-degree heart blocks, ventricular asystole, and other arrhythmias resulting in symptomatic bradycardia.

5. A pacer spike is a straight line observed on the ECG strip.

6. To treat permanent arrhythmias, permanent pacemakers are surgically implanted.

7. The electrodes are attached to a battery-operated pace generator, which fires impulses at a specific rate continuously, or to a demand-type pacer, which fires if the patient’s heart rate slows to a pre-set rate.

8. The RCP must know whether the patient has a temporary pacemaker before beginning a treatment, such as CPT, because this type of pacemaker can be dislodged with vigorous movement.

L. Holter Monitoring

1. A Holter monitor is a portable, battery-powered recording device that records the patient’s ECG tracing while the patient conducts daily activities. The monitoring is generally done over 24 h.

2. The patient keeps a diary of activity throughout the day so that it can be compared with the ECG recording. The patient records any symptoms in the diary, which are later correlated to the ECG at that specific time.

3. Because arrhythmias and inadequate blood flow to the heart may occur only briefly or unpredictably, this method of monitoring is useful in patients experiencing irregular heart beats on an inconsistent basis.

II. HEMODYNAMIC MONITORING

CRT Exam Content Matrix: IA8b, IB9i, IB10i, IC10, IIIE3e, IIIE4c

RRT Exam Content Matrix: IA8b, IB9i, IB9r, IB10m, IB10s, IC11-12, IIA9a-b, IIIE3d, IIIE4a, IIIJ6

A. Arterial Catheter (Arterial “Line”)

1. Systemic arterial blood pressure is most accurately measured by placing a catheter directly into a peripheral artery.

2. Peripheral arterial lines should be used in patients with hemodynamic instability. Along with the measurement of blood pressure, these lines provide a direct route for the frequent blood samples drawn from these patients.

3. The most common peripheral artery sites are as follows

a. Radial: most common because of easy access and good collateral circulation (with ulnar artery). The Allen test must be performed before puncture to determine whether collateral circulation is present. (See Chapter 10 on ABG interpretation.)

b. Brachial

c. Femoral

4. Sterile technique should be used when the 18- or 20-gauge catheter is placed into the artery by either surgical cutdown or percutaneous puncture. The catheter is connected to a system that delivers a continuous flow of fluid from an IV bag to maintain patency of the system. The IV bag, which should contain normal saline with added heparin, is pressurized by a hand-bulb pressure pump.

5. The system is also equipped with stopcocks to allow for calibration with atmospheric pressure and for arterial sampling.

6. A strain gauge pressure transducer (the most commonly used transducer) is connected to the system to provide a display of the pressure waveform and a digital reading of the arterial pressure in millimeters of mercury.

FIGURE 9-22

7. Pressures measured on the arterial waveform

a. Systolic pressure: equal to the peak of the waveform (normally 90 to 140 mm Hg). Systole occurs as the heart contracts, forcing blood through the aorta (to the systemic circulation) and pulmonary arteries (to the lungs).

b. Diastolic pressure: measured at the lowest point of the waveform (normally 60 to 90 mm Hg). Diastole occurs in between the contractions of the atria and ventricles (or while the heart is at rest), as these chambers begin refilling with blood.

c. Pulse pressure: the difference between the systolic and diastolic pressures (normally about 40 mm Hg).

d. Mean arterial pressure: represents the average pressure during the cardiac cycle (normally 80 to 100 mm Hg).

e. Note the dicrotic notch on the waveform. It represents the closing of the aortic valve. If the dicrotic notch is not visible, the pressure is most likely inaccurate, in that the values are lower than the patient’s actual pressure. The dicrotic notch may disappear when the systolic pressure drops below 50 to 60 mm Hg. At this point it is difficult to palpate or hear a cuff pressure.

8. Complications of arterial catheters

a. Infection: risk may be reduced with removal of the catheter within 4 days.

b. Hemorrhage: make sure all connections in the system are tight.

c. Ischemia: note the color and temperature of the skin distal to the insertion site to determine distal perfusion.

d. Thrombosis and embolization: a weak pulse distal to the puncture site may indicate thrombosis. A continuous flush of saline and heparin through the system helps to avoid clot formation.

