PV PVE PVR qid RA RAS RBBB RBC RCA RF RFA RHC RIJ rtPA RV RVA RVAD RVF RVH RVOT RVSP SACT S AH SAM SAN SBE SBP SC SCD SCM SCV SK SL SLE SND SNRT SPECT SR SS STEMI SV pulmonary valve prosthetic valve endocarditis pulmonary vascular resistance four times a da y rheumatoid arthritis; right atrium, atrial renal artery stenosis right bundle branch bloc k red blood cells right coronary artery radiofrequency; rheumatoid factor radio frequency a blation right heart catheterization right interior jugular recombinant tissue-type plasmino gen activator right ventricular; regurgitant volume right ventricular apex right ventricula r assist device right ventricular failure right ventricular hypertrophy right ventricular o ut \202 ow tract right ventricular systolic pressure sinoatrial conduction time subarachno id hemorrhage systolic anterior motion sinoatrial node subacute bacterial endocarditis syst olic blood pressure subcutaneous; subcostal sudden cardiac death sternocleidomastoid subcla vian vein streptokinase sublingual systemic lupus erythematosus sinal node dysfunction sinu s node reentrant tachycardia single photon electron computed tomography sinus rhythm supras ternal ST elevation myocardial infarction stroke volume SYMBOLS AND ABBREVIATIONS xxxiii SVC SVG SVT TAA TB TCL TDI TdP TEE TFT TGF-B TIA tid TOF TR TS TSH TST TTE TV TVI UA UFH VF VLDL VMA VPB VPC V/Q VSD VT VVI WBC WCL WCT WHO WMSI WPW superior vena cava saphenous vein graft supraventricular tachycardia thoracic aortic aneury sm tuberculosis tachycardia cycle length tissue Doppler imaging torsades de pointes transes ophageal echocardiography thyroid function test transforming growth factor B transient isch emic attack three times a day tetralogy of Fallot tricuspid regurgitation tricuspid stenosi s thyroid-stimulating hormone tuberculin skin test transthoracic echocardiogram tricuspid v alve time \200\223velocity index unstable angina unfractionated heparin ventricular \201 brillation very low density lipoprotein vanilmandelic acid ventricular premature beats vent ricular premature complex ventilation \200\223perfusion ratio ventricular septal defect ven tricular tachycardia ventricular demand pacing white blood cells Wenckebach cycle length wi de complex tachycardia World Health Organization wall motion score index Wolff \200\223Park inson \200\223White (syndrome) This page intentionally left blank 1 Chapter 1 Cardiovascular emergencies and practical procedures Hypertensive encephalopathy 39 Aortic dissection: assessment 40 Aortic dissection: investig ations 43 Cardiovascular emergencies Adult basic life support 2 Adult advanced life support 5 Universal treatment algorithm 7 Ac ute pulmonary edema: Aortic dissection: management 45 Acute pericarditis: assessment 48 Acute pericarditis: mana gement 50 Cardiac tamponade: presentation 51 Cardiac tamponade: management 53 assessment 9 Pulmonary edema: causes 11 Pulmonary edema: management 12 Pulmonary edema: speci \201 c conditions 15 Acute aortic regurgitation 16 Acute mitral regurgitation 18 Deep vein thrombosis: Practical procedures Central line insertion 55 Internal jugular vein cannulation 57 assessment 20 Deep vein thrombosis: management 22 Subclavian vein cannulation 59 Pulmonary artery Pulmonary embolism (PE): assessment 24 catheterization 61 Pulmonary embolism: investigations 25 Pulmonary embolism: management 27 Indications for temporary pacing 66 Temporary ventricular pacing 68 Temporary atrial pacing 71 AV sequential pacing 72 Temporar y pacing: complications 73 Pericardiocentesis 75 DC cardioversion 78 Intra-aortic balloon Fat embolism 29 Hypertensive emergencies 31 Hypertensive emergencies: management 33 Drugs for hypertensive emergencies 35 Hypertensive emergency with retinopathy (accelerated and malignant hypertension) 37 counterpulsation 80 CHAPTER 1 Cardiovascular emergencies 2 Cardiovascular emergencies Adult basic life support Basic life support (BLS) is the backbon e of effective resuscitation follow- ing a cardiorespiratory arrest. The aim is to maintain adequate ventilation and circulation until the underlying cause for the arrest can be reve rsed. A period of 3 \200\2234 minutes without adequate perfusion (less if the patient is hy poxic) will lead to irreversible cerebral damage. Occasionally you will be the \201 rst to discover the unresponsive patient, and it is imp ortant to rapidly assess the patient and begin cardiopulmon- ary resuscitation (CPR). The v arious stages in BLS are described here and summarized in Figure 1.1. CHECK RESPONSIVENESS Shake and shout OPEN AIRWAY Head tilt/chin lift If breathing: recovery position Look, listen, and feel CHECK BREATHING BREATHE 2 effective breaths ASSESS 10 secs only Signs of a circulation CIRCULATION PRESENT continue rescue breathing NO CIRCULATION Compress chest Check circulation every minute 100 per minute 30:2 ratio Send or go for help as soon as possible according to guidelines Figure 1.1 Stages in basic life support. For further information, see BLS/ACLS AHA/ACC guid elines. ADULT BASIC LIFE SUPPORT 3 1. Assessment of the patient \200 \200 Ensure safety of rescuer and victim. Check whether the patient is responsive ask loudly, \200\234Are you all right? \200\235 \200 \200 . Gently shake the victim and If the victim responds, place them in recovery position and get help. If the victim is unre sponsive, shout for help and move on to assess airway (see below). 