Cardiovascular Emergencies - Part 10 doc

of these signs to appear indicates that the catheter has not crossed the valve and is merely curling round in an enlarged right atrium: deflate the balloon and start again. (4) The balloon should now “turn the corner” and face cranially: pausing for a few seconds may facilitate this, as may asking the patient to take a deep breath. (5) Advancing the catheter will result in the balloon crossing the pulmonary valve signalled by an increase in diastolic pressure, usually around the 40 cm mark. (6) Feed the catheter forward into the pulmonary artery (it usually lodges on the right side and at around 40–50 cm). (7) The catheter should migrate distally into the wedged position. This can be confirmed by the characteristic forward motion of the catheter tip when the balloon is inflated and the bifid pressure trace. Deflation of the balloon should be followed by movement of the balloon backwards into the pulmonary artery, the restoration of pulsatile motion and the re-appearance of the characteristic arterial pressure tracing (Figure 14.5). Cardiovascular Emergencies 350 Figure 14.5 Pressure tracings obtained during pulmonary artery catheterisation. 1318 BMJ Cardio Emergencies 29/5/01 3:52 pm Page 350 The three most important rules in PA catheter placement are: • Never leave the catheter with balloon wedged for longer than it takes to make a PCWP measurement (< 40 seconds). • Never pull the catheter back with the balloon still inflated. • Always inflate the balloon slowly and monitor the pressure tracing during inflation. PCWP readings only represent left atrial pressure if the pulmonary capillary wedge pressure (PCWP) value is less than alveoiar pressure. 6 This condition is only satisfied for the basal one-third of the lungs (so called zone 3). This region is readily identified in erect patients where a useful rule is to ensure that the catheter tip is always below the level of the left atrium. However, in a supine patient this region can only be identified with a lateral chest x ray and this is unacceptably cumbersome for routine use. As the majority of catheters spontaneously lodge in zone 3 (due to its higher flow), a suggested compromise is to resort to a lateral chest x ray if the PCWP data do not fit into the overall clinical picture. As the catheter is manufactured from PVC, it becomes progressively less rigid following insertion. Thus it is important to attempt to cross the tricuspid valve and to negotiate the curve of the RV (the two most difficult manoeuvres) as soon as possible after insertion. 14.3.3 Interpretation The commonly encountered haemodynamic patterns are listed in Table 14.1. The normal range of the right heart pressures are given in Table 14.2. It is important to appreciate that the accuracy of the pressure data is limited and should be viewed in terms of a series of bands (low: 0–13, mid 14–23, and high > 24 mmHg) as opposed to absolute values. In particular, a change in pressure in response to fluid loading, diuresis, etc. is more significant than isolated values. Importantly, the relationship between pressure and volume (i.e. the degree of pressure change one would expect for a given change in volume) is non-linear and varies with time due to changes in circulatory capacitance. Formulae for the derived variables are listed in Box 14.1, however, these all Practical procedures 351 1318 BMJ Cardio Emergencies 29/5/01 3:52 pm Page 351 depend on thermodilution derived cardiac output, which is frequently inaccurate. For the majority of cardiac patients, calculation of these values adds little to patient management and use of a non-thermodilution catheter is satisfactory. In patients with obstructive airways disease, pulmonary fibrosis, mechanical ventilation, mitral stenosis, or following cardiopulmonary bypass, PCWP values tend to be higher than LV filling pressures. Conversely, aortic regurgitation, pneumonectomy and pulmonary embolus are all associated with PCWP readings in excess of true LV filling pressures. Table 14.1 Haemodynamic patterns in shock. Condition RA PA PCWP CI PVR SVR LV infarction ǟǞ orȆǟǞ ȆȆȇȇȆ RV infarction Ȇ ȇ ȇȇȇȆ <1.5 ϫ RA Ventricular septal ǟǞ orȆ Ȇ ȆȆȆȆ defect Papillary muscle ǟǞ orȆ Ȇ ȆȆȇȆȆ rupture Massive pulmonary ȆȆȇȇȆȆȆ embolus Tamponade ȆȆ ȇ ϭ to RA ȇǟǞȆ Early septicaemia ȇ ȇ ȇȆȇȇ Late septicaemia ǟǞ orȆǟǞ orȆȆȇȆȆ Hypovolaemia ȇȇȇȇǟǞȆ RA: right atrium, PA: pulmonary artery; PCWP: pulmonary capillar y wedge pressure; CI: cardiac index; PVR: pulmonary vascular resistance; SVR: systemic vascular resistance. Notes These represent general trends, to which there are many exceptions (for example pulmonary artery resistance and pressure may both rise in septicaemic shock, whilst both RA and PCWP may be normal despite marked hypovolaemia). Large “V” waves may be present in the PCWP tracing of patients with both ventricular septal defects and acute mitral regurgitation. The thermodilution cardiac index in patients with VSDs will reflect pulmonary flow and will therefore br higher than expected. Saturation measurements in patients with VSDs will demonstrate the characteristic “step-up” between the RA and RV samples. Cardiovascular Emergencies 352 1318 BMJ Cardio Emergencies 29/5/01 3:52 pm Page 352 Table 14.2 Normal ranges of right heart pressures Site Pressure/mmHg Right atrium (RA) range 0–5 Right ventricle (RV) systolic 15–30 diastolic 0–6 Pulmonary artery (PA) systolic 15–30 diastolic 5–13 range 10–18 Pulmonary wedge (PCWP) range 2–12 Box 14.1 Derived data formulae Systemic vascular resistance ϭ 80 (MAPϪCVP) 1000–1500 dynes/s/cm Ϫ 5 CO Pulmonary vascular resistance ϭ 80 (MPAPϪPCWP) 120–250 dynes/s/cm Ϫ 5 CO Cardiac index ϭ CO 2.5–4.5 l/min/m 2 body surface area COϭcardiac output, MPAPϭmean pulmonary artery pressure, CVPϭcentral venous pressure, PCWPϭpulmonar y capillary wedge pressure 14.3.4 Potential problems Failure to wedge is usually due to the balloon failing to migrate distally enough. Deflate the balloon and attempt to manoeuvre it into another lung segment. If the catheter will not wedge despite this then the pulmonary artery diastolic pressure may be used as a substitute for PCWP. Damped traces respond to flushing the system or slight withdrawal of the catheter. Effects of mechanical ventilation and PEEP may be minimised by taking all recordings at end expiration. Practical procedures 353 1318 BMJ Cardio Emergencies 29/5/01 3:52 pm Page 353 Right bundle branch block occurs in 5% of patients due to the balloon coming into contact with the exposed section of the right bundle (moderator band) as it tracks across the right ventricular floor. This may produce complete heart block in patients with pre-existing left bundle branch block in whom a prophylactic temporary wire is required. Pulmonary artery rupture, presenting as haemoptysis, may occur when the balloon is inflated too rapidly in a small peripheral branch: this emphasises the importance of slow and gentle balloon inflation. Catheter knotting is a risk if screening is not used and the distances for the appearance of the various changes in waveform are exceeded. Once knotted it may prove impossible to withdraw the catheter into the sheath and a surgical venotomy may be needed. 14.4 DC cardioversion The degree of preparation appropriate will depend on the urgency of the situation. 7,8 Prior to performing DC cardioversion, check the plasma potassium and correct this if time permits, though bear in mind that two oral potassium tablets will have little effect on total body potassium levels. Similarly, for elective conversion of atrial fibrillation or flutter with durations > 48 hours adequate anticoagulation (INR > 2.5 in general, but 3.5–4 with mechanical valves) both at the present time and over the preceding month should be confirmed. An alternative is to perform a transoesophageal echo to confirm the absence of intracardiac thrombi and then perform cardioversion with acute heparin. In conscious patients adequate sedation is essential and this is best obtained with general anaesthesia. Light sedation for cardioversion, other than in extreme emergencies, is unacceptable. Deep sedation using iv midazolam combined with flumazenil recovery is an alternative only in experienced hands and requires the presence of a second doctor to administer. Digoxin need not be withheld prior to cardioversion, but caution should be exercised in patients in whom digoxin toxicity is suspected. Cardiovascular Emergencies 354 1318 BMJ Cardio Emergencies 29/5/01 3:52 pm Page 354 (1) Connect the patient to the defibrillator. (2) Switch lead orientations until a QRS of adequate amplitude is obtained. (3) Change the defibrillator to synchronous shock mode and check that the sensing algorithm marks each R wave with a sensing artifact. (4) Place the paddles or self adhesive pads either anterolaterally (apex and right praecordium) or anteroposteriorly (apex and posterior). (5) Charge to the appropriate energy (see below). (6) Check that everyone is clear, issue the “everyone clear” warning and depress the discharge button: there is a disconcerting pause of approximately 1–2 seconds (depending on heart rate) before discharge. (7) If cardioversion is successful then a 12-lead ECG should be obtained. If