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<HTML> <HEAD> <META NAME="GENERATOR" CONTENT="Adobe PageMill 2.0 Win"> <TITLE>ACLS Chapter 14</TITLE> </HEAD> <BODY TEXT="#bafddc" LINK="#ffcc66" VLINK="#5cf373" BGCOLOR="#006666" ALINK= "#fb1814"> <H1>Chapter 14 Invasive Therapeutic Techniques<HR ALIGN=LEFT></H1> <H1><A NAME="anchor1845"></A>14.1 Introduction</H1> The ACLS provider course presents three invasive therapeutic techniques: pericardiocentesis, intracardiac injections, and relief of tension pneumothorax.<HR ALIGN=LEFT> <A NAME="anchor1"></A> <H1><A NAME="anchor2142"></A>14.2 Pericardiocentesis</H1> <H2>14.2.1 Overview</H2> Pericardiocentesis, or needle aspiration of fluid from the pericardium, is indicated to obtain fluid for diagnostic study, obtain information regarding the physiological mechanism of venous pressure elevation, and relieve cardiac tamponade.<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0001" TARGET="Footnote #1">1</A> This section describes the pathophysiology of cardiac tamponade, the clinical diagnosis of tamponade, and the technique of pericardiocentesis. <A NAME="anchor2"></A> <H2>14.2.2 Anatomy of the Pericardium<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0002" TARGET="Footnote #2">2</A></H2> The pericardium encloses the heart and the first few centimeters of the great vessels in a serous sac lined by mesothelial cells. The visceral pericardium lies close to the heart surface as the epicardium. The pericardial sac normally contains up to 50 mL of fluid with similar or the same composition as serum. In the adipose tissue beneath the visceral pericardium and on the mediastinal aspect of the parietal pericardium are arteries, veins, lymphatics, and nerves. The pericardium reacts to injury by exuding fluid, fibrin, or cells. <A NAME="anchor3"></A> <H2>14.2.3 Cardiac Tamponade</H2> <H3>Pathophysiology</H3> In cardiac tamponade ventricular diastolic filling is impaired. This occurs because of increased pressure from accumulation of fluid within the pericardial sac.<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0003" TARGET= "Footnote #3">3-6</A> Tamponade is most commonly related to one of three causes: (1) trauma, which may be direct or indirect, penetrating or nonpenetrating; (2) infection; and (3) neoplastic disease.<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0007" TARGET="Footnote #7">7</A> Myocardial rupture following acute myocardial infarction, uremia, and collagen-vascular diseases are also important causes of tamponade. Iatrogenic cardiac tamponade may follow cardiac surgery, CPR, or perforation of the heart by a vascular catheter or transvenous pacemaker, or it may be due to radiation or drug reactions, such as to hydralazine or procainamide.<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0008" TARGET="Footnote #8">8</A> <A NAME="anchor4"></A> As fluid is added to the pericardial space, the rate of rise of the pressure within the pericardial space depends on several factors. With acute increases in fluid, as little as 200 mL may produce a marked rise in intrapericardial pressure. This explains why the removal of only small amounts of fluid may be followed by a dramatic decrease in intrapericardial pressure and improvement of the patient. However, with slow accumulation of pericardial fluid over weeks or months, there is a gradual stretching of the pericardium, with an increase in its compliance. More than 2 L of fluid may then accumulate without a severe rise in intrapericardial pressure. <A NAME="anchor5"></A> Hypovolemia may mask the usual clinical manifestations of cardiac tamponade, including jugular venous distention. The dynamics of tamponade may become apparent in some patients only after volume administration. While hypervolemia can accentuate the clinical manifestations of tamponade, cardiac output can be enhanced temporarily by the initial increase in ventricular filling pressure that accompanies volume loading and results in a transient increase in stroke volume.<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0001" TARGET= "Footnote #1">1</A> <A NAME="anchor6"></A> <H3>Diagnostic Considerations<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0001" TARGET="Footnote #1">1-9</A></H3> Pulsus paradoxus, defined as a decline greater than 10 mm Hg in systolic arterial pressure with normal inspiration, is usually present with tamponade. However, considerable effusion may exist without pulsus paradoxus, especially if such effusion complicates left ventricular dysfunction manifested by high left ventricular diastolic pressure, atrial septal defect, aortic insufficiency, positive-pressure breathing, or pulmonary arterial obstruction.