2. Airway assessment \200 Open the airway tilt the head up. If this fails, place your \201 ngers behind the angles of the lower jaw and apply steady pressure upward and forward. Remove ill- \201 tting dentures and any obvious obstruction. If the patient starts breath ing, roll patient over into the recovery position and try to keep the airway open until an orophyrangeal airway can be inserted. Use jaw thrust without head extension, if trauma is s uspected (see Fig. 1.2). . With two \201 ngertips under the point of the chin, Jaw lift to open the airway Jaw thrust (thrust the angle of the mandible upward) Figure 1.2 Opening the airway. Reproduced with permission from Ramrakha PS, Moore KPK (2004 ). Oxford Handbook of Acute Medicine. Oxford, UK: Oxford University Press. CHAPTER 1 Cardiovascular emergencies 4 Keep the airway open; look, listen, and feel for breathing chest movements, listen at the v ictim \200\231s mouth for breathing sounds, and feel for air on your cheek (for no more tha n 10 seconds). \200 . Look for If the patient is breathing, turn patient into the recovery position, check for continued b reathing, and get help. If the patient is not breathing or is making occasional gasps or we ak attempts at breathing, send someone (or go for help if alone). (On return) Start rescue breaths by giving two slow effective breaths, each resulting in a visible rise and fall in the chest wall; a mouth-to- barrier device may be used. 3. Assessment of circulation \200 Assess signs of circulation by feeling the carotid pulse for no more than 10 seconds. \200 If there are signs of circulation but no breathing, continue rescue breaths and check for s igns of breathing every 10 breaths. If there are no signs of circulation, start chest compr ession. Combine rescue breaths and compression at the rate of 30 compressions to two effect ive breaths, repeating this cycle 5 times in approximately 2 minutes. The ratio of compressions to lung in \202 ation remains the same for resuscitation with tw o persons. ADULT ADVANCED LIFE SUPPORT 5 Adult advanced life support It is unlikely that an effective spontaneous cardiac activity w ill be restored by BLS without more advanced techniques (intubation for effective ventilati on, drugs, de \201 brillation, etc.). Do not waste time. As soon as help arrives, delegate CPR to someone less experienced in advanced cardiac life support (ACLS), so that you are a ble to continue. \200 Attach the patient to an automated external de \201 brillator (AED) as soon as possible to determine if there is a shockable rhythm and treat appropriately (see p. 7 for the univers al treatment algorithm). Oropharyngeal or nasopharyngeal airways help maintain the patency of the airway by keeping the tongue out of the way (see Fig. 1.3). Endotracheal (ET) intuba tion is the best method of securing the airway. Do not attempt this if you are inexperience d. Establish venous access. Central vein cannulation (internal jugular or subclavian) is id eal but requires more training and practice and is not for the inexperienced. If venous acc ess fails, drugs may be given via an intraosseous (IO) route (more effective than an ET tub e) or ET tube into the lungs (except for bicarbonate and calcium salts). Double the dose of drug if using this route, as absorption is less ef \201 cient than when given intravenous ly (IV). Post resuscitation care \200 Try to establish the events history, staff, witnesses, and h ospital notes of the patient. Is there an obvious cause (myocardial infarction [MI], hypoxi a, hypoglycemia, stroke, drug overdose or interaction, electrolyte abnormality, etc.)