unsuccessful then the energy level should be increased and/or an anteroposterior position attempted. • Patients who transiently convert to sinus rhythm (SR) but then degenerate back to their initial arrhythmia will not remain in SR any longer despite higher energy shocks. • Optimum results are obtained from anteroposterior paddle positions 9 (best achieved with self adhesive pads) and end expiration. It is important to appreciate that firm pressure is still required even when pads are used. • Previous recommendations for the initial energy settings started at inappropriately low levels and the recent demonstration that myocardial damage does not occur during routine cardioversion has encouraged the use of higher initial energy levels. 10,11 For atrial fibrillation, we currently use a starting energy of 200 J followed by 360 J, 12 whilst for atrial flutter, a minimum energy of 100 J is recommended. 13 The position is less clear for ventricular tachycardia, but we currently recommend 200 J. • Unlike troponins, 10,11 “cardiac” enzymes (including creatinine kinase MB fraction (CKMB)) are elevated following cardioversion due to skeletal muscle damage, and blood for these should be obtained taken prior to the procedure (from the sample used to check the K ϩ ). Practical procedures 355 1318 BMJ Cardio Emergencies 29/5/01 3:52 pm Page 355 • There is preliminary evidence to suggest an increased rate of successful conversion following the administration of 1 mg atropine in patients with atrial fibrillation who do not successfully convert to SR. 14 • Patients require one month of anticoagulation following successful cardioversion of atrial fibrillation (restoration of mechanical activity lags behind the electrical function by several weeks). Potential problems Ventricular fibrillation occasionally follows cardioversion (even with correct synchronisation). Before a defibrillating shock can be administered it is essential to switch to asynchronous mode without which no shock will be delivered despite frantic depression of the discharge buttons (the defibrillator cannot synchronise on VF). Fulminant pulmonary oedema may complicate successful cardioversion. Peripheral embolisation occurs in 1–2% of cases. Permanent pacemakers may be disabled by shocks delivered < 10 cm of the pulse generator, resulting in profound bradycardia following cardioversion. A pacing magnet will revert the system to asynchronous mode (VOO/DOO) and overcome this. Skin burns are more common with higher energy levels (both total and cumulative 15 ) and are traditionally treated with 1% hydrocortisone cream. 14.5 Pericardiocentesis 14.5.1 Clinical presentation of cardiac tamponade The classical features, encompassing Beck’s triad, are of a falling blood pressure, rising venous pressure and quiet heart sounds. Added to this are pulsus paradoxus, a rise in central venous pressure with inspiration and occasionally the Cardiovascular Emergencies 356 1318 BMJ Cardio Emergencies 29/5/01 3:52 pm Page 356 presence of a pericardial friction rub. Unfortunately, the possibility of tamponade is often not considered and treatment is frequently delayed. 16 14.5.2 Investigations The ECG may demonstrate small voltage QRS complexes (a subjective observation of little practical use). The cardiac silhouette appears globular on chest x ray. Echocardiography will demonstrate the presence of a pericaridal effusion. Unfortunately, confusion exists between the anatomical demonstration of pericardial fluid and the physiological diagnosis of tamponade. The degree of compression, and thus the restriction to cardiac filling, exerted by pericardial fluid depends upon the rate of its accumulation and the degree of pericardial distensibility. Thus the rapid accumulation of small volumes (<1 cm effusion) of fluid into a rigid pericardium may produce acute tamponade whilst the gradual accumulation of much larger amounts may not. Echo and Doppler features to determine the haemodynamic consequences of pericardial fluid do exist (Box 14.2) but the more sophisticated of these are rarely performed. In addition, it is important to appreciate that inexperienced echocardiographers may mistake pleural fluid for a pericardial effusion. Box 14.2 Echo/Doppler quantification of haemodynamic consequences of pericardial fluid Right ventricular collapse with inspiration > 20% change in mitral or 40% change in tricuspid velocities with respiration (mitral flow ȇ with inspiration, tricuspid flow Ȇ) For these reasons the primary determinant of the need for emergency (as opposed to diagnostic) pericardiocentisis must be made on the basis of the degree of