<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0010" TARGET="Footnote #10">10-12</A> The term pulsus paradoxus is a misnomer in that the decrease in arterial pressure during inspiration is merely an exaggeration of a normal phenomenon. Without tamponade there is a normal inspiratory decline in systolic pressure of less than 10 mm Hg that is due both to the transmission of the inspiratory decline in intrathoracic pressure to the heart and aorta and to the delay in transit through the lungs of the normal inspiratory increase of right ventricular stroke volume. In the presence of cardiac tamponade there is a normal decrease in intrapericardial pressure with inspiration and a normal increase in right ventricular filling. However, because of competition of the ventricles for space within the distended and restricted pericardial sac and a shift of the ventricular septum to the left, there is selective impairment of left ventricular filling and a decrease in left ventricular stroke volume. There is also increased capacity of the pulmonary veins since there is a greater fall in pulmonary venous pressure than in intrapericardial pressure; this also leads to reduced left ventricular filling. <A NAME="anchor7"></A> Echocardiography may be used not only to document the presence of pericardial effusion but also to show evidence of cardiac tamponade.<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0013" TARGET="Footnote #13">13-16</A> In the presence of tamponade, there is right ventricular compression evidenced by a markedly reduced end-expiratory, end-diastolic dimension due to a sudden increase in anterior motion of the interventricular septum toward the right rather than the left ventricular cavity. Right ventricular compression disappears following pericardiocentesis and is not present with pericardial effusion without tamponade. <A NAME="anchor8"></A> As the rise in pericardial pressure becomes severe, stroke volume decreases and systemic vascular resistance increases, resulting in a fall in systolic pressure, a rise in diastolic pressure, and a narrowing of the arterial pulse pressure. However, hypotension in the presence of tamponade is usually a late finding. <A NAME="anchor9"></A> The electrocardiogram (ECG) often shows low voltage and nonspecific ST-T wave abnormalities. Electric alternans, a beat-to-beat change in the axis of the ECG that is due to a swinging motion of the heart within the pericardial effusion, may be present. Total alternans, which involves the P wave as well as the QRS, may be more specific for pericardial effusion.<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0017" TARGET="Footnote #17">17</A> Electromechanical dissociation also may be a manifestation of cardiac tamponade. <A NAME="anchor10"></A> <H3>Treatment<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0001" TARGET="Footnote #1">1-6</A>,<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0018" TARGET="Footnote #18">18</A></H3> The specific therapy for cardiac tamponade is drainage of the pericardial fluid. However, until drainage can be performed, the following measures may be helpful. <A NAME="anchor11"></A> Volume infusion increases stroke volume in cardiac tamponade by increasing ventricular filling pressure. Rapid intravenous (IV) administration of fluid will provide temporary hemodynamic support for the patient with acute tamponade. The first 500 mL of fluid should be given over a 10-minute period, followed by 100 to 500 mL/h thereafter, according to the patient's response to the initial volume load. The administration of fluid volume appears most beneficial with an acute tamponade<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0019" TARGET="Footnote #19">19</A> but is of limited value when tamponade follows a subacute or chronic pericardial effusion.<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0020" TARGET="Footnote #20">20</A> <A NAME="anchor12"></A> <H2>14.2.4 Description of Pericardiocentesis</H2> Decompression of a pericardial effusion producing cardiac tamponade is always indicated. Surgical decompression is preferred. Needle pericardiocentesis is indicated when cardiac tamponade represents an immediate threat to life, ie, when it produces increasingly severe hemodynamic impairment. In general, pericardiocentesis should be performed in any patient with acute tamponade and respiratory distress, progressive hypotension with jugular venous distention, or other signs of circulatory compromise. Open drainage is safer and more effective. Procedures include subxiphoid pericardiotomy, which not only allows for drainage of pericardial fluid but also permits a biopsy specimen that is especially helpful for the diagnosis of granulomatous and lymphomatous invasion of the pericardium; parietal pericardiectomy (pericardial window) via a left thoracotomy, which provides for continuing drainage of fluid and thereby prevents recurrence; and visceral pericardiectomy, which is necessary for effusive constrictive pericarditis and constrictive pericarditis.