Exam Note

The catheter site and points distal to it should be assessed frequently by the respiratory therapist for signs of the above complications.

9. Troubleshooting for arterial lines

a. “Damped” pressure tracing; causes include

(1) Occlusion of the catheter tip by a clot: correct by aspiration of the clot and flushing with heparinized saline.

(2) Catheter tip resting against the wall of the vessel: correct by repositioning catheter while observing waveform.

(3) Clot in transducer or stopcock: correct by flushing system and, if no improvement is seen in the waveform tracing, change the stopcock and transducer.

(4) Air bubbles in the line: correct by disconnecting transducer and flushing out air bubbles.

b. Abnormally high or low pressure readings; causes include

(1) Improper calibration: correct by recalibration of monitor and strain gauge.

(2) Improper transducer position: correct by ensuring the transducer is kept at the level of the patient’s heart.

c. No pressure reading; causes include

(1) Improper scale selection: correct by selecting appropriate scale.

(2) Transducer not open to catheter: correct by checking system and making sure the transducer is open to the catheter.

B. Flow-Directed Pulmonary Artery Catheter (Swan-Ganz Catheter)

FIGURE 9-23

1. The Swan-Ganz catheter is a balloon-tipped catheter made of polyvinyl chloride that is used to measure central venous pressure (CVP), pulmonary artery pressure (PAP), and pulmonary capillary wedge pressure (PCWP), sometimes referred to as pulmonary artery wedge pressure (PAWP).

2. The catheter also allows for the aspiration of blood from the pulmonary artery for mixed venous blood gas sampling and injection of fluids to determine cardiac output.

3. The distal channel (lumen) is used for the measurement of PAP and for obtaining mixed venous blood from the pulmonary artery.

4. The proximal channel (lumen) is used for the measurement of CVP or right atrial pressure and for the injection of fluids to determine cardiac output.

5. The balloon inflation channel controls the inflation and deflation of a small balloon, located about 1 cm from the distal tip of the catheter, and is used to measure PCWP.

6. The fourth channel is an extra port for the continuous infusion of fluid, when necessary.

7. This catheter is also equipped with a computer connector to measure cardiac output with the use of the thermodilution technique.

Some catheters are equipped with only two channels, the distal channel and the balloon inflation channel.

8. Insertion of the Pulmonary Artery Catheter

a. The catheter is inserted through the brachial, femoral, subclavian, or internal or external jugular vein.

b. Continuous monitoring of the catheter pressure and waveform is necessary along with ECG monitoring.

c. Once the vein is entered, the catheter is advanced into the right atrium, at which time the balloon is inflated and the catheter flows through the right atrium, right ventricle, and into the pulmonary artery, where it “wedges” into a distal branch.

d. Pressures and pressure waveform tracings are recorded as the catheter passes through the right side of the heart.

e. Once the catheter “wedges” in a distal branch of the pulmonary artery, the PCWP may be measured, and the balloon should then be deflated, allowing blood flow past the tip of the catheter. Because blood flow is stopped distal to the wedge position when the balloon is inflated, it should not be inflated any longer than 15 to 20 s or pulmonary infarction may occur.

C. Monitoring of CVP, PAP, and PCWP

FIGURE 9-24 A normal pressure waveform tracing of the right atrium (RA), right ventricle (RV), pulmonary artery (PA), and pulmonary artery wedge pressure (PAWP).

Wilkins RL, Stoller JK, Kacmarek R, Egan’s fundamentals of respiratory care, ed 9, St Louis, 2009, Mosby.

1. CVP may be monitored with a pulmonary artery catheter or from a separate CVP catheter that is inserted through the subclavian, jugular, or brachial vein. The CVP catheter is connected to a water manometer, which reads the pressure in cm H₂O. Measuring the CVP with a pulmonary artery catheter gives the pressure in mm Hg.

