 \200 Bradycardia not associated with acute myocardial infarction \200 \200 Asystole Second- or third-degree AV block with hemodynamic compromise or syncope at rest Ve ntricular tachyarrhythmias secondary to bradycardia Elective \200 \200 Support for procedures that may promote bradycardia General anesthesia with: \200 \200 \200 \200 Second- or third-degree AV block Intermittent AV block First degree AV block with bifascicu lar block First degree AV block and LBBB Cardiac surgery (not usual) \200 \200 Aortic surgery Tricuspid surgery Ventricular septal defect closure Ostium primum repair \200 Rarely considered for coronary angioplasty (usually to right coronary artery) Overdrive suppression of tachyarrhythmias Ryan TJ, et al. (1996). ACC/AHA guidelines for the management of patients with acute myocar dial infarction. J Am Coll Cardiol 28:1328 \200\2231428. Reproduced with permission from Ga mmage MD (2000). Temporary cardiac pacing. Heart 83:715 \200\223720. CHAPTER 1 Cardiovascular emergencies 68 Temporary ventricular pacing For a checklist for inserting a pacing wire, see Box 1.12. \200 Cannulate a central vein: right interior jugular (RIJ) approach but is more comfortable for the patient via the right subclavian (SC) vein. The LIJ approach is best avoided as there are many acute bends to negotiate and a stable position is dif \201 cult to achieve. Avoid the left subclavicular area as this is the preferred area for permanent pacemaker insertio n and should be kept \200\234virgin \200\235 if possible. The femoral vein may be used (in cidence of DVT and infection is high). Insert a sheath (similar to that for PA catheterizat ion) through which the pacing wire can be fed. Pacing wires are commonly 5F or 6F and a she ath at least one size larger is necessary. Most commercially available pacing wires are pre packed with an introducer needle and plastic cannula similar to an Abbocath , which may be used to position the pacing wire. However, the cannula does not have a hemostatic seal. Th e plastic cannula may be removed from the vein, leaving the bare wire entering the skin, on ce a stable position has been achieved. This reduces the risk of wire displacement but also makes repositioning of the wire more dif \201 cult should this be necessary, and infectio n risk is higher. Pass the wire the introducer sheath and advance into the upper right atri um (see Fig. 1.11) but do not unfurl the cover yet. The wire is much easier to manipulate w ith gloved hands without the hindrance of the plastic cover. Advance the wire may cross the tricuspid valve easily. If it fails to cross, point the tip to the lateral wall of the atr ium and form a loop. Rotate the wire and the loop should fall across the tricuspid valve in to the ventricle. The wire is easiest to manipulate via the through the sterile plastic cover that accompanies with the tip pointing toward the right ventricle; it Advance and rotate the wire so that the tip points inferiorly as close to the apex of the r ight ventricle (laterally) as possible. Box 1.12 Checklist for pacing wire insertion \200 Check that the \202 uoroscopy and monitoring equipment and de \201 brillator are working . Check the type of pacing wire: atrial wires have a preformed \200\234J \200\235 that all ows easy placement in the atrium or appendage and are very dif \201 cult to manipulate int o a satisfactory position in the ventricle. Ventricular pacing wires have a more open, gent le \200\234J. \200\235 Check the pacing box (single vs. dual or sequential pacing box) and leads to attach to the wire(s). Familiarize yourself with the controls on the box; you may need to connect up in a hurry if the patient \200\231s intrinsic rhythm slows further. Rem ember to put on the lead apron before wearing the sterile gown, mask, and gloves. TEMPORARY VENTRICULAR PACING 69 SVC Pulmonary artery RV Tricuspid valve IVC Figure 1.11 Insertion of a ventricular pacing wire (see text for details). Reproduced with permission from Ramrakha P, Moore K (2004). Oxford Handbook of Acute Medicine, 2nd ed. Oxfo rd, UK: Oxford University Press. If the wire does not rotate down to the apex easily, it may be because you are in the coron ary sinus rather than in the right ventricle. (The tip of the wire points to the left shoul der). \200 Withdraw the wire in the wire; the \201 nal appearance should be like the outline of a so ck with the \200\234heel \200\235 in the right atrium, the \200\234arch \200\235 over the tricuspid valve and the \200\234big toe \200\235 at the tip of the right ventricle. Conne ct the wire Ventricular pacing thresholds should be <1.0 V, but threshold up to 1.5 V is ac ceptable if another stable position cannot be achieved. Check for positional stability. tha n the intrinsic heart rate, ask the patient to take some deep breaths, cough forcefully, an d sniff. Watch for failure of capture; if this