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figure 17-1 Internal jugular veins. (From Bickley L: Bates' Guide to Physical Examination and Health History [8th Ed], p 32. Philadelphia, Lippincott Williams & Wilkins, 2003.)
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figure 17-2 Assessment of jugular venous pressure. Place the patient supine in bed and gradually raise the head of the bed to 30, 45, 60, and 90 degrees. Using tangential lighting, note the highest level of venous pulsation. Measure the vertical distance between this point and the sternal angle. Record this distance in centimeters and the angle of the head of the bed.
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figure 17-3 Areas of auscultation. I. Aortic area (second intercostal space to the right of the sternum). II. Pulmonic area (second intercostal space to the left of the sternum). III. Tricuspid area (fifth intercostal space to the left of the sternum). IV. Mitral or apical area (fifth intercostal space midclavicular line). (From Bickley L: Bates' Guide to Physical Examination and Health History [8th Ed], p 278. Philadelphia, Lippincott Williams & Wilkins, 2003.)
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figure 17-4 First heart sound.
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figure 17-5 Second heart sound. The second heart sound is produced by the closure of the semilunar valves (aortic and pulmonary). During inspiration, there is an increase in venous return to the right side of the heart, which causes a delay in the emptying of the right ventricle and the closure of the pulmonic valve. This allows the two components of the second heart sound to separate or split during inspiration.
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figure 17-6 Third heart sound. An S3 or ventricular gallop is heard in early diastole, shortly after the second heart sound. The presence of a pathological S3 may be indicative of heart failure.
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figure 17-7 Fourth heart sound. An S4 is a late diastolic sound that occurs just prior to S1. It is a low-frequency sound heard best with the bell of the stethoscope.
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figure 17-8 Summation gallop. With rapid heart rates, S3 and S4 may become audible as a single, very loud sound that occurs in mid-diastole. This sound is a summation gallop.
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figure 17-9 Murmur associated with aortic or pulmonic stenosis. Blood flow through a stenotic aortic or pulmonic valve produces a crescendo-decrescendo midsystolic ejection murmur.
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figure 17-10 Murmur associated with tricuspid or mitral regurgitation. A holosystolic murmur is caused by the regurgitant flow of blood through an incompetent mitral or tricuspid valve. Flow of blood from the left ventricle to the right ventricle through a ventricular septal defect also produces this type of murmur.
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figure 17-11 Murmur associated with aortic or pulmonic insufficiency. Regurgitant flow through an incompetent aortic or pulmonic valve produces a diastolic decrescendo murmur.
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figure 17-12 Murmur associated with tricuspid or mitral stenosis. This low-frequency murmur is heard best with the bell of the stethoscope. It occurs after S1 and has a decrescendo-crescendo configuration.
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figure 17-14 Electrocardiogram electrode placement. The standard left precordial leads are V1, fourth intercostal space, right sternal border; V2, fourth intercostal space, left sternal border; V3, diagonally between V2 and V4; V4, fifth intercostal space, left midclavicular line; V5, same horizontal line as V4, anterior axillary line; V6, same horizontal line as V4 and V5, midaxillary line. The right precordial leads, placed across the right side of the chest, are the mirror opposite of the left leads. For the posterior leads, V7 is placed at the left posterior axillary line, V8 is placed at the left midscapular line, and V8 is placed at the left border of the spine. All are placed on the same horizontal line as V6.
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figure 17-15 Frontal plane leads = standard limb leads, I, II, III, plus augmented leads aVR, aVL, and aVF. This allows an examination of electrical conduction across a variety of planes (e.g., left arm to leg, right arm to left arm).
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figure 17-16 Echocardiographic views of the heart. A cross-section of the heart shows the structures through which the ultrasonic beam passes as it is directed from the apex (1) toward the base (4) of the heart. CW, chest wall; T, transducer; S, sternum; ARV, anterior right ventricular wall; RV, right ventricular cavity; IVS, interventricular septum; LV, left ventricle; PPM, posterior papillary muscle; PLV, posterior left ventricular wall; AMV, anterior mitral valve; PMV, posterior mitral valve; AO, aorta; LA, left atrium.
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figure 17-17 Views of the heart from a transesophageal echocardiogram. (A) Horizontal scan plane of aortic arch and distal portion of aorta. (B) Basal short-axis (transverse), long-axis (sagittal) views, and short-axis views of both atria. (C) Four-chamber and left atrioventricular long-axis views. Sagittal scan plane can image a cross-section of the left ventricle. (D) Transgastric short-axis view of left and right ventricles. (E) Transverse and sagittal scan sections of descending aorta.