Exam Note

When CVP is monitored with a water manometer, the manometer must be level with the heart while the patient is lying flat. This method of monitoring CVP is not as accurate as using a Swan-Ganz catheter and is not commonly used.

a. CVP is a measurement of right atrial pressure, which reflects systemic venous return and right ventricular preload. The normal value is less than 8 cm H₂O or less than 6 mm Hg.

b. Conditions that increase CVP

(1) Hypervolemia (volume overload)

(2) Pulmonary hypertension

(3) Right ventricular failure

(4) Pulmonary valve stenosis

(5) Tricuspid valve stenosis

(6) Pulmonary embolism

(7) Arterial vasodilation, resulting in increased blood volume in the venous system

(8) Left heart failure

(9) Improper transducer placement (below the level of the right atrium)

(10) Positive pressure ventilator breath (measure CVP at end of expiration)

(11) Severe flail chest or pneumothorax: these conditions may compress the superior and inferior vena cavae, which would decrease venous return and increase CVP as a result of compression of the heart.

Exam Note

To determine what effect PEEP has on venous return and CVP, measure CVP while the patient continues using PEEP. To determine CVP without the effects of PEEP, discontinue PEEP for the measurement in some patients. However, remember that patients with critical lung conditions using high levels of PEEP cannot tolerate being removed from PEEP; therefore, CVP must be measured while the patient continues using PEEP.

c. Conditions that decrease CVP

(1) Hypovolemia (inadequate circulating blood volume)

(2) Vasodilation (from decreased venous tone)

(3) Leaks or air bubbles in the pressure line

(4) Improper transducer placement (above the level of the right atrium)

2. PAP is an important measurement in the care of critically ill patients with sepsis, ARDS, pulmonary edema, and MI.

a. It is especially important to monitor PAP and PvO₂ values in patients using at least 10 cm H₂O of PEEP because high levels of PEEP may compromise the cardiac status of the patient by decreasing cardiac output and oxygen delivery to the tissues.

b. Mixed venous blood sampling (to measure PvO₂) is achieved by obtaining blood from the pulmonary artery. Normal PvO₂ is 35 to 45 mm Hg. PvO₂ reflects tissue oxygenation. If this level drops after the initiation of or increase in PEEP, then a decrease in tissue oxygenation has occurred, caused by a drop in cardiac output because of PEEP. PEEP should be decreased to maintain an adequate PvO₂. (See Chapter 11 on ventilator management.)

c. Normal systolic PAP is 20 to 30 mm Hg. Normal diastolic PAP is 5 to 15 mm Hg. Normal mean PAP is 10 to 20 mm Hg.

d. Conditions that increase PAP

(1) Pulmonary hypertension (resulting from hypercapnia, acidemia, or hypoxemia, for example)

(2) Mitral valve stenosis

(3) Left ventricular failure

e. Conditions that decrease PAP

(1) Decreased pulmonary vascular resistance (pulmonary vasodilation); caused by improved oxygenation, for example

(2) Decreased blood volume

3. PCWP

a. When the balloon at the distal end of the catheter is inflated, it “wedges” in a branch of the pulmonary artery, blocking blood flow from the right side of the heart. The transducer measures the back pressure through the pulmonary circulation, which is equal to pressure in the left atrium and the left ventricular end-diastolic pressure (LVEDP).

b. PCWP, therefore, is a measurement of pressure in the left side of the heart.

c. As stated, the balloon should not be inflated any longer than 15 to 20 s because blood flow obstructed for any longer may cause pulmonary infarction.

d. The normal PCWP value is 4 to 12 mm Hg. A PCWP value of more than 18 mm Hg usually indicates impending pulmonary edema.

Exam Note

PCWP is elevated in patients with cardiogenic pulmonary edema and is normal in patients with noncardiogenic pulmonary edema.

e. Conditions that increase PCWP

(1) Left ventricular failure

(2) Mitral valve stenosis

(3) Aortic valve stenosis

(4) Systemic hypertension

f. Conditions that decrease PCWP

(1) Hypovolemia

(2) Pulmonary embolism (PCWP may be normal or decreased)

D. Complications of Pulmonary Artery Catheter Insertion

1. Damage to tricuspid valve

2. Damage to pulmonary valve

3. Pulmonary infarction

4. Pneumothorax

5. Cardiac arrhythmias

6. Air embolism

7. Ruptured pulmonary artery

E. Measurement of Cardiac Output

1. Cardiac output may be measured through the pulmonary artery catheter with the use of the thermodilution technique. A cold saline or dextrose solution is injected through the proximal port of the catheter. Heat loss occurs from the injection port to the distal tip of the catheter. The rate of blood flow determines the amount of heat loss and is measured on the cardiac output computer.