<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0002" TARGET="Footnote #2">2</A>,<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0021" TARGET="Footnote #21">21</A> If time and resources permit, most cardiologists now drain pericardial effusions in the catheterization laboratory using fluoroscopy, echocardiography, and flexible catheters introduced by the Seldinger technique. <A NAME="anchor13"></A> Needle pericardiocentesis should be performed only by a skilled and experienced physician. It is optimally performed in the presence of large amounts of pericardial fluid. When time permits, pericardial fluid is best documented and localized by echocardiography. During pericardiocentesis the patient's ECG should be continuously monitored, and ideally, invasive hemodynamic monitoring should be used as well. Full resuscitative equipment, as well as personnel experienced in its use, must be available. Different approaches have been advocated.<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0018" TARGET="Footnote #18">18</A> Some echocardiographic<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0022" TARGET="Footnote #22">22</A>,<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0023" TARGET="Footnote #23">23</A> and autopsy<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0024" TARGET= "Footnote #24">24</A> data suggest that the left fifth intercostal approach <A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/fig14_01.htx" TARGET="_blank">(Fig 1)<IMG SRC="Book_ACLS/ACLS_Source_Art/ico14_01.gif" ALIGN="BOTTOM" WIDTH="41" HEIGHT="32" NATURALSIZEFLAG="3"></A> may be optimal. <A NAME="anchor14"></A> The following technique should be used when the resources of a fully equipped catheterization laboratory are not immediately available. Ideally the ECG V lead should be connected to the needle with a sterile alligator clip with care to ensure that the patient limb leads are attached. If ST-segment elevation occurs as the needle is advanced, ventricular contact is suggested; if PR-segment elevation occurs, atrial contact is suggested. Elevation of both ST and PR segments may also indicate pericardial contact with no intervening fluid within the pericardial sac. However, these are signs indicating need for withdrawal of the needle. Other signs of epicardial contact include atrial and ventricular arrhythmias and atrioventricular conduction abnormalities. Monitoring the ECG from the pericardiocentesis needle may prevent entry of the needle into the pericardium when there is no cushioning layer of fluid present. It also immediately signals entry of the needle into the myocardium, allowing the operator to withdraw the needle and minimize any myocardial or coronary artery laceration. If blood or fluid is obtained without the appearance of ST- or PR-segment shift or cardiac arrhythmias, this is an indication that the fluid was obtained from the pericardial sac rather than the cardiac chamber. However, in the presence of myocardial scarring due to old transmural infarction or infiltrative myocardial disease, the needle may enter an electrically silent area of the myocardium and not produce PR- or ST-segment elevation or cardiac arrhythmias.<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0025" TARGET="Footnote #25">25-27</A> <A NAME="anchor15"></A> If immediate pericardiocentesis is necessary to sustain the life of the patient, an alternative approach is to use the Seldinger technique with a thin scout needle to locate the pericardial space. Once the pericardial space is entered, the guidewire is passed and used to facilitate placement of a large-bore catheter into the space. <A NAME="anchor16"></A> <H3>Equipment Needed</H3> <BLOCKQUOTE> 1. A short-bevel, large-bore needle at least 16 gauge and 9 cm long (a Seldinger catheter set for central venous lines may also be used) <A NAME="anchor17"></A> 2. A 30- or 50-mL syringe <A NAME="anchor18"></A> 3. Sterile alligator connector to ECG V lead <A NAME="anchor19"></A> 4. Povidone-iodine solution for skin preparation <A NAME="anchor20"></A> 5. Syringe with small-bore needle and 1% lidocaine without epinephrine for local anesthetic <A NAME="anchor21"></A> 6. Sterile gloves and sterile drapes; ideally, sterile gowns and face masks <A NAME="anchor22"></A> </BLOCKQUOTE> <H3>Technique <A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/fig14_01.htx" TARGET="_blank">(Fig 1)<IMG SRC= "Book_ACLS/ACLS_Source_Art/ico14_01.gif" ALIGN="BOTTOM" WIDTH="41" HEIGHT="32" NATURALSIZEFLAG="3"></A></H3> <BLOCKQUOTE> 1. Have the patient in a supine position or with the upper torso elevated 20° to 30°. <A NAME="anchor23"></A> 2. Prepare the anterior midthorax with povidone-iodine solution. <A NAME="anchor24"></A> 3. If the patient is conscious or responsive to pain, infiltrate the skin and subcutaneous tissues immediately to the left of the sternum in the fifth intercostal space with 1% lidocaine without epinephrine. A small skin incision with a scalpel blade will facilitate entry of the large-bore needle. <A NAME="anchor25"></A> 4. Attach the large-bore needle to the syringe and connect the alligator clamp with ECG V lead to the needle. Insert the large-bore needle attached to the syringe perpendicular to the frontal plane. Aspiration should be continuous. As the needle is advanced beneath the skin, the resistance of the taut pericardium may be felt, and entry into the pericardial space may produce a distinct "giving" sensation. Contact of the needle against the epicardium may be accompanied by a scratching sensation or by PR- and ST-segment elevation if the ECG V lead is connected to the pericardiocentesis needle as described above. <A NAME="anchor26"></A> 5. If grossly bloody fluid is obtained, it should not clot if from the pericardial space. A spun hematocrit may also denote a difference between venous and bloody pericardial fluids. <A NAME="anchor27"></A> </BLOCKQUOTE> It may be advantageous to insert a catheter into the pericardial space. This avoids the potential epicardial or coronary artery injury that might be produced by the sharp tip of a needle. It also allows for continuous drainage of fluid from the pericardial space. As noted above, use of a Seldinger (guidewire) system is useful for this indication. Use of the wire allows a larger catheter to be passed into the pericardial space than can be inserted through a needle.<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0028" TARGET="_blank">28</A> <A NAME="anchor28"></A> <H3>Alternative Approach<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0018" TARGET="Footnote #18">18</A></H3> Some clinicians prefer the xiphisternal or subxiphoid approach for pericardiocentesis <A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/fig14_02.htx" TARGET="_blank">(Fig 2)<IMG SRC="Book_ACLS/ACLS_Source_Art/ico14_02.gif" ALIGN="BOTTOM" WIDTH="44" HEIGHT="32" NATURALSIZEFLAG="3"></A>. This technique is performed like the fifth intercostal approach, although the needle is inserted between the xiphoid process and the left costal margin at a 30° to 45° angle to the skin. The heart is located between the neck and left shoulder when the needle is directed in the coronal plane. <A NAME="anchor29"></A> <H3>Hazards<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0007" TARGET="Footnote #7">7</A>,<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0018" TARGET="Footnote #18">18</A>,<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0021" TARGET="Footnote #21">21</A>,<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0029" TARGET="Footnote #29">29</A>,<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0030" TARGET="Footnote #30">30</A> </H3> Significant risks accompany pericardiocentesis. Cardiac arrhythmias, including ventricular fibrillation and asystole, may occur. Puncture or laceration of the cardiac chambers or the coronary arteries is a possibility. Air may be inadvertently injected into the cardiac chambers if a catheter or needle placed into a cardiac chamber is left open to air. Hemothorax, pneumothorax, or both may occur. Hemorrhage from myocardial or coronary artery puncture or laceration following pericardiocentesis may in itself produce cardiac tamponade, especially in the patient with thrombocytopenia or if thrombolytic therapy has been used. <A NAME="anchor30"></A> <H3>Intracardiac Injections</H3> Intracardiac injections are not recommended. However, in desperate clinical situations when an IV cannot be started or an endotracheal tube placed, intracardiac injections can be used to administer epinephrine to treat ventricular fibrillation, asystole, or PEA.