happens, reposition the wire. and re-cross the tricuspid valve. Leave some slack to the pacing box and check the threshold. With the box pacing at a rate higher CHAPTER 1 Cardiovascular emergencies 70 to 5 V and the box on \200\234demand. \200\235 If the patient is in Set the output sinus r hythm and has an adequate blood pressure, set the box rate to just below the patient \200 \231s rate. If there is complete heart block or bradycardia, set the rate at 70 \200\22380/ min. Dress sterilely. sheath and wire securely to the skin. Loop the rest of the wire and \201 x to the patient \200\231s skin with adhesive dressing. When the patient returns to t he ward, obtain a CXR to con \201 rm satisfactory positioning of the wire and to exclude a pneumothorax. Cover the wire with the plastic sheath and suture Temporary pacemaker placement can be done with ECG guidance (clip lead V1 to end of pacing wire) but \202 uoroscopy guidance is preferred. If it is anticipated that a temporary pacer will be needed for more than a short period of time (infected or hemodynamically unstable patient), a permanent screw-in pacemaker lead ma y be placed, externalized, and connected to a nonsterile permanent pacemaker generator whic h is then secured to the patient \200\231s skin. This is especially useful if \200\234temp orary \200\235 atrial or dual chamber pacing is needed. TEMPORARY ATRIAL PACING 71 Temporary atrial pacing The technique of inserting an atrial temporary wire is similar to t hat of ventricular pacing. \200 \200 Advance the atrial wire until the \200\234J \200\235 is re-formed in the right atrium. Rot ate the wire and withdraw slightly to position the tip in the right atrial appendage. Aim f or a threshold of <1.5 V. If atrial wires are not available, a ventricular pacing wire may be manipu- lated into a si milar position or passed into the coronary sinus for left atrial pacing. Alternatively, a s crew-in permanent lead may be used as described on p. 398. CHAPTER 1 Cardiovascular emergencies 72 AV sequential pacing In critically ill patients with impaired cardiac pump function and sym p- tomatic bradycardia (especially with right ventricular infarction), cardiac output may b e increased by up to 20% by maintaining atrioventricular syn- chrony. This requires two pac ing leads, one atrial and one ventricular, and a dual pacing box. Patients most likely to bene \201 t from AV sequential pacing \200 \200 Acute MI (especially RV infarction) \200\234Stiff \200\235 left ventricle: aortic stenosis , hypertrophic cardiomyopathy (HCM), hypertensive heart disease, amyloidosis Low cardiac ou tput states (cardiomyopathy) Recurrent atrial arrhythmias \200 TEMPORARY PACING: COMPLICATIONS 73 Temporary pacing: complications 1. Ventricular ectopy or tachycardia Nonsustained ventricular tachycardia (VT) is common as the guide or pacing wire crosses the tricuspid valve (especially in patients receiving a c atecholamine infusion) and does not require treatment. Try to avoid long runs of VT and, if necessary, withdraw the wire into the atrium and wait until the rhythm has settled. If ectopy persists after the wire is positioned, try adjusting the amount of slack in the w ire in the region of the tricuspid valve (either more or less). Pacing the right ventricular out \202 ow tract can provoke runs of VT. 2. Failure to pace and/or sense It is dif \201 cult to get low pacing thresholds (<1.0 V) in patients with exten- sive myocardial infarction (especially of the inferior wall) or car diomyop- athy or who have received class I antiarrhythmic drugs. Accept a slightly higher v alue if the position is otherwise stable and satisfactory. If the position of the wire appears satisfactory and yet the pacing thresh- olds are high, the wire may be in a left hepatic vein or may have perfo- rated. Pull the wire back into th e atrium and try again, looking speci \201 cally for the ventricular ectopy as the wire cr osses the tricuspid valve. Monitor closely for signs of hemodynamic compromise. \200 The pacing threshold commonly doubles in the \201 rst few days due to endocardial edema. If the pacemaker suddenly fails, the most common reason is usually wire displacement. Incre ase the pacing output of the box. Check all the connections of the wire and the battery of the box. Try moving the patient to the left lateral position until arrangements can be made to reposition the wire. \200 \200 3. Perforation A pericardial rub may be present in the absence of perforation (especially p ost-MI). Presentation Watch for pericardial chest pain, increasing breathlessness, falling blood pre ssure, enlarged cardiac silhouette on CXR, signs of cardiac tamponade, left diaphragmatic p acing at low output, increased threshold. Management If there are signs of cardiac tamponade, arrange for urgent ECHO, drain- age of \202 uid, and repositioning of the wire. Monitor the