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figure 17-18 Ventricular segments of the heart projected on radionuclide planar views. ANT, anterior; LAO, left anterior oblique; LLAT, left lateral.
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figure 17-19 Three-electrode monitoring system. Leads placed in this position allow the nurse to monitor leads I, II, or III. The left leg electrode must be placed below the level of the heart. LA, left arm; LL, left leg; RA, right arm.
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figure 17-20 Einthoven's triangle. Leads I, II, and III are known as the standard leads. When placed together over the chest, they form what is known as Einthoven's triangle.
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figure 17-22 Waveforms of the electrocardiogram. Schematic representation of the electrical impulse as it traverses the conduction system, resulting in depolarization and repolarization of the myocardium.
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figure 17-23 Configurations of the QRS complex. A Q wave is a negative deflection before an R wave, an R wave is a positive deflection, and an S wave is a negative deflection after an R wave.
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figure 17-24 Method for estimating heart rate. Using this method, the heart rate is approximately 85 beats/min.
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figure 17-25A Sinus rhythms. (A) Normal sinus rhythm. (Heart rate = 60-100 beats/min.) (Difference between shortest and longest R-R interval.)
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figure 17-25B Sinus rhythms. (B) Sinus tachycardia. (Heart rate = 100-180 beats/min.) (Difference between shortest and longest R-R interval.)
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figure 17-25C Sinus rhythms. (C) Sinus bradycardia. (Heart rate < 60 beats/min.) (Difference between shortest and longest R-R interval.)
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figure 17-25D Sinus rhythms. (D) Sinus arrhythmia. (Difference between shortest and longest R-R interval.)
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figure 17-26 Sinoatrial block. The pause is a multiple of the basic PP interval.
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figure 17-27 Sick sinus syndrome. Atrial fibrillation is followed by atrial standstill. A sinus escape beat is seen at the end of the strip.
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figure 17-28 Premature atrial contraction.
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figure 17-29 Paroxysmal supraventricular tachycardia, which begins with a premature atrial contraction.
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figure 17-30 Atrial flutter. (Atrial rate = 250-350 beats/min. P wave shows characteristic sawtoothed pattern.)
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figure 17-31 Atrial fibrillation. (Atrial rate = 400-600 beats/min with a variable ventricular response. Characteristic atrial fibrillatory waves seen.)
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figure 17-32 Multifocal atrial tachycardia. (The atrial rate exceeds 100 beats/min with three or more different P-wave morphologies.)
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figure 17-33A Junctional rhythm. (A) A junctional rhythm in which the inverted P wave appears before a normal QRS complex.
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figure 17-33B Junctional rhythm. (B) A junctional rhythm in which the inverted P wave is buried inside the QRS complex.
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figure 17-33C Junctional rhythm. (C) A junctional rhythm in which the inverted P wave follows the QRS complex.
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figure 17-34 Premature junctional contraction.
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figure 17-35 Ventricular arrhythmias. (A) Premature ventricular contractions (PVCs). (B) Ventricular bigeminy. (Every other beat is a PVC.) (C) Multiformed PVCs. (D) Couplet (two PVCs in a row). (E) Triplet. (Short run of ventricular tachycardia [VT]; the first three beats are VT with the rhythm converting to sinus rhythm with first-degree heart block.)
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figure 17-36 R-on-T premature ventricular contraction. (From Huff J: ECG Workout [4th Ed], p 195. Philadelphia, Lippincott Williams & Wilkins, 2002.)
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figure 17-37 Ventricular tachycardia. (From Huff J: ECG Workout [4th Ed], p 197. Philadelphia, Lippincott Williams & Wilkins, 2002.)
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figure 17-38 Torsades de pointes.
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figure 17-39 Ventricular fibrillation.
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figure 17-40 Accelerated idioventricular rhythm. The first three beats are of ventricular origin. The fourth beat (arrow) represents a fusion beat. The subsequent two beats are of sinus origin.
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figure 17-41 Heart block rhythms. (A) First-degree heart block. (From Huff J: ECG Workout [4th Ed], p 156. Philadelphia, Lippincott Williams & Wilkins, 2002.) (B) Second-degree heart block: Mobitz type I. (From Huff J: ECG Workout [4th Ed], p 150. Philadelphia, Lippincott Williams & Wilkins, 2002.) (C) Second-degree heart block: Mobitz type II. Arrows denote blocked P wave (2:1 block). (D) Third-degree heart block (complete atrioventricular block). Arrows denote P waves. Note the lack of relationship between the atria (P wave) and ventricles (QRS).