<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0031" TARGET="Footnote #31">31-33</A> Anecdotal data suggest that intracardiac epinephrine may have been effective in restoring cardiac contractions in asystole or electromechanical dissociation when IVepinephrine was ineffective. Whether the needle stick or the drug itself was effective has not been resolved. Regardless, IV and endotracheal routes should always be attempted initially. <A NAME="anchor31"></A> <H3>Equipment Needed </H3> Equipment for intracardiac injections should include the following: <A NAME="anchor32"></A> <BLOCKQUOTE> 1. Povidone-iodine solution for skin sterilization <A NAME="anchor33"></A> 2. A 19-gauge, 3½-inch (<IMG SRC= "Book_ACLS/ACLS_Source_Art/wavy_equals.gif" ALIGN="BOTTOM" WIDTH="10" HEIGHT= "10" NATURALSIZEFLAG="3">9-cm) needle attached to a syringe filled with the drug to be injected <A NAME="anchor34"></A> 3. Sterile gloves to be worn for optimal asepsis <A NAME="anchor35"></A> </BLOCKQUOTE> <H3>Technique </H3> As with pericardiocentesis, the parasternal and subxiphoid approaches are preferred. The steps in the process of intracardiac injections are as follows: <A NAME="anchor36"></A> <BLOCKQUOTE> 1. Place the patient in a supine position. <A NAME="anchor37"></A> 2. Cleanse the area of insertion with povidone-iodine solution. <A NAME="anchor38"></A> 3. Insert the needle using one of the sites and approaches previously described for pericardiocentesis. <A NAME="anchor39"></A> 4. Maintain suction on the syringe and stop once blood appears. If no blood appears when the needle is fully advanced, continue maintaining suction and slowly withdraw the needle. If no blood appears, withdraw the needle altogether and repeat the attempt. <A NAME="anchor40"></A> 5. When brisk filling of the syringe occurs, the needle is inside the ventricular cavity. The medication can now be injected. <A NAME="anchor41"></A> </BLOCKQUOTE> <H3>Complications<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0031" TARGET="Footnote #31">31-33</A></H3> The major hazard of an intracardiac injection is the need to interrupt CPR during injection. Although uncommon, complications may follow intracardiac injection — pneumothorax, pneumopericardium, hemopericardium (with or without tamponade), myocardial laceration, coronary artery laceration, internal mammary artery laceration, and intramyocardial injection.<HR ALIGN=LEFT> <A NAME="anchor42"></A> <H1><A NAME="anchor93655"></A>14.3 Tension Pneumothorax</H1> <H2>14.3.1 What is Pneumothorax ?</H2> Intrapleural pressure is normally subatmospheric throughout the respiratory cycle. Because of elastic recoil of the lung, the intra-alveolar pressure is at all times greater than intrapleural pressure. Thus transpulmonary pressure, which is alveolar pressure minus intrapleural pressure, is always positive.<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0034" TARGET="Footnote #34">34</A>,<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0035" TARGET="Footnote #35">35</A> The transpulmonary pressure gradient is markedly increased during coughing, breathing against an airway obstruction, and positive-pressure ventilation. <A NAME="anchor43"></A> If a break occurs in the alveolar-pleural barrier, air enters the pleural space, and the elasticity of the lung causes it to collapse. This condition is called a pneumothorax. As long as the transpulmonary gradient is maintained, the air leak will continue. Lung collapse ceases when either the communication is sealed or intra-alveolar and intrapleural pressures become equal.<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0034" TARGET="Footnote #34">34-37</A> <A NAME="anchor44"></A> <H2>14.3.2 Causes of Pneumothorax</H2> There are four general causes of pneumothorax<A HREF= "http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0038" TARGET="Footnote #38">38</A>: <A NAME="anchor45"></A> Group 1: Alveoli become overdistended and rupture. <A NAME="anchor46"></A> Group 2: The facial planes of the neck are injured by being either incised at operation or lacerated by trauma, allowing entry of air into the mediastinum, producing mediastinal emphysema. <A NAME="anchor47"></A> Group 3: There is a direct connection of the distal airway to the pleural space. High airway pressure from either positive-pressure ventilation or coughing may cause rupture of a bleb on the surface of the lung. Fractured ribs caused by nonpenetrating injuries to the chest wall may puncture both the parietal and visceral pleura and tear the underlying lung, or a needle introduced through the chest wall into the pleural space may