patient carefully over the next few days with repeat ECHOs to detect incipient cardiac tamponade. CHAPTER 1 Cardiovascular emergencies 74 4. Diaphragmatic pacing High-output pacing (10 V), even with satisfactory position of the v entricu- lar lead, may cause pacing of the left hemidiaphragm. At low voltages this suggest s perforation (see above). Right hemidiaphragm pacing may be seen with atrial pacing and stimula- tion of the right phrenic nerve. Reposition the wire if symptomatic (painful twitching, dyspnea). Box 1.13 Complications of temporary pacing \200 \200 \200 \200 \200 \200 \200 \200 Complications associated with central line insertion Ventricular ectopy Nonsustained VT Per foration Pericarditis Diaphragmatic pacing Infection Pneumothorax PERICARDIOCENTESIS 75 Pericardiocentesis Equipment Establish peripheral venous access and check that full facilit ies for resusci- tation are available. Pre-prepared pericardiocentesis sets may be availabl e. You will need the following: \200 Table for central line insertion with chlorhexidine for skin, dressing pack, sterile drapes , local anesthetic (lidocaine 2%), syringes (including a 50 mL), needles (25G and 22G), No 11 blade, and silk sutures Pericardiocentesis needle (15 cm, 18G) or similar Wallace cannul a J-guide wire ( Dilators (up to 7 French) Pigtail catheter ( Drainage bag and connectors F acilities for \202 uoroscopy or echocardiographic screening Often done with a pulmonary a rtery catheter in place to document initial \201 lling pressures and improvement \200 \200 \200 \200 \200 \200 (cid:116)80 cm, 0.035 diameter) (cid:116)60 cm with catheter with multiple side holes) Technique \200 Position the patient at 30 . This allows the effusion to pool inferiorly and anteriorly w ithin the pericardium. Sedate the patient lightly with midazolam (2.5 \200\2237.5 mg IV) an d fentanyl 50 \200\223200 g IV) if necessary. Use with caution, as this may drop the BP i n patients already compromised by the effusion. Wearing a sterile gown and gloves, clean th e skin from mid-chest to mid-abdomen and put the sterile drapes on the patient. In \201 lt rate the skin and subcutaneous tissues with local anesthetic starting 1 \200\2231.5 cm belo w the xiphoid and just to the left of midline, aiming for the left shoulder and staying as close as possible to the inferior border of the rib cartilages. The pericardiocentesis need le is introduced into the angle between the xiphoid and the left costal margin angled at 3 0 . Advance slowly, aspirating gently and then injecting more lidocaine every few millimet ers, aiming for the left shoulder. As the parietal pericardium is pierced, you may feel a \200\234give \200\235 and \202 uid will be aspirated. Remove the syringe and introduce th e guide wire through the needle (see Fig. 1.12). Check the position of the guide wire by sc reening. It should loop within the cardiac silhouette only and not advance into the SVC or pulmonary artery. Remove the needle, leaving the wire in place. Enlarge the skin incision s lightly using the blade and dilate the track. Insert the side-hole catheter over the wire i nto the pericardial space and remove the wire. Measure intrapericardial pressure. Take spec imens for microscopy, culture (and inoculate a sample into blood culture bottles), cytology , and hematocrit if blood stained (a CBC tube; ask the hematologists to run on the Coulter counter for rapid estimation of Hb). CHAPTER 1 Cardiovascular emergencies 76 Figure 1.12 Pericardial aspiration. Reproduced with permission from Ramrakha P, Moore K (20 04). Oxford Handbook of Acute Medicine, 2nd ed. Oxford, UK: Oxford University Press. Aspirate to dryness, watching the patient carefully. Symptoms and hemodynamics (tachycardia ) often start to improve with removal of as little as 100 mL of pericardial \202 uid. If the \202 uid is heavily blood stained, withdraw \202 uid cautiously \200\223if the pigt ail is in the right ventricle, withdrawal of blood may cause cardiovascular collapse. Arran ge for urgent Hb/hematocrit. Leave on free drainage and attached to the drainage bag. Sutur e the pigtail to the skin securely and cover with a sterile occlusive dressing. \200 Aftercare \200 Closely observe the patient for recurrent tamponade (obstruction of drain) and follow repea t ECHO studies. Discontinue anticoagulants. Remove the drain after 24 hours or when the dra inage stops. Consider the need for surgery (drainage, biopsy, or pericardial window) or spe ci \201 c therapy (chemotherapy if malignant effusion, antimicrobials if bacterial, dialys is if renal failure, etc.). \200 \200 PERICARDIOCENTESIS 77 Tips and pitfalls A summary of complications of pericardiocentesis is provided in Box 1.14. 1. If the needle touches the heart \200\231s epicardial surface, you may feel a \200\234t icking \200\235 sensation transmitted down the needle: withdraw the needle a few millimeter s, angulate the needle more super \201 cially, and try cautiously again, aspirating as you advance. 