? Reco rd the duration of the arrest in the notes with the interventions, drugs (and doses) in chr onological order. Examine the patient ventilated; check for ribs that may have broken durin g CPR. Listen for any cardiac murmurs. Check the neck veins. Examine the abdomen for an ane urysm or signs of peritoneal irritation. Insert urinary catheter. Consider a nasogastric (N G) tube if the patient remains unconscious. Record the Glasgow Coma Score and perform a bri ef neurological assessment. ECG (electrocardiogram; looking for MI, ischemia, tall Investig ations: T-waves [suggesting hyperkalemia]); ABG (arterial blood gas; mixed metabolic and re spiratory acidosis is common and usually responds to adequate oxygenation and ventilation o nce the circulation is restored); CXR (chest X-ray; check position of ET tube, look for pne umothorax); and glucose, CBC (complete blood count). After early and successful resuscitati on from a primary cardiac arrest, the patient may rapidly recover completely. The patient m ust be transferred to an appropriate location (ICU) for monitoring and treatment. Change an y venous lines that were inserted at the time of arrest for central lines inserted with ste rile technique. Insert an arterial line and consider pulmonary artery (PA) catheter (Swan \200\223Ganz) if requiring inotropes. that precipitated the arrest from the to check that both lung \201 elds are being CHAPTER 1 Cardiovascular emergencies 6 Remember to talk to the relatives. Keep them informed of events and give a realistic pictur e of the arrest and possible outcomes. When appropriate, consider the possibility of organ donation and do not be frightened to discuss this with the relatives. Even if discussion wi th the relatives is delayed, remember that corneas and heart valves may be used up to 24 ho urs after death. Consider hypothermia for patients who do not immediately wake up, or who w ere \200\234down \200\235 for a period of time. Insertion of oropharyngeal airway Insertion of nasopharyngeal airway Figure 1.3 Insertion of nasopharyngeal airway. Reproduced with permission from Ramrakha PS, Moore KPK (2004). Oxford Handbook of Acute Medicine. Oxford, UK: Oxford University Press. UNIVERSAL TREATMENT ALGORITHM 7 Universal treatment algorithm Cardiac rhythms of cardiac arrest can be divided into two gro ups: 1. Ventricular \201 brillation/pulseless ventricular tachycardia (VF/VT). 2. Other c ardiac rhythms, which include asystole and pulseless elec- trical activity (PEA). The principle difference in treatment of the two groups of arrhythmias is the need for atte mpted de \201 brillation in the VF/VT group of patients. Figure 1.4 summarizes the algorithm for management of both groups of patients. VF/VT VF/VT are the most common rhythms at the time of cardiac arrest. Success in treatment of VF/VT is dependent on the delivery of prompt de \201 brillation. With each minute the chances of successful de \201 brillation declines by 7% \200\22310%. \200 Chest compressions and ventilation should be undertaken until the monitor and de \201 bril lator are available. Typically, 120J to 200J for a biphasic de \201 brillator and 360J for a monophasic de \201 brillator is delivered in one shock. Continue CPR x 5 cycles then re assess. If there is persistent VF/VT a second shock is delivered, biphasic at an energy spe ci \201 c to the device and monophasic at 360J. At this time, epinephrine 1 mg IV/IO or va sopressin 40 U IV/IO can be given and repeated. Next, another shock is delivered and if the re is persistent VF/VT, then antiarrhythmics (amiodarone 300 mg IV/IO once, then 150 mg IV/ IO once, or lidocaine 1.0 \200\2231.5 mg/kg \201 rst dose and then 0.5 \200\2230.75 mg/kg IV/IO for a maximum of 3 mg/kg) should be considered After each shock CPR is resumed immed iately for 5 cycles, after which the carotid pulse should be palpated only if the waveform changes to one usually capable of providing a cardiac output. Shock cycle is repeated every minute if VF/VT persists. Myocardial and cerebral viability must be maintained after each shock cycle with chest compressions and ventilation. In between cycles of de \201 brillati on, reversible factors must be identi \201 ed and corrected, the patient intubated (if pos sible), and venous access obtained. \200 Non-VF/VT rhythms The outcome from these rhythms is generally worse than that with VF/VT un less a reversible cause can be identi \201 ed and treated promptly. \200 Chest compressi ons and ventilation should be undertaken for 3 minutes with each loop of the algorithm (1 m inute if directly after a shock). With each cycle, attempts must be made to intubate the pa tient, gain IV access, and give adrenaline. Asystole \200 \200 Atropine 3 mg IV should be given to block all vagal output. In the presence of p waves on t he ECG strip/monitor, pacing (external or transvenous) must be considered. CHAPTER 1 Cardiovascular emergencies 8 Pulseless electrical activity (PEA) \200 Identi \201 cation of the underlying cause and its correction are both vital for successfu l resuscitation. Resuscitation must be continued while reversible causes are being sought. 