tear the lung; the tear may be inapparent until positive pressure is applied to the airway. Each of these produces a pneumothorax. <A NAME="anchor48"></A> Group 4: Breaks in the parietal pleura can connect the pleural space with an extrathoracic source of air, producing pneumothorax. Causes include traumatic esophageal pleural fistulas, emergency tracheostomy, thoracotomy, diaphragmatic tears (both traumatic and during abdominal operations), or a needle in the pleural space that is open to air, such as during thoracentesis. <A NAME="anchor49"></A> <H2>14.3.3 Causes of Tension Pneumothorax</H2> Air under pressure in the pleural space is referred to as a tension pneumothorax. A simple pneumothorax may be converted to a tension pneumothorax if there is a ball-valve mechanism at the site of the leak that permits air to enter but not to leave the pleural space; at each inspiration the volume of gas in the pleural space increases, and the pressure becomes markedly elevated during exhalation.<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0034" TARGET="Footnote #34">34</A>,<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0037" TARGET="Footnote #37">37</A> If positive pressure is applied to the airway, such as during positive-pressure ventilation or coughing,<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0039" TARGET="Footnote #39">39</A>,<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0040" TARGET="Footnote #40">40</A> intra-alveolar pressure becomes markedly elevated, air leak increases, and air under pressure rapidly accumulates in the pleural space.<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0040" TARGET="Footnote #40">40</A> <A NAME="anchor50"></A> Direct causes of a tension pneumothorax include (1) barotrauma from positive-pressure ventilation alone (especially with positive end-expiratory pressure) and with endobronchial intubation and (2) malfunctioning exhalation valves on bag-valve–mask units,<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0041" TARGET="Footnote #41">41</A>,<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0042" TARGET="Footnote #42">42</A> ventilators, or anesthesia machines,<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0043" TARGET="Footnote #43">43</A> especially with preexisting chronic obstructive pulmonary disease, acute necrotizing pneumonitis, or pulmonary infarction.<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0044" TARGET= "Footnote #44">44-48</A> Tension pneumothorax has also been reported following fiberoptic bronchoscopy with closed lung biopsy<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0049" TARGET="Footnote #49">49</A> and with pneumoperitoneum.<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0036" TARGET="Footnote #36">36</A>,<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0037" TARGET="Footnote #37">37</A>,<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0040" TARGET="Footnote #40">40</A>,<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0050" TARGET="Footnote #50">50</A>,<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0051" TARGET="Footnote #51">51</A> <A NAME="anchor51"></A> <H2>14.3.4 Clinical Manifestations</H2> In this syndrome the spontaneously breathing patient experiences dyspnea and may complain of chest pain. Examination reveals tachypnea, tachycardia, and distended neck veins with florid facies. The patient may be hypertensive initially, with hypotension a later finding. Compared with the contralateral side, the hemithorax under tension may be more prominent and hyper-resonant with diminished breath sounds; wheezing may be audible.<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0036" TARGET="Footnote #36">36</A> The trachea may be deviated contralaterally. However, significant tension pneumothorax may be present without these typical physical findings. <A NAME="anchor52"></A> In the patient being treated with positive-pressure ventilation, an increase in peak pressure is needed to deliver the tidal volume because of increased pleural pressure; there is a diminution of expiratory volume because the air leaks from the lungs. There may be increased end-expiratory pressure even with the discontinuation of positive end-expiratory pressure.<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0040" TARGET="Footnote #40">40</A>,<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0052" TARGET="Footnote #52">52</A> <A NAME="anchor53"></A> If a pulmonary artery catheter is in position, a sudden increase in pulmonary artery pressure will be noted, presumably due to both the compressive effect of the pneumothorax and hypoxic pulmonary arterial vasoconstriction.