2. If you do not enter the effusion, and the heart is not encountered: \200 Withdraw the needle slightly and advance again, aiming slightly deeper, but still toward th e left shoulder. If this fails, try again, aiming more medially (mid-clavicular point or ev en suprasternal notch). Consider trying the apical approach (starting laterally at cardiac apex and aiming for right shoulder), if echo con \201 rms suf \201 cient \202 uid at th e cardiac apex). 3. If available, intrathoracic ECG can be monitored by a lead attached to the needle as it is advanced. This is seldom clinically useful in our experi- ence. Penetration of the myoca rdium results in ST elevation, suggesting that the needle has been advanced too far. 4. If there is dif \201 culty with inserting the side-hole catheter: \200 \200 This may be due to insuf \201 cient dilatation of the tract (use a larger dilator). Holdin g the wire taught (by gentle traction) while pushing the catheter may help; take care not t o pull the wire out of the pericardium. 5. With hemorrhagic effusion vs. blood \200 \200 Compare the Hb of the pericardial \202 uid with the venous blood Hb. Place some of the \202 uid in a clean container; blood will clot, whereas hemorrhagic effusion will not, as t he \200\234whipping \200\235 action of the heart tends to de \201 brinate it. Con \201 r m the position of the needle by \201 rst withdrawing some \202 uid and then injecting 1 0 \200\22320 mL of contrast; using \202 uoroscopy, see if the contrast stays within the c ardiac silhouette. Alternatively, if using ECHO guidance, inject 5 \200\22310 mL saline int o the needle, looking for \200\234microbubble contrast \200\235 in the cavity containing t he needle tip. Injecting 20 mL saline rapidly into a peripheral vein will produce \200\234 contrast \200\235 in the right atrium and ventricle and may allow them to be distinguished from the pericardial space. Connect a pressure line to the needle; a characteristic wavefor m will con \201 rm penetration of the right ventricle. Box 1.14 Complications of pericardiocentesis \200 \200 \200 Penetration of a cardiac chamber (usually right ventricle) Laceration of an epicardial vess el Arrhythmia (atrial arrhythmias as the wire is advanced, ventricular arrhythmias if the R V is penetrated) Pneumothorax Perforation of abdominal viscus (liver, stomach, colon) Ascen ding infection \200 \200 CHAPTER 1 Cardiovascular emergencies 78 DC cardioversion Relative contraindications \200 \200 \200 Digoxin toxicity Electrolyte disturbance ( Fever and ongoing metabolic abnormalities dNa+, dK+, iK, dCa2+, dMg2+, acidosis) Checklist for DC cardioversion \200 De \201 brillator Check that this is functioning, with a fully equipped crash cart on hand in case of arrest. Unless life-threatening emergency AF, \202 utter, SVT, VT, signs of ischemia or digoxin. If ventricular rate is slow, have an external (transcu- taneous) pacing system nearby in c ase of asystole. For at least 6 hours Does the patient require anticoagulants? Is the INR > 2.0? (Has it been so for >3 weeks?) Check that this is >3.5 mmol/L. Check that there are n o features of digoxin toxic- ity. If taking (cid:116)250 g/day, check that renal function and recent digoxin level are normal. If there is frequent ventricular ectopy, give IV Mg2+ 2 g. Treat thyrotoxicosis or myxedema \201 rst, if patient is stable. Peripheral venous cannula Short general anesthesia (propofol) is preferable to sedation with benzodiazepine a nd fentanyl. Bag the patient with 100% oxygen. See Box 1.16. Check that this is selected on the de \201 brillator for all shocks (unless the patient is in VF or hemodynamically unst able). Adjust the ECG gain so that the machine is only sensing QRS complexes and not P or T waves. Conductive gel pads should be placed between the paddles and the skin or, preferabl y, self- adhesive patches should be used. Place one anteriorly just left of the sternum, an d one posteriorly to the left of midline. Alternatively, position one just to the right of the sternum and the other to the left of the left nipple (anterior \200\223mid-axillary lin e). Check that no one is in contact with the patient or with the metal bed. Ensure your own legs are clear of the bed! Apply \201 rm pressure on the paddles if they are used. \200 Informed consent 12 lead ECG \200 Nothing by mouth Anticoagulation \200 Potassium Digoxin Thyroid function \200 IV access Sedation \200 Select energy Synchronization Paddle placement Cardioversion DC CARDIOVERSION 79 Successful Repeat ECG. Place patient in recovery position until awake. Monitor for 2 \200\2234 hours a nd ensure that effects of sedation have passed. If being discharged, patients should be acc ompa- nied home by a friend or relative. In addition, they