2. Cardiac output may be calculated with the use of the Fick equation

QT = cardiac output (L/min)

VO₂ = oxygen consumption (mL/min)

[CaO₂ − CVO₂] = arterial and mixed venous oxygen content difference (milliliters of oxygen per deciliter of blood), also called vol%

Milliliters per deciliter (mL/dL) must be converted to mL/L to express the cardiac output in L/min. This is accomplished by multiplying the oxygen content difference by 10. Normal cardiac output is 5 L/min.

EXAMPLE:

Calculate a patient’s cardiac output given the following information:

F. Measurement of Arterial and Venous O₂ Content

1. O₂ content refers to the total amount of O₂ dissolved in the plasma and bound to Hb in arterial or mixed venous blood.

2. The difference between arterial and venous O₂ content (arteriovenous O₂ content difference) is used to calculate cardiac output and cardiopulmonary shunting.

3. Total O₂ content of arterial blood (CaO₂) is calculated with the use of the following formula:

1.34 mL of O₂ is capable of binding with 1 g of Hb, and 0.003 mL of O₂ is dissolved in the plasma for each 1 mm Hg of PaO₂.

EXAMPLE:

Calculate the total arterial O₂ content from the following data:

Hb	15 g%
SaO₂	98%
PaO₂	86 mm Hg

4. CVO₂ is calculated with the following formula

EXAMPLE:

Calculate the total venous O₂ content, given the following data.

Hb	15 g%
SvO₂	75%
PvO₂	40 mm Hg

Exam Note

The normal C(a − v)O₂, or arteriovenous O₂ content, difference is 4 to 6 mL/dL (or vol%). In the above calculations, the C(a − v)O₂ is

An arteriovenous O₂ content difference of less than 4 vol% may be the result of increased cardiac output (less time for tissues to extract O₂; therefore arterial and venous O₂ are closer in value), septic shock, or anemia.

An arteriovenous O₂ content difference of more than 6 vol% may be the result of decreased cardiac output (more time for tissues to extract O₂ because of slower blood flow; therefore a greater difference is seen between arterial and venous O₂ values).

C(a − v)O₂ is useful in determining the effects that PEEP and mechanical ventilation have on the patient’s cardiac output and in evaluating the patient’s need for more circulatory support.

G. Intrapulmonary Shunting

1. Intrapulmonary shunting is defined as the portion of the cardiac output that perfuses through the lungs without coming in contact with ventilated alveoli. This portion of the cardiac output therefore passes through the lungs and into the left side of the heart without being oxygenated.

2. In a healthy person, intrapulmonary shunting occurs. This results from blood flow through the bronchial, pleural, and thebesian veins. These veins return blood to the left atrium, thus bypassing the oxygenation process in the lungs (called an anatomic shunt). Normally, intrapulmonary shunting is about 2% to 5% of the cardiac output and is primarily caused by anatomic shunting.

3. Physiologic shunting represents only a small portion of the normal anatomic shunt. Increased physiologic shunting results in a worsening cardiopulmonary status.

4. Conditions that increase physiologic shunting

5. The amount of shunt may be determined with the use of the clinical shunt formula

This formula requires a 100% Hb saturation of O₂ in arterial blood.

6. If measurement of PvO₂ is not available (via pulmonary artery catheter), the modified shunt equation may be used:

EXAMPLE:

Calculate a patient’s percentage of shunt given the following data

pH	7.37
PaCO₂	45 mm Hg
PAO₂	60 mm Hg
FiO₂	0.40
PB	747 mm Hg

This means that almost 10% of the patient’s cardiac output is not being oxygenated in the lungs.

Exam Note

A simplified method of calculating shunt is as follows: A−a gradient/20 + 4%. Although not as accurate, it should work fine on the NBRC exams.

7. Interpreting calculated shunt values

a. Less than 10% is normal.

b. Abnormal intrapulmonary status is 10% to 20% and is usually of no significance clinically.

c. Significant intrapulmonary disease is 20% to 30%, may be life-threatening, and requires cardiopulmonary support.

d. More than 30% is a serious, life-threatening condition that requires aggressive cardiopulmonary support.