1 PULSELESS ARREST BLS algorithm: Call for help, give CPR \200 Give oxygen \200 Attach monitor/defibrillat or 2 Check rhythm Shockable rhythm? Not Shockable Shockable 9 3 Asystole/PEA VF/VT 4 Give 1 shock \200 Manual biphasic: device-specific (typically 120 to 200 J) Note: if un known, use 200 J \200 AED: device specific \200 Monophasic: 360 J Resume CPR immediatel y 10 Resume CPR immediately for 5 cycles When IV/IO available, give vasopressor \200 Epinep hrine 1 mg IV/IO Repeat every 3 to 5 min or May give 1 dose of vasopressin 40 U IV/IO to replace first or second dose of epinephrine Give 5 cycles of CPR* 5 No Consider atropine 1 mg IV/IO for asystole or slow PEA rate Repeat every 3 to 5 min (up to 3 doses) Check rhythm Shockable rhythm? Shockable 6 Give 1 shock \200 Manual biphasic: device-specific (same or higher dose as first shock) Note: if unknown, use 200 J \200 Monophasic: 360 J Resume CPR immediately When IV/IO ava ilable, give vasopressor \200 Epinephrine 1 mg IV/IO Repeat every 3 to 5 min or Give 5 cycles of CPR* 11 Check rhythm Shockable rhythm? 12 \200 If asystole, go to Box 10 \200 If electrical activity, check pulse. If no pulse , go to Box 10 \200 If pulse present, begin post-resuscitation care Avoid: \200\223 hype rventilation \200\223 hypotension \200\223 hypo-/hyperglycemia \200\223 hypothermia Not Shockable 13 Go to Box 4 Shockable May give 1 dose of vasopressin 40 U IV/IO to replace first or second dose of epinephrine Give 5 cycles of CPR* NOTE: After an advanced airway is placed, give about 2 min of CPR (instead of 5 cycles) 7 No Check rhythm Shockable rhythm? During CPR \200 Secure and search for contributing factors: Shockable 8 Give 1 shock Push hard and fast (100/min) \200 Ensure full chest recoil \200 Minimize interruption i n chest compressions \200 One cycle of CPR: 30 compressions then 2 breaths: 5 cycles appr ox. 2 min \200 Establish IV/IO access \200 Secure airway and confirm placement \200 A fter an advanced airway is placed, give 6 to 10 breaths/min without pausing compressions, a void hyperventilation Manual biphasic: device-specific (same or higher dose as first shock) Note: if unknown, use 200 J \200 AED: device specific \200 Monophasic: 360 J Resume CPR immediately Consider antiarrhythmics: amiodarone (300 mg IV/IO once, then consider additional 150 mg IV/IO once ) or lidocaine (1 to 1.5 mg/kg first dose then 0.5 to 0.75 mg/kg IV/IO maximum 3 doses or 3 mg/kg Consider magnesium, loading dose 1 to 2 g IV/IO for torsades de pointes After 5 cycl es of CPR, * go to Box 5 above \200\223 Hypovolemia \200\223 Hypoxia \200\223 Hydrogen ion (acidosis) \200\223 Hypo-/h yperkalemia \200\223 Hypoglycemia \200\223 Hypothermia \200\223 Toxins \200\223 Tampona de, cardiac \200\223 Tension pneumothorax \200\223 Thrombosis (coronary or pulmonary) \200\223 Trauma Consider termination of CPR if no response Figure 1.4 Advanced cardiac life support pulseless arrest algorithm. Reprinted with permiss ion from 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and E mergency Cardiovascular Care Part 7.2: Management of Cardiac Arrest. Circulation 2005; 112( Suppl IV):IV58 \200\223IV66. 2005, American Heart Association, Inc. ACUTE PULMONARY EDEMA: ASSESSMENT 9 Acute pulmonary edema: assessment Presentation \200 \200 \200 Acute breathlessness, cough, frothy blood-stained (pink) sputum Collapse, cardiac arrest, o r shock Associated features may re \202 ect underlying cause: \200 Chest pain or palpitations \200\224? ischemic cardiomyopathy (ICMP)/MI, arrhythmia Precedin g history of dyspnea on exertion \200\224? ICMP, poor left ventricular (LV) function Oligur ia, hematuria \200\224? acute renal failure Seizures, signs of intracranial bleed \200 Causes A diagnosis of pulmonary edema or \200\234heart failure \200\235 is not adequate. U nderlying causes must be sought in order to direct treatment appropri- ately. These may be divided into the following: \200 \200 \200 Increased pulmonary capillary pressure (hydrostatic) Increased pulmonary capillary permeabi lity Decreased intravascular oncotic pressure Often a combination of factors is involved (e.g., pneumonia, hypoxia, car- diac ischemia). See Table 1.1. The main differential diagnosis is acute exacerbation of chronic obstructive pulmonary dise ase (COPD) (previous history, quiet breath sounds wheeze, fewer crackles). It may be dif \201 cult to differentiate the two clinically. Principles of management 1 Stabilize the patient \200\224relieve distress and begin de \201 nitive treatment. 2 Look for an underlying cause. 3 Address hemodynamic and respirator y issues. 