should not drive or operate heav y equipment for 24 hours. Special situations Pregnancy DC shock during pregnancy appears to be safe. Auscultate the f etal heart before and after cardioversion and, if possible, fetal ECG should be moni- tored . Because of the increased risk of gastric re \202 ux, airway protection (intubation) is u sually necessary. Pacemakers/AICDs There is a danger of damage to the pacemaker generator box or the junc- ti on at the tip of the pacing wire(s) and endocardium. Position the paddles away from the gen erator, and not in the same vector as the device. Facilities for backup pacing (external or transvenous) should be avail- able. Check the pac emaker/ICD post-cardioversion \200\224both early and late problems have been reported. Thes e problems are very rare with newer devices and are minimized by not delivering a shock ove r the generator. The presence of a de \201 brillator is not a contraindication to an external shock if this is needed. Box 1.15 Complications of DC cardioversion \200 \200 \200 \200 \200 \200 Asystole/bradycardia Ventricular \201 brillation Thromboembolism Transient hypotension Sk in burns Aspiration pneumonitis. Box 1.16 Suggested initial energies for DC shock for elective cardioversion \200 \200 \200 \200 \200 Sustained monomorphic VT Atrial \201 brillation Atrial \202 utter Other SVTs If the ini tial shock is unsuccessful, increase the energy (50, 100, 200, 360 J) and repeat. If still unsuccessful, consider changing paddle position and try 200 J again. 200 J biphasic 50 \200\223200 J 50 J 50 J Synchronized Synchronized Synchronized Synchronized CHAPTER 1 Cardiovascular emergencies 80 Intra-aortic balloon counterpulsation Indications \200 \200 \200 \200 Cardiogenic shock post-MI Acute severe mitral regurgitation Acute ventricular septal defect Preoperative (LM disease, triple-vessel disease with severely depressed EF with high \201 lling pressures) Weaning from cardiopulmonary bypass Rarely \200 \200 \200 Treatment of ventricular arrhythmias post-MI. Unstable angina (as a bridge to CABG) Hemodyn amic support as a bridge to transplant or assist device placement Contraindications \200 \200 \200 \200 Aortic regurgitation Aortic dissection Severe aortoiliac atheroma. Bleeding diathesis Dilated cardiomyopathy (if patient is not a candidate for transplantatio n) Complications \200 \200 \200 \200 \200 \200 Aortic dissection Arterial perforation Limb ischemia Infection Principle The device consist s of a catheter with a balloon (34 mL up to 40 mL size) at its tip, which is positioned in the descending thoracic aorta. Trombocytopenia Peripheral embolism/stroke Balloon rupture The balloon in \202 ation and de \202 ation is synchronized to the ECG. The balloon shoul d in \202 ate just after the dicrotic notch (in diastole), thereby increasing pressure in the aortic root and increasing coronary perfusion. The balloon de \202 ates just before ve ntricular systole, thereby decreasing afterload and improving left ventricular performance (see Fig. 1.13). Counterpulsation has a number of bene \201 cial effects on the circulation: Increased in c oronary perfusion in diastole Reduced LV end-diastolic pressure Reduced myocardial oxygen c onsumption Increased cerebral and peripheral blood \202 ow \200 \200 \200 The IAB cannot assist the patient in asystole or VF. It is often less effective in the sett ing of severe tachycardia (rapid atrial \201 brillation or atrial \202 utter). It requi res a minimum cardiac index of 1.2 \200\2231.4 L/min/m2, often necessitat- ing additional i notropes. Technique Balloon insertion Previous experience is essential. Formerly, a cut-down to the f emoral artery was required, but newer balloons come equipped with a sheath that may be intr oduced percutaneously. INTRA-AORTIC BALLOON COUNTERPULSATION 81 Balloon deflated to allow systemic perfusion during systole Balloon inflated to increase coronary perfusion during diastole Coronary perfusion (a) Cardiac diastole (b) Cardiac systole Figure 1.13 Operation of intra-aortic balloon pump. Reproduced with permission from Ramrakh a P, Moore K (2004). Oxford Handbook of Acute Medicine, 2nd ed. Oxford, UK: Oxford Universi ty Press. Using \202 uoroscopy, the balloon is positioned in the descending thoracic aorta with the tip just below the origin of the left subclavian artery. Fully anticoagulate the patient w ith IV heparin. Some units routinely give IV antibiotics (vancomycin) to cover against Staph. infection. Triggering and timing The balloon pump may be triggered either from the patient \200\231s E CG (R wave) or from the arterial pressure waveform. Slide switches on the pump console allo w precise timing of in \202 ation and de \202 ation during the cardiac cycle. Set the pum p to 1:2 to allow you to see the effects of aug- mentation on alternate beats (see Fig. 1.1 4). Troubleshooting Seek help from