H. Measuring Cardiac Index

1. Cardiac output varies according to the patient’s body surface area (BSA). The cardiac index (CI) correlates the patient’s cardiac output for his or her specific BSA.

2. Formula for calculation

3. Normal CI is 2.6 to 4.3 L/min/m²

4. Factors that increase CI

a. Drugs that increase cardiac contractility (e.g., dopamine, epinephrine, digitalis)

b. Hypervolemia

c. Decreased vascular resistance

d. Septic shock (early stages)

5. Factors that decrease CI

a. Drugs that decrease cardiac contractility (e.g., propranolol and metoprolol)

b. Hypovolemia

c. CHF

d. Increased vascular resistance

e. MI

f. Septic shock (late stages)

g. Positive pressure ventilation

h. PEEP and CPAP

I. Measuring Stroke Volume

1. Stroke volume (SV) is the amount of blood ejected from the ventricle during ventricular contraction.

2. Formula for calculation

3. Normal SV is 60 to 120 mL/beat.

J. Measuring Systemic Vascular Resistance

1. Systemic vascular resistance (SVR) is a measurement of the resistance that the left ventricle must overcome to eject its volume of blood. This is known as afterload.

2. SVR is calculated with the use of the following formula

MSAP = mean systemic arterial pressure

This resistance formula may be multiplied by 80 to convert to resistance units of dyne × s × cm⁻⁵.

3. Normal SVR is 10 to 18 mm Hg/L/min, or 900 to 1450 dyne × s × cm⁻⁵.

4. Factors that increase SVR

a. Vasoconstrictors (dopamine, epinephrine)

b. Hypovolemia

c. Hypocapnia

5. Factors that decrease SVR

a. Vasodilators (nitroprusside sodium, morphine, nitroglycerin)

b. Hypercapnia

c. Septic shock (early stages)

K. Measuring Pulmonary Vascular Resistance

1. Pulmonary vascular resistance (PVR) is a reflection of the afterload of the right ventricle.

2. PVR is calculated with the use of the following formula

MPAP = mean pulmonary artery pressure

QT = cardiac output (L/min)

PAWP = pulmonary artery wedge pressure

This resistance formula may be multiplied by 80 to convert to resistance units of dyne × s × cm⁻⁵.

3. Normal PVR is 1.5 to 3.0 mm Hg/L/min, or 150 to 250 dyne × s × cm⁻⁵.

4. Factors that increase PVR

a. Vasoconstrictors (dopamine, epinephrine)

b. Hypercapnia

c. Hypoxemia

d. Acidemia

e. Pulmonary embolism

f. Pneumothorax

g. Positive pressure ventilation

h. PEEP and CPAP

5. Factors that decrease PVR

a. Improved oxygenation (pulmonary vasodilator)

b. Alkalemia (hypocapnia)

c. Vasodilating agents

L. Measurement of O₂ Consumption (VO₂)

1. VO₂ is defined as the amount of O₂ (in milliliters) extracted by the peripheral tissues in 1 min. It is also a measurement of the O₂ uptake in the lung.

2. VO₂ may be calculated with the use of the following formula, which is based on the Fick equation

10 = factor to convert C(a − v)O₂ to milliliters of O₂ per liter

EXAMPLE:

Given the following data, calculate a patient’s O₂ consumption (uptake).

QT	5 L/min
CaO₂	20 vol%
CVO₂	14.5 vol%

3. Normal O₂ consumption is 150 to 275 mL/min.

4. Factors that increase VO₂

5. Factors that decrease VO₂

a. Hypothermia

b. Cyanide poisoning

c. Musculoskeletal relaxation

III. CARDIOPULMONARY STRESS TESTING

CRT Exam Content Matrix: IB9r, IB10r, IIIE7e

RRT Exam Content Matrix: IB9s, IB10t, IIIE7e

A. Exercise Stress Testing

1. Exercise stress testing is used to evaluate a patient’s cardiopulmonary reserve capacity.

2. The cardiopulmonary stress test is usually conducted with the patient either pedaling a cycle or walking on a treadmill.