4 Optimize and introduce long-term therapy. Initial rapid assessment \200 If the patient is unstable (e.g., unable to speak, hypoxic, systolic blood pressure [SBP] < 100 mmHg), introduce stabilizing measures and begin treatment immediately before detailed e xamination and investigations (see p. 12). If the patient is stable and/or if there is doub t as to the diagnosis, give oxygen and diuretic, but await the outcome of clinical examinat ion, CXR, and blood tests such as B-type natriuretic peptide (BNP) level before deciding on de \201 nitive treatment. CHAPTER 1 Cardiovascular emergencies 10 Urgent investigations for all patients \200 ECG Sinus tachycardia most common. ? Any cardiac arrhythmia (SVT, VT). ? Evidence of acute ST c hange (ACS). ? Evidence of underlying heart disease (LVH, P mitrale). To con \201 rm diagn osis, looking for interstitial shadowing, enlarged hila, prominent upper lobe vessels, pleu ral effusion, and Kerley B lines. Cardiomegaly may or may not be present. Also exclude pneu mothorax, pulmon- ary embolus (oligemic lung \201 elds), and consolidation. ? Pre-existin g renal impairment. Regular K+ and Mg measurements (once on IV diuretics). Anemia. Signs of infection. As soon as practical to assess LV function, valve abnor- malities, ventricular septal defect (VSD), or pericardial effusion. Typically low PaO2, PCO2 levels may be low (h yper- ventilation) or increased depending on severity. Pulse oximetry may be inadequate if peripheral vasoconstric- tion is present. CXR Laboratory ECHO ABG PULMONARY EDEMA: CAUSES 11 Pulmonary edema: causes Table 1.1 Look for an underlying cause for pulmonary edema Increased pulmonary capillary pressure (hydrostatic) i Left atrial (LA) pressure \200 Mitral valve disease Arrhythmia (e.g., AF) with pre-existing mitral valve disease Left atri al myxoma \200 \200 \200 \200 \200 \200 \200 i Left ventricular end diastolic pressure (LVEDP) Ischemia Arrhythmia Aortic valve disease Cardiomyopathy Uncontrolled hypertension Pericardi al constriction Fluid overload High-output states (anemia, thyrotoxicosis, Paget \200\231s, atrioventricular (AV) \201 stula, beri-beri) Renovascular disease \200 l R shunt (e.g. , VSD) L \200 Veno-occlusive disease \200 Intracranial hemorrhage \200 Cerebral edema \200 Postictal i Pulmonary venous pressure Neurogenic High-altitude pulmonary edema Increased pulmonary capillary permeability Acute lung injury Acute respiratory distress syndrome (ARDS) Decreased intravascular oncotic pressure Hypoalbuminemia i \200 \200 d \200 Losses (e.g., nephrotic syndrome, liver failure) Production (e.g., sepsis) Dilution (e.g., crystalloid transfusion). Note: the critical LA pressure for hydrostatic edema (cid:32)(cid:3)serum albumin (g/L) x 0 .57. CHAPTER 1 Cardiovascular emergencies 12 Pulmonary edema: management Stabilize the patient Patients with acute pulmonary edema shoul d initially be continuously monitored and managed where full resuscitation facilities are a vailable. \200 \200 \200 Sit the patient up in bed. Give 100% oxygen by facemask, unless contraindicated, i.e., COPD . If the patient is severely distressed, the patient may require continuous positive airway pressure (CPAP) or mechanical ventilation. Treat any hemodynamically unstable arrhythmia ( urgent synchronized DC shock may be required, (p. 78). Give \200 \200 Secure venous acc ess and send blood for urgent blood work. Unless thrombolysis is indicated, take ABG. If SB P \200 \200 Morphine 2.5 \200\2235 mg IV (caution: abnormal ABGs) Frusemide 40 \200\223120 mg slow IV i njection \200 \200 (cid:116)90 mmHg and the patient does not have aortic stenosis: Give sublingual nitroglycerin spray (2 puffs). Start IV nitroglycerin infusion 1 \200\22310 mg/hr; increase the infusion rate every 15 \200\22320 minutes, titrating against blood pre ssure (aiming to keep SBP 100 mmHg). \200 \200 If SBP <90 mmHg, treat patient as cardiogenic shock. Insert a urinary catheter to monitor u rine output. + if the clinical condition deteriorates or fails to Repeat ABG and K improve, or after 2 hours if there is improvement and the original sample was abnormal. Monitor pul se, BP, respiratory rate, O oximeter (if an accurate reading can be obtained), and urine ou tput. 2 saturation with a pulse Further management The subsequent management of the patient is aimed at ensuring adequate v entilation/gas exchange, ensuring hemodynamic stability, and correcting any reversible prec ipitants of acute pulmonary edema. If the patient stabi- lizes, begin investigations lookin g for a cause. If the patient remains unstable and/or deteriorates conduct the assess- ments listed next. Assess patient \200\231s respiratory function Wheeze may be caused by interstitial pulmonar y edema. If there is a his- tory of asthma, give nebulized salbutamol (2.5 \200\2235 mg), n ebulized ipratro- pium bromide (500 g), and hydrocortisone (200 mg) IV. Indications for further respiratory support \200 \200 \200 \200 Patient exhaustion or continuing severe breathlessness Persistent hypoxemia Rising P aCO2 P ersistent or worsening acidosis (pH < 7.2) PULMONARY EDEMA: MANAGEMENT 13 Continuous positive airway pressure (CPAP) This may be tried for cooperative