an expert! There is usually an on-call cardiac perfusionist or technician or senior cardiac physician or surgeon. Counterpulsation is inef \201 cient with heart rates over 130/min. Consider antiarrhythmics or 1:2 augmentation instead. Triggering and timing For ECG triggering, select a lead with most pronounced R wave; ensure that the pump is set to trigger from ECG, not pressure. Permanent pace- makers may interfe re with triggering \200\224select a lead with a negative and the smallest pacing artifact. Alternatively, set the pump to be triggered from the external pacing device. A good arterial waveform is required for pressure triggering; the tim- ing will vary slight ly depending on the location of the arterial line (slightly earlier for radial artery line than femoral artery line). Be guided by the hemodynamic effects of balloon in \202 ation a nd de \202 ation rather than precise value of delay. See Figure 1.15 for timing errors. CHAPTER 1 Cardiovascular emergencies 82 Diastolic augmentation \206\221 Coronary perfusion 140 Unassisted systole Assisted systole 120 g H m m 100 Balloon inflation 80 Unassisted aortic end diastolic pressure 60 Assisted aortic end diastolic pressure \206\223MVO2 demand Figure 1.14 Arterial waveform variations during 1:2 IABP therapy. Limb ischemia is exacerbated by poor cardiac output, adrenaline, nor- adrenaline, and perip heral vascular disease. Wean patient off and remove the balloon. Thrombocytopenia is commonly seen; it does not require transfusion unless there is overt bl eeding and returns to normal once the balloon is removed. IABP removal The patient may be progressively weaned by gradually reducing the coun- terpul sation ratio (1:2, 1:4, 1:8, etc.) and checking that the patient remains hemodynamically st able. \200 Stop the heparin infusion and wait for the ACT (activated clotting time) to fall <150 secon ds (APTT <1.5 normal). Using a 50 mL syringe, have an assistant apply negative pressure to the balloon. Pull the balloon down until it abuts the sheath; do not attempt to pull the ba lloon into the sheath. Withdraw both balloon and sheath and apply \201 rm pressure on the femoral puncture site for at least 30 minutes or until the bleeding is controlled. INTRA-AORTIC BALLOON COUNTERPULSATION 83 (a) Inflation of the IAB prior to aortic valve closure Diastolic augmentation Unassisted systole Waveform characteristics: Inflation of IAB prior to dicrotic notch \200 Diastolic augmentation encroaches onto syst ole (may be unable to distinguish) Assissted systole Physiologic effects: Potential premature closure of aortic valve \200 Potential increase in LVEDV and LVEDP or PCWP \200 Increased left ventricular wall stress or afterload \200 Aortic reguragitati on \200 Increased MVO2 demand Assisted aortic end-diastolic pressure Diastolic augmentation (b) Inflation of the IAB markedly after closure of the aortic valve Waveform characteristic s: Unassisted systole Assisted systole Inflation of the IAB after the dicrotic notch \200 Absence of sharp V \200 Sub-optimal diastolic augmentation Physiologic effects: Dicortic notch Sub-optimal coronary artery perfusion Assisted aortic end-diastolic pressure (c) Premature deflation of the IAB during the diasstolic phase Diastolic augmentation Waveform characteristics: Assisted systole Deflation of IAB is seen as a sharp drop following diastolic augmentation \200 Sub-optima l diastolic augmentation \200 Assisted aortic end-diastolic pressure may be equal to or l ess than the unassisted aortic end-diastolic pressure \200 Assisted systolic pressure may rise Physiologic effects: \200 Sub-optimal coronary perfusion \200 Potential for retro grade coronary and carotid blood flow \200 Angina may occur as a result of retrograde cor onary blood flow \200 Sub-optimal afterfoad reduction \200 Increased MVO2 demand Unassisted aortic end-diastolic pressure Assisted aortic end-diastolic pressure (d) Deflation of the IAB as the aortic valve is beginning to open Diastolic augmentation Unassisted systole Waveform characteristics: \200 Assisted aortic end-diastolic pressure may be equal to the unassisted aortic end-diastolic pressure \200 Rate of rise of assisted systole is proton ged \200 Diastolic augmentation may appear widened Prolonged rate of rise assisted systole Widened appearance Physiologic effects: Afterload reduction is essentially absent \200 increased MVO2 consumption due to the left ventricle ejecting against a greater resistance and a prolonged isovolumetric contraction phase \200 IAB may impede left ventricular ejection and increase the afterload Assisted aortic end-diastolic pressure Figure 1.15 Timing errors. (a) Early in \202 ation; (b) late in \202 ation; (c) early de \202 ation; (d) late de \202 ation. This page intentionally left blank 85 Chapter 2 Chapter 2 Coronary artery disease Angina pectoris 86 Acute coronary syndromes 89 