3. Before testing, perform a patient history and physical examination.

The examination should include

a. Pulmonary function tests

b. Carbon monoxide diffusion capacity

c. Arterial blood gas measurements

d. Blood pressure

e. Before and after bronchodilator study (if airflow obstruction exists)

f. Resting ECG

4. Some patients are not ideal candidates for cardiopulmonary stress testing. Below is a list of conditions in which stress testing is contraindicated.

e. Uncontrolled cardiac arrhythmias

f. Dissecting aneurysm

g. Third-degree heart block

h. Myocarditis

5. A physician should always be present during the stress test as well as the following emergency equipment

a. Defibrillator

b. Oxygen source

c. Manual resuscitator with mask

d. Oral airway

e. Laryngoscope and endotracheal tubes

f. IV setup with 5% dextrose

g. Cardiac medications

B. Cardiac Stress Test

1. The patient performs incremental work using either a cycle ergometer or treadmill.

2. The patient’s heart rate, blood pressure, and ECG are monitored before the test.

3. These same variables are measured at the end of each stage of the test and for at least 15 min after the test or until any cardiopulmonary problems decline.

4. Most healthy individuals are able to complete all four stages of the exercise without difficulty. Patients with coronary artery disease may not be able to complete all stages because of dyspnea and angina.

5. This stress test is very useful in diagnosing and treating coronary artery disease but is limited in diagnosing other cardiopulmonary diseases.

C. Cardiopulmonary Stress Test

1. This test requires a cycle ergometer or a treadmill, a system for analyzing exhaled gases, a device for recording ventilation variables, and an oximeter for measuring oxygen saturation or an arterial line for obtaining blood gas measurements.

2. This test also requires the patient to exercise at certain workload increments.

3. Values measured during this test include

e. Oxygen saturation or blood gases

f. Oxygen consumption

g. CO₂ production

h. Respiratory quotient

i. Oxygen pulse (volume of oxygen removed from the blood with each heartbeat; calculated by dividing oxygen consumption by the heart rate)

j. VD/VT ratio

k. Maximum voluntary ventilation (MVV)

l. Anaerobic threshold (the point at which the oxygen requirements of the exercising muscles cannot be met and anaerobic metabolism begins providing the cellular energy supply)

m. The test is discontinued when the patient reaches a predetermined heart rate or if the following signs or symptoms occur

(1) Physical exhaustion

(2) Excessive chest pain

(3) Excessive dyspnea

(4) Excessive fatigue in the legs

(5) PVCs

(6) Ventricular tachycardia

(7) Heart blocks

(8) Hypotension

(9) Patient requests the test to be stopped

POSTCHAPTER STUDY QUESTIONS

1. List four causes of a “damped” arterial pressure waveform.

2. List five conditions that cause an increased CVP.

3. List four conditions that cause a decreased CVP.

4. What are three drugs used to treat PVCs.

5. What is the treatment for ventricular tachycardia?

6. List three conditions that cause an increased PAP.

7. List two conditions that cause a decreased PAP.

8. PAWP is a measurement of what function?

9. List four conditions that cause an increased PCWP.

10. List two conditions that cause a decreased PCWP.

11. List the normal values for CVP, PAP, and PCWP.

12. Calculate the QT of a patient who has a VO₂ of 240 mL/min and a C(a − v)O₂ of 6 vol%.

13. In a healthy person, what percentage of the cardiac output makes up the intrapulmonary shunt?

14. Calculate the C(a − v)O₂, given the following information

15. List four conditions that increase physiologic shunting.

16. Calculate the percentage of intrapulmonary shunt given the following information

17. List four factors that cause an increased SVR.

18. List three factors that cause a decreased SVR.

19. List five factors that cause an increased PVR.

20. List three factors that cause a decreased PVR.

21. Calculate the oxygen consumption given the following information

QT 4.5 L/min

CaO₂ 19 vol%

CVO₂ 14 vol%

22. List four factors that cause an increased O₂ consumption.

23. List three factors that cause a decreased O₂ consumption.

See answers at the back of the text.

Respiratory Care Exam Review Review for the Entry Level and Adva

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