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figure 17-42 Electrocardiographic views of the heart.
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figure 17-43 Determining electrical axis. To determine the axis of the heart, examine the direction of the QRS complex in leads I and aVF.
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figure 17-44A Comparison of right versus left bundle branch block. (A) A normal V1 tracing. Note the small narrow R and deep narrow S wave.
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figure 17-44B Comparison of right versus left bundle branch block. (B) V1 tracing showing the wide QRS complex and double-peaked R wave, indicating a right bundle branch block.
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figure 17-44C Comparison of right versus left bundle branch block. (C) A normal V6 tracing. Note the tall narrow R wave and absent S wave.
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figure 17-44D Comparison of right versus left bundle branch block. (D) A V6 tracing showing the side QRS complex and double-peaked R wave, indicating a left bundle branch block.
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figure 17-44E Comparison of right versus left bundle branch block. (E) A V1 tracing. Note the small narrow R and deep wide S wave, indicating a left bundle branch block.
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figure 17-45 Right versus left atrial enlargement. (A) The normal P wave in leads II and V1. (B) Right atrial enlargement. Note the increased amplitude of the early, right atrial component of the P wave in V1 and the tall, pointed P wave in lead II. (C) Left atrial enlargement. Note the increased amplitude and duration of the P wave in V1 and the broad, notched P wave in lead II.
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figure 17-46 The effect of hyperkalemia on an ECG. (A) This waveform is produced when the serum potassium level falls within the normal range-usually considered to be 3.5 to 5 mEq/L. (B) When the serum potassium level rises above 5.5 mEq/L, the T wave begins to peak (see highlighted area). The P wave and QRS complex are normal. (C) When the potassium level exceeds 6.5 mEq/L, the P wave grows wider and its amplitude falls. The QRS complex also widens (see highlighted area) as intraventricular conduction velocity diminishes. (D) When the potassium level reaches 10 mEq/L, the P wave becomes almost indiscernible; the QRS complex is slurred and widened (see highlighted area). (E) When the potassium level ranges from 10 to 12 mEq/L, the P wave is undetectable (see highlighted area), because the atria are no longer excitable. (F) When the potassium level exceeds 12 mEq/L, the QRS complex is no longer identifiable. The waves are known as sine waves (see highlighted area). Ventricular fibrillation and cardiac arrest follow. (From Springhouse: ECG Interpretation: Clinical Skillbuilders, p 113. Springhouse, PA, author, 1990.)
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figure 17-47 The effect of hypokalemia on an ECG. (A) When the potassium level is normal-usually considered to be 3.5 to 5 mEq/L-the T wave is much higher than the U wave (see highlighted area).(B) When the potassium level falls to 3 mEq/L, the T wave and U wave are almost the same height (see highlighted area). (C) When the potassium level falls to 2 mEq/L, the U wave starts rising above the T wave (see highlighted area). (D) As the potassium level reaches 1 mEq/L, the U wave starts to resemble a T wave (see highlighted area). The duration of the QT interval remains the same, but it cannot be measured because the two waves are fusing. (From Springhouse: ECG Interpretation: Clinical Skillbuilders, p 114. Springhouse, PA, author, 1990.)
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figure 17-48 The effects of hypercalcemia and hypocalcemia on an ECG. Changes in serum calcium levels are reflected in phase 2 of the action potential. Hypercalcemia shortens the QT interval, whereas hypocalcemia lengthens it (see highlighted areas). (From Springhouse: ECG Interpretation: Clinical Skillbuilders, p 115. Springhouse, PA, author, 1990.)
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figure 17-49 Indwelling arterial catheter. The catheter is attached by pressure tubing to a transducer. The transducer is connected to an amplifier/monitor that visually displays a waveform and systolic, diastolic, and mean pressure values. The system is composed of a flush solution under pressure, a continuous flush device, and a series of stopcocks. The stopcock closest to the insertion site is used to draw blood samples from the artery, and the stopcock located near the transducer is used for zeroing.
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figure 17-50 Square wave test. (A) Optimally damped system: Activation of the fast flush device generates a sharp vertical upstroke, horizontal line, and straight vertical downstroke ending with one or two oscillations (minimal ringing) and quick return to the baseline. (B) Overdamped system: Activation of the fast flush device generates a slurred upstroke and downstroke with no oscillations above or below the baseline. Causes of an overdamped system include system leaks, blood clots, or air bubbles in the tubing or transducer. (C) Underdamped system: Activation of the fast flush device (more than three) above and below the baseline. Usually caused by a small air bubble in the system. (From Darovic GO: Hemodynamic Monitoring: Invasive and Noninvasive Clinical Application, p 161. Philadelphia, W. B. Saunders, 1995.)