ST elevation myocardial infarction (STEMI) 9 1 STEMI: diagnosis 93 STEMI: general measures 96 STEMI: reperfusion therapy (thrombolysis) 98 STEMI: reperfusion by primary PCI 101 Surgery for acute STEMI 103 STEMI: additional meas ures 104 Right ventricular (RV) infarction 105 STEMI: predischarge risk strati \201 cation 107 STEMI: complications 109 Ventricular septal defect post-MI 111 Acute mitral regurgitat ion post-MI 113 Pseudoaneurysm and free wall rupture 114 Cocaine-induced MI 115 Ventricular tachyarrhythmias post-MI 117 Atrial tachyarrhythmia post-MI 117 Bradyarrhythmias and indic ations for pacing 118 Bradyarrhythmias post-MI 118 Hypotension and shock post-MI 119 Cardio genic shock 120 Non-ST elevation myocardial infarction (NSTEMI)/unstable angina (UA) 122 NSTEMI/UA: diagnosis 124 NSTEMI/UA: risk strati \201 cation 125 NSTEMI/UA: late risk strat i \201 cation 127 NSTEMI/UA: medical management 128 NSTEMI: invasive vs. noninvasive strat egies 131 Discharge and secondary prevention 132 CHAPTER 2 Coronary artery disease 86 Angina pectoris Angina pectoris refers to the pain caused by myocardial ischemia. Ischemia is usually caused by mismatched oxygen demand (tachycardia, anemia, aortic stenosis, left v entricular hypertrophy of other etiologies) and deliv- ery in the setting of a hemodynamica lly signi \201 cant coronary stenosis due to atheroma, but it may have other causes such a s coronary artery spasm (Prinzmetal \200\231s variant angina). In more unusual cases the etiology is not completely understood \200\224e.g., syndrome X (c hest pain with normal coronary arteries). Alternatively, these conditions may coexist and b e exacerbated by emotional stress. History and examination Angina pectoris is characterized by a deep and diffusely distribute d cen- tral chest discomfort. Certain features of pain are of discriminative value. Patient s will not be able to point to where the pain is coming from with one \201 nger but will use an open palm or \201 st over the center or left para- sternal aspect of their chest. \200 \200 The pain is not sharp (some patients confuse \200\234sharp \200\235 with \200\234severe \200\235). Pain lasts longer than a few seconds and rarely exceeds an hour without varying in severity. Most episodes will last 1 \200\2235 minutes. The response to nitroglycerin, if any, will be almost immediate. Generally, responses taking more than 5 minutes are unlikel y to be related to the drug. Chest wall tenderness suggests musculoskeletal pain and does not accom- pany angina. Dyspnea, fatigue, nausea, and recurrent belching may also represent underlying ischemia and can occur in the absence of the classical central chest pain. The clue to underlying ische mic heart disease (IHD) lies in their precipitation by exertion or emotional stress. Angina is often classi \201 ed according to its temporal pattern and its rela- tion to exertion because this loosely re \202 ects prognosis. \200 Stable angina constant level of exertion. Unstable angina is characterized by pain on minor exertion or at rest, which is either new onset or a dramatic worsening of existing angina. Also, it can present as pain on ever-diminishing levels of exertion, usually over a period of days. is characterized by pain occurring after a relatively The Canadian Cardiovascular Society (CCS) system provides a quantitative means to describe exertional capacity and is divided into four classes: I. Minimal limitation of ordinary activity. Angina occurs with strenuous, rapid, or prolonged exertion at work or recreation. II. Slight limitation of ordinary activity; angina occurs on walking or climb- ing stairs r apidly; walking in cold, in wind, or under emotional stress. III. Marked limitation of ordinary physical activity; angina occurs on walking 50 \200\223100 m on level ground or climbing 1 \202 ight of stairs at a normal pa ce in normal conditions. Inability to perform any physical activity without discomfort; ang ina symptoms may be present at rest. IV. ANGINA PECTORIS 87 Physical examination \200 Measure the pulse rate. This may be slowed by inferior ischemia due to atrioventricular (AV ) node ischemia. A resting tachycardia, if present, usually represents activation of the sy mpathetic nervous system but may be due to an arrhythmia precipitated by ischemia. Blood pr essure measurement is essential to look for evidence of hypertension (predisposing to ather oma) or hypotension (may re \202 ect cardiac dysfunction or overmedication). Precordial ex amination should include palpation for left ventricular hypertrophy (LVH), cardiac enlargem ent, or dyskinesis, and auscultation for added heart sounds (heart failure or acute ischemi a), aortic stenosis, or mitral regurgitation (due to papillary muscle dysfunction). Examine for signs of heart failure by listening for \201 ne, late-inspiratory crackles at the lu ng bases and looking