patients who c an protect their airway, have adequate respiratory muscle strength, and who are not hypoten sive. The positive pressure reduces venous return to the heart and may com- promise BP. Endotracheal intubation and mechanical ventilation This may be required, and some positive end expiratory pressure (PEEP) should be used. PEEP may also lower SBP. Discuss the patient with the on-call anesthesiologist and ICU team early. Assess patient \200\231s hemodynamic status It is important to distinguish between cardioge nic and noncardiogenic pulmonary edema, as further treatment is different for the two group s. Making this distinction may be dif \201 cult clinically. A central venous or PA (Swan \200\223Ganz) catheter must be inserted if the patient \200\231s condition will allow this procedure. Management The general approach involves a combination of diuretics, vasodilators, inotr opes. Patients may be divided into two groups: \200 \200 Patients in shock (with SBP <90 mmHg) Hemodynamically stable patients with SBP >90 mmHg Patients with SBP <90 mmHg The choice of inotropic agent depends on the clinical condition of the patient and, to some extent, the underlying diagnosis: SBP <90 mmHg give: \200 Dopamine to direct and indirect inotropic effects and may be used at higher doses (10 \200 \22320 g/kg/min) if the blood pressure remains low. However, it tends to raise the pulmon ary capillary \201 lling pressure further and should be combined with vasodilators (e.g., nitroprusside or hydralazine) once the blood pressure is restored (see below). Beware of a rrhythmias at these dosages. infusion may be preferred to high-dose dopamine Epinephrine as an alternative inotrope. Once the blood pressure is restored (>100 mmHg), vasodilators suc h as nitroprusside/hydralazine or nitroglycerin infusion should be added to counteract the pressor effects. Epinephrine can be combined with dobutamine and/or a phosphodiesterase inh ibitor, especially in the context of a poor ventricle. Dobutamine infusion 10 \200\22315 mi nutes to a maximum of 20 g/kg/min until BP >100 mmHg. This may be combined with dopamine (2.5 \200\2235 g/kg/min). However, tachycardia and/or hypotension secondary to peripheral vasodilation may limit its effectiveness. Phosphodiesterase inhibitors dobutamine fails. at doses of >2.5 g/kg/min has a pressor action in addition at 5 g/kg/min, increasing by 2.5 g/kg/min every (milrinone) should be considered where CHAPTER 1 Cardiovascular emergencies 14 Intra-aortic balloon counterpulsation without inotropes in the context of a potentially rev ersible cause for the pulmonary edema and shock (e.g., ongoing myocardial ischemia, VSD, ac ute mitral regurgitation [MR]). Further doses of diuretic may be given. should also be used with or Patients with SBP (cid:1)90 mmHg \200 Further doses of diuretic may be given (furosemide 40 \200\22380 mg IV q3 \200\2234h or as a continuous infusion [10 \200\22380 mg/hr]). Continue the nitroglycerin infusion, increasi ng the infusion rate every 15 \200\22320 minutes up to 10 mg/hr, titrating against blood pr essure (aiming to keep SBP 100 mmHg). Long-term management \200 Unless a contraindication exists, start an angiotensin-converting enzyme (ACE) inhibitor, i ncreasing the dose to as near the recommended maximum dose as possible. In the context of L V impairment, ACE inhibitors have signi \201 cant prognostic bene \201 t. If ACE inhibito rs are contraindicated or not tolerated, consider use of hydralazine and long-acting oral n itrate in combination. If the patient is already on high doses of diuretics and ACE inhibit ors, consider addition of spironolactone (25 \200\22350 mg) (monitor renal function and ser um potassium). In the context of stable patients (no clinical features of failure) and poor LV function, B-blockers have signi \201 cant mortality and some symptomatic bene \201 t (start with very small dose and increase gradually every 2 weeks with regular monitoring). Bisoprolol, carvedilol, and metoprolol can all be used. Ensure that all arrhythmias are tre ated. Digoxin can be used for symptomatic improvement. Consider cardiac resynchronization t herapy (biventricular pacing) in the context of severe LV dysfunction, broad QRS complex MR on ECHO. Patients in atrial \201 brillation (AF) or with poor LV function should be c onsidered for long-term anticoagulation. Patients <60 years with severe irreversible LV dys function and debilitating symptoms must be considered for cardiac transplantation. \200 \200 PULMONARY EDEMA: SPECIFIC CONDITIONS 15 Pulmonary edema: speci \201 c conditions Diastolic LV dysfunction This typically occurs in elderly hypertensive patients with left ventricular hypertrophy (LVH), where there is impa ired relaxation of the ventricle in diastole. There is marked