<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0053" TARGET="Footnote #53">53</A> The ECG may show a rightward shift in the mean frontal axis, a diminution in precordial voltage, and precordial T-wave inversion. Hypoxemia, caused both by intrapulmonary shunting and decreased cardiac output, may be present. <A NAME="anchor54"></A> A chest x-ray film generally will show the ipsilateral lung collapsed toward the hilum.<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0036" TARGET= "Footnote #36">36</A>,<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch14/ch14_ref.htx#anchor0037" TARGET="Footnote #37">37</A> However, there may be localized tension pneumothorax with various degrees of lung collapse if there is coexistent pulmonary or pleural disease. The trachea and the heart are usually displaced contralaterally, whereas the ipsilateral intercostal spaces are widened and the hemidiaphragm is pushed downward. The hemidiaphragm may be inverted if the pneumothorax occurs on the left side, but this effect is prevented on the right side by the liver. <A NAME="anchor55"></A> <H2>14.3.5 Treatment</H2> Since a tension pneumothorax may produce cardiovascular collapse and cardiac arrest, emergency relief of pressure must be accomplished as soon as the clinical diagnosis is apparent. This may allow little time for x-ray film confirmation. A diagnostic needle tap with a large-bore needle should be performed in the second or third anterior intercostal space. Since the internal mammary artery parallels the sternum approximately the breadth of one or two fingers from its edge, the needle is best inserted in the midclavicular line to avoid serious bleeding from this vessel. In addition, the needle should be inserted over the top of a rib to avoid the intercostal artery and vein that run on the lower border of each rib. <A NAME="anchor56"></A> In the presence of cardiovascular collapse from a tension pneumothorax, simply inserting a catheter-over-needle device into the chest, removing the needle, and leaving the catheter open to the air is appropriate. Air escaping through the needle with a hissing noise is proof of tension pneumothorax. Although this maneuver technically produces a pneumothorax in itself, an external open pneumothorax is less likely to be lethal than an internal closed valve-like tension pneumothorax. With open pneumothorax, positive-pressure ventilation or spontaneous exhalation against resistance can reexpand the lung. <A NAME="anchor57"></A> <H3>Equipment Needed </H3> <BLOCKQUOTE> 1. Povidone-iodine solution for skin preparation <A NAME="anchor58"></A> 2. A 14-gauge catheter-over-needle device <A NAME="anchor59"></A> </BLOCKQUOTE> <H3>Technique </H3> <BLOCKQUOTE> 1. Cleanse the overlying skin with povidone-iodine solution. <A NAME="anchor60"></A> 2. Insert the 14-gauge catheter-over-needle device into the second intercostal space in the midclavicular line just above the top of the third rib. Entry into the pleural space and confirmation of air under tension will be evident by hearing the escape of air through the open needle. <A NAME="anchor61"></A> 3. Remove the needle and leave the catheter in the pleural space open to atmospheric air. <A NAME="anchor62"></A> 4. As soon as possible, perform tube thoracostomy with underwater seal drainage for definitive treatment. <A NAME="anchor63"></A> </BLOCKQUOTE> <H3>Complications of Treatment </H3> The most common complication is due to misdiagnosis. If a pneumothorax is present but not under tension, inserting the needle will convert it from a closed pneumothorax to an open pneumothorax. If there is no pneumothorax, insertion of a needle open to the atmosphere will produce a pneumothorax. This can be easily treated with a tube thoracostomy. <A NAME="anchor64"></A> Insertion of either a steel needle or a Teflon catheter may lacerate the lung and produce a significant pulmonary injury or hemothorax. If the needle is inserted adjacent to the sternum, the internal mammary artery may be punctured. If the needle is inserted at the lower margin of the rib, the intercostal vessels may be lacerated. Either event may lead to significant hemothorax. Also, the catheter may become kinked or displaced, permitting a closed pneumothorax to reaccumulate. Since simple needle placement will not expand most pneumothoraces, chest tube placement and application of negative pressure should follow needle placement as soon as possible.<HR ALIGN=LEFT> <A NAME="anchor65"></A> end of Chapter 14 </BODY> </HTML>