for dependent pitting edema (typically bilateral ankle leg edema, b ut sacral edema may be the only manifestation if the patient has been recumbent for some ti me). Look for evidence of peripheral vascular disease by palpating for aortic aneurysm; fee ling the carotid and limb pulses; listening for carotid, renal, or femoral artery bruits; a nd assessing tissue integrity and capillary re \201 ll of the legs and feet. Examine for s igns of hypercholesterolemia: the eyes for xanthelasmata and corneal arcus, and the skin an d tendons (especially the Achilles) for xanthomata. Differential diagnosis The differential diagnosis of anginal chest pain is wide and include s \200 \200 \200 \200 \200 \200 Anxiety and hyperventilation Musculoskeletal chest wall pain Cervical or thoracic root pain Pneumothorax, pneumonia, or pulmonary embolus Esophageal problem (in \202 ammation/spasm) Other upper gastrointestinal (GI) problem (gastritis, peptic ulcer, pancreatitis, cholecys titis) Pericarditis Aortic dissection Mitral valve prolapse Coronary emboli (LV mural throm bus, atrial myxoma) \200 \200 \200 Investigations Further risk strati \201 cation will add to the diagnostic certainty achiev ed by history and examination. Measure complete blood count (CBC), chemis- tries, a full fa sting lipid pro \201 le (total, LDL and HDL cholesterol and triglyc- eride levels), and bl ood glucose. Chest X-ray (CXR) is not mandatory but should be performed if there is suspicion of heart f ailure, aortic dissection, a pulmonary condition or an abnormality of the bony structures o f the chest wall. CHAPTER 2 Coronary artery disease 88 12 Lead ECG A resting electrocardiogram (ECG) may not con \201 rm the diagnosis but can po int toward ischemic heart disease. The presence of Q waves suggests previous myocardial inj ury. The presence of ST depression and, to a lesser extent, T-wave inversion during pain is a marker of ischemia and patients with these signs should be further investigated. If ST-s egment deviation is observed at rest, an acute coronary syndrome must be excluded. A 12-lead ECG can also help identify other causes of chest pain (LVH, arrhythmia, pericarditis). Tests for inducible ischemia Tests such as exercise ECG, stress echocardiogram (ECHO), or m yocar- dial perfusion scanning are useful adjuncts to con \201 rm the diagnosis and aid ma nagement. Management Lifestyle Smoking cessation is of paramount importance. Encourage daily aerobic exercise within limits of exercise capacity. Look at the patient \200\231s occupa- tional n eeds and advise adjustment if symptom level is not compatible. Advise a healthy diet, colla borating with dieticians if required. Aspirin Provide aspirin in all cases unless there is active peptic ulcer disease, allergy ( desensitizing may be required), or bleeding diathesis. Those with past peptic ulcer disease may take a gastroprotective agent such as an H2 antagonist or proton pump inhibitor. Anti-anginals B \200 Blockers: First line (e.g., atenolol 25 \200\223100 mg qd or metoprolol 25 \200\22350 mg bi d). Start on suspicion of ischemic heart disease. Avoid only if contraindicated (asthma wit h con \201 rmed B-agonist response (mortality improved in patients with angina and concomi tant COPD if they can tolerate bronchospasm), uncontrolled severe LV dysfunction, bradycard ia, coronary artery spasm). Calcium antagonists contraindicated or concern for vasospasm, c alcium antagonists become the drug of choice. Nitrates (e.g., nitroglycerin): Used for cont rol of breakthrough angina. Long-acting nitrates (e.g., isosorbide mononitrate 60 \200\2231 20 mg qd) are a useful addition to B-blockers for prevention of attacks. (e.g., amlodipine or diltiazem): If B-blocker Statins Statins (HMG-CoA reductase inhibitors) reduce mortality by approxi- mately one-thir d in all risk groups. However, the underlying risk of events must be taken into account whe n considering starting the drug, because absolute risk reduction in young patients with low -risk IHD may be very small, with possible harm of myositis, hepatic failure, and reduced c ompli- ance with other medications. ACUTE CORONARY SYNDROMES 89 Acute coronary syndromes Acute coronary syndrome (ACS) is a term used to describe a constel lation of symptoms resulting from acute myocardial ischemia. An ACS resulting in myocardial injury is termed myocardial infarction (MI). ACS includes the diagnosis of unstable angina (UA), non-ST elevation myocardial infarction (NSTEMI), and ST elevation myocardial infarct ion (STEMI). De \201 nition The current nomenclature divides ACS into two major groups on the basis of delivered treatment modalities (see Fig. 2.1). ST elevation myocardial infarction (STEMI) \200\224an ACS in which patients present with ch est discomfort and ST-segment elevation on ECG. This group of patients must undergo reperfu sion therapy on presentation.