hypertension, pulmonary edema , and normal, or only mild, systolic LV impairment. With tachycardia, diastolic \201 lling time shortens. As the ventricle is \200\234stiff \200\235 in diastole, LA pressure is increased and pulmonary edema occurs (exac- erbated by AF as \201 lling by atrial systole is lost). Treatment involves control of hypertension with IV nitrates (and/or nitroprusside), calcium blockers (verapamil or nifedipine), and even cer- tain B-blockers (e.g., carvedilol, bisop rolol) and, if appropriate, restoration of sinus rhythm. Fluid overload Standard measures are usually effective. \200 Check that the patient is not anemic (Hb blood via cannula in a large vein and repeat if ne cessary. If anemic (e.g., renal failure) and acutely unwell, consider dialysis. (cid:116)10 g/dL). Remove 500 mL Known (or unknown) renal failure \200 Unless the patient is permanently anuric, large doses of IV furosemide may be required in a ddition to standard treatment. If this fails or the patient is known to be anuric, dialysis will be required. In patients not known to have renal failure an underlying cause should b e sought. Anemia \200 Cardiac failure may be worsened or precipitated by the presence of signi \201 cant anemia. Symptoms may be improved in the long term by correcting this anemia. If the anemia is thou ght to be exacerbating pulmonary edema, ensure that an adequate diuresis is obtained prior to transfusion. Give slow transfusion (3 \200\2234 hours per unit) of packed cells, with IV furosemide 20 \200\22340 mg before each transfusion. Hypoproteinemia \200 Treatment involves diuretics, cautious albumin replacement, spironolactone (if there is sec ondary hyperaldosteronism), and treatment of the underlying cause for hypoproteinemia. CHAPTER 1 Cardiovascular emergencies 16 Acute aortic regurgitation Presentation \200 Sudden, severe aortic regurgitation (AR) presents as cardiogenic shock and acute pulmonary edema. The hemodynamic changes are markedly different from those seen in chronic AR. The pr evious normal-sized LV results in a smaller effective forward \202 ow and higher LVEDP fo r the same degree of AR. Patients are often extremely unstable, tachycardic, and peripheral ly vasoconstricted and often have pulmonary edema. Unlike chronic AR, pulse pressure may be near normal. If available, ask about history of previous valvular heart disease, hypertens ion, features of Marfan \200\231s syndrome (family history), and risk factors for infective endocarditis. Physical signs of severe AR include a quiet aortic closure sound (S2); an ej ection systolic murmur over the aortic valve (turbulent \202 ow); high-pitched and short, early diastolic murmur (AR); quiet S1 (premature closure of the mitral valve). Examine spe ci \201 cally for signs of an underlying cause. Where there is no obvious underlying cause (e.g., acute MI), assume infective endocarditis until proven otherwise. \200 Causes \200 \200 \200 \200 \200 \200 Infective endocarditis Ascending aortic dissection Collagen vascular disorders (e.g., Marfa n \200\231s) Connective tissue diseases (large- and medium-vessel arteritis) Trauma Dehisce nce of a prosthetic valve Diagnosis Diagnosis is based on a combination of clinical features and transthoracic and/or transesophageal ECHO. Management Acute AR is a surgical emergency and all other management measures are only aime d at stabilizing the patient until urgent aortic valve replacement (AVR) can take place. Th e patient \200\231s clinical condition will determine the urgency of surgery (and risk of m ortality). General measures \200 \200 \200 \200 \200 Admit the patient to intensive care unit (ICU). Give oxygen and begin treating any pulmonar y edema with diuretics. Monitor blood gasses; mechanical ventilation may be necessary. Bloo d cultures Serial ECG: watch for developing atrioventricular (AV) block or conduction defec ts in endocarditis. x 3 are essential. ACUTE AORTIC REGURGITATION 17 Speci \201 c measures \200 \200 Every patient must be discussed with a cardiothoracic surgeon. In the context of good syste mic BP, vasodilators such as sodium nitroprusside or hydralazine may temporarily improve fo rward \202 ow and relieve pulmonary edema. Inotropic support may be necessary if the pati ent is hypotensive. However, inotropes are best avoided as any increase in systemic pressur es and peripheral vasoconstriction may worsen AR. All patients with hemodynamic compromise should have immediate or urgent AVR. Infective endocarditis Intra-aortic balloon pump (IABP ) must be avoided, as it will worsen AR. \200 : indications for surgery are given on p. 208. CHAPTER 1 Cardiovascular emergencies 18 Acute mitral regurgitation Presentation \200 Patients most commonly present with acute shortness of breath and severe pulmonary edema. S