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figure 17-51 Modified Allen's test.
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figure 17-52 Normal features of an arterial pressure wave. These include a prominent pulse pressure (50 mm Hg in this patient) and a dicrotic notch (N) signifying closure of the aortic valve. The crisp dicrotic notch indicates a properly responsive catheter system.
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figure 17-53 Measuring central venous pressure (CVP) using a water manometer. (A) System 1 allows for fluid administration. System 2 fills the manometer with fluid. System 3 allows the flow of fluid from the manometer to the patient and determines the CVP reading. (B) Steps in measuring CVP. (1) Stopcock turned so that IV fluid flows to patient. (2) Stopcock in position to fill manometer with fluid. (3) Stopcock turned so that it is open from manometer to patient to obtain reading. (4) Stopcock returned to first position so that IV fluid flows to patient.
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figure 17-54 Pulmonary artery catheter. PAWP, pulmonary capillary wedge pressure. (From Springhouse: Critical Care Made Incredibly Easy, p C1. Springhouse, PA, author, 2004.)
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figure 17-55 Types of pulmonary artery (PA) catheters. (A) Four-lumen catheter. (B) Five-lumen catheter that includes an additional venous infusion port (VIP) into the right atrium. (C) Seven-lumen catheter that includes a VIP port and two additional lumens for continuous cardiac output (CCO) and thermal filament, and continuous mixed venous oxygen saturation (Sv-O2) monitoring (optical module connector). An additional option is to combine use of the CCO filament and the thermistor response time to calculate end-diastolic volume monitoring.
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figure 17-56 Position of the pulmonary artery catheter in the right atrium, right ventricle, and the pulmonary artery. When the balloon is inflated and the catheter is in the wedge position, there is an unrestricted vascular channel between the tip of the catheter and the left ventricle in diastole. Pulmonary artery wedge pressure thus reflects left ventricular end-diastolic pressure, an important indicator of left ventricular function. (Courtesy of Hewlett Packard.)
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figure 17-57 Normal pulmonary artery (PA) waveforms. During PA insertion, the waveforms change as the catheter advances through the heart. (A) When the catheter enters the right atrium, a waveform with two small upright waves appears. The a waves represent the right ventricular end-diastolic pressure; the v waves, right atrial filling. (B) When the catheter reaches the right ventricle, a waveform with sharp systolic upstrokes and lower diastolic dips appears. (C) When the catheter "floats" into the PA, a PA pressure (PAP) waveform appears. Note that the upstroke is smoother than on the right ventricle waveform. The dicrotic notch indicates pulmonic valve closure. (D) When the catheter "floats" into a distal branch of the pulmonary artery, the balloon wedges where the vessel becomes too narrow for it to pass, and a pulmonary artery wedge pressure (PAWP) waveform, with two small upright waves, appears. The a wave represents left ventricular end-diastolic pressure; the v wave, ventricular filling. ECG, electrocardiogram. (From Springhouse: Critical Care Made Incredibly Easy, p 173. Springhouse, PA, author, 2002.)
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figure 17-58 Normal values and wave configurations produced by the pulmonary artery catheter.
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figure 17-59 Pulmonary artery wedge pressure (PAWP) tracing showing respiratory variation from positive pressure mechanical ventilation. Measurement of PAWP is made at the mean point of end expiration.
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figure 17-60 Dubois body surface chart (as prepared by Boothby and Sandiford of the Mayo Clinic). To find the body surface area of a patient, locate the height in inches (or centimeters) on scale I and the weight in pounds (or kilograms) on scale II, and place a straightedge (ruler) between these two points, which intersect scale III at the patient's surface area.
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figure 17-61 A closed injectate system for measurement of cardiac output.
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figure 17-62A Thermodilution curves produced on a strip chart recorder. (A) Smooth recording is accurate.
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figure 17-62B Thermodilution curves produced on a strip chart recorder. (B) Irregular recording is distorted, probably because of irregular or uneven emptying of the injectate syringe.
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figure 17-63 Delivery-dependent oxygen consumption curve reflecting the change in oxygen consumption related to oxygen delivery. At the point of critical oxygen delivery, oxygen delivery is sufficient to meet oxygen demand, and oxygen consumption does not increase further. However, any decrease in oxygen delivery from this point results in a decrease of oxygen consumption due to an inadequate supply of oxygen.
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