ymptoms may be less severe, or spontaneously improve as left atrial compliance increases. T here may be a history of previous murmur, angina, or myocardial infarction. The signs are d ifferent from those seen in chronic MR because of the presence of a nondilated and relative ly noncompliant LA. Acute MR results in a large LA systolic pressure wave (v wave) and henc e pulmonary edema. Patients may be acutely ill with tachycardia, hypotension, peripheral va soconstriction, and pulmonary edema, and a pan-systolic murmur of MR. Later in the illness, probably because of sustained high left atrial and pulmonary venous pressures, right heart failure develops. Examine for signs of any underlying conditions. When there is no obvious underlying cause (e.g., acute MI; see Box 1.1), assume the patient has infective endocardi tis until proven otherwise. \200 Diagnosis Diagnosis is based on a combination of clinical features and ECHO. Transthoracic echocardiography (TTE) can be used to readily diagnose and quantify MR. It also provides in formation on LV status (in particular regional wall motion abnormalities that can give rise to MR). TEE can provide speci \201 c information about etiology of valve dysfunc- tion, including papillary muscle rupture and MV lea \202 et (anterior and posterior) structural abnormalit ies. This information will be vital for a decision regarding de \201 nitive management. Th e important differential diagnosis is a VSD. TTE and Doppler studies can readily differentiate between the two con- ditions. Alternative ly, if ECHO is not available, pulmonary artery catheter- ization in acute MR will exclude t he presence of a left-to-right shunt and the pulmonary capillary wedge pressure (PCWP) trac e will demonstrate a large v-wave. General measures \200 \200 \200 \200 \200 Admit patient to ICU. Give oxygen and begin treating any pulmonary edema with diuretics. Mo nitor blood gasses; mechanical ventilation may be necessary. Blood cultures If present, MI should be treated in the standard manner. x 3 are essential. Speci \201 c measures Pulmonary edema may be very resistant to treatment. \200 In the presence of good BP, reduction in preload (nitroglycerin infusion) and afterload, es pecially with ACE inhibitors, is important. Systemic vasodilators such as hydralazine (12.5 \200\223100 mg tid) can also be added. ACUTE MITRAL REGURGITATION 19 \200 An IABP will help decrease LVEDP and increase coronary blood \202 ow. Patients may requir e inotropic support. There are multiple combinations and etiologies of MR and hemodynamic s tatus, and local policy and expertise should dictate choice of agent. CPAP and intubation a nd positive-pressure ventilation are extremely useful and must be considered in all severe and/or resistant cases. Hemodynamic disturbance and severe pulmonary edema in the context o f acute MR is a surgical emergency. Infective endocarditis: Post-infarct MR: following resu scitation. Patients who are stabilized may have mitral valve replacement (MVR) deferred bec ause of risks of surgery in the post-infarct patient. Preoperative management should consis t of diuretics and vasodilators, including ACE inhibitors, if tolerated. Opening the infarc t-related artery (angioplasty) may improve acute MR. \200 indications for surgery are given on p. 208. management depends on the patient \200\231s co ndition Box 1.1 Causes of acute mitral regurgitation \200 \200 \200 Infective endocarditis Papillary muscle dysfunction or rupture (post-MI). Rupture of chorda e tendinae (e.g., infection, myxomatous degeneration, systemic lupus erythematosus [SLE]) T rauma (to lea \202 ets, papillary muscle, or chordae) Prosthetic valve malfunction (e.g., secondary to infection) Left atrial myxoma Acute rheumatic fever Collagen vascular disorder s (e.g., Marfan \200\231s) Connective tissue diseases (large- and medium-vessel arteritis) \200 \200 \200 \200 \200 CHAPTER 1 Cardiovascular emergencies 20 Deep vein thrombosis: assessment Presentation \200 Deep vein thrombosis (DVT) is most commonly asymptomatic. Minor leg discomfort or isolated swelling (>65%) in the affected limb are the most common clinical features. Breathlessness or chest pain may be secondary to pulmonary embolism (PE). Signs include erythema and swell ing of the leg, dilated super \201 cial veins, and calf discomfort on dorsi \202 exion of the foot (Homan \200\231s sign). The thrombus may be palpable as a \201 brous cord in th e popliteal fossa. Con \201 rm the presence of swelling (>2 cm) by measuring the limb circ umference 15 cm above and 10 cm below the tibial tuberosity. In all cases of leg swelling, abdominal and rectal (and pelvic in women) examination must be carried out to exclude an ab dominal cause. See Table 1.2 for risk factors for DVT. Investigations \200 