haemodynamic compromise (hypotension with > 20 mmHg paradox) and not simply the presence of pericardial fluid per se. Failure to appreciate this may lead to severe complications from a procedure that was never likely to have benefitted the patient in the first place. Practical procedures 357 1318 BMJ Cardio Emergencies 29/5/01 3:52 pm Page 357 14.5.3 Blind pericardiocentesis The traditional procedure should now only be used as a last resort: actual or impending cardiac arrest due to pulseless electrical activity (PEA). Connecting an ECG lead to the needle makes it no less barbaric and only wastes time. (1) Attach a 16 gauge needle to a 25 ml syringe: use either a spinal needle or one taken from a central line set. (2) Palpate just beneath the xiphisternum. (3) Angle the needle 45° downwards and 45° to the left (aiming for the left shoulder) (4) Advance the needle with continuous negative pressure, stopping the moment blood is aspirated. (5) Place the aspirated blood into a plain glass test tube: ventricular blood clots, but pericardial fluid does not. 14.5.4 Echo-guided pericardiocentesis This is now the procedure of choice, but is still hazardous and should only be performed by those with experience. If time permits, a clotting screen and platelet count should be checked. (1) Scan the patient to determine the region with the optimum combination of fluid width and accessability, mark the skin at the proposed point of entry. (2) Prepare a sterile field and consider the use of light sedation. (3) Infiltrate both the superficial and deep layers with local anaesthetic. (4) Make a small nick in the skin at the marked entry site. (5) Open a sterile glove and ask an assistant to place echo gel and the echo transducer into this to provide a sterile transducer. Re-scan from the point of skin incision to the point of proposed pericardial penetration, noting the depth in centimetres from the display. (6) Gradually advance the pericardiocentisis needle parallel Cardiovascular Emergencies 358 1318 BMJ Cardio Emergencies 29/5/01 3:52 pm Page 358 to the echo probe an appropriate distance to puncture the pericardium (the needle itself is often poorly visualised on the scan). (7) Aspirate fluid. If there is uncertainty about the needle’s position, gently re-inject a small volume of the fluid: echo contrast will appear within the cardiac chambers if ventricular perforation has occurred. (8) Remove the syringe and advance the guidewire into the pericardium before removing the needle. (9) Advance the dilator over the wire and then remove it. (10) Advance the pericardial drainage pigtail catheter over the wire. (11) Aspirate fluid whilst intermittently confirming that the effusion is indeed decreasing, send samples for cytology and culture as appropriate. (12) When no further fluid can be aspirated (a small posterior collection often remains), re-insert the guidewire and remove the pigtail. Failure to re-insert the guidewire may result in the curled up end of the pigtail catheter lacerating the coronary veins. Leaving a drain in the pericardium should be avoided if possible: if recurrent fluid accumulation occurs then a pericardial window should be considered. (13) A chest x ray should be obtained following the procedure, as pneumothorax is a potential complication. 14.5.5 Potential problems Perforation of the cardiac chamber (usually the right ventricle) is the most common problem. The chances of this occurring are minimised by echo guidance and by avoiding drainage of effusions of < 1 cm depth at the proposed entry site. As noted above, the appearance of an echo contrast effect within the heart, when a small volume of the aspirate is injected, is diagnostic. Injection of radiocontrast and screening is an alternative. If only the needle has perforated the myocardium, matters may resolve spontaneously once it has been removed (although the effusion will enlarge); if the dilator has been Practical procedures 359 1318 BMJ Cardio Emergencies 29/5/01 3:52 pm Page 359 [...]... ventricular damage 57–8, 132, 136, 137 left ventricular dysfunction atrial fibrillation 204 causes 110, 111 mechanism for 107 10 systolic vs diastolic 109 , 110 valvular vs non-valvular 110 left ventricular hypertrophy 123–4, 170, 307 acute chest pain 20 hypertensive 46, 109 narrow complex tachycardia 246 lidocaine (lignocaine) 373 antiarrhythmic 269, 270, 279, 282 cardiac arrest 315 central venous access... unstable angina 94 alveolar oedema 104 alveolar shadowing 107 , 123, 135 alveolar thickening 102 American Heart Association protocols 311 amiloride 116 amiodarone 66–7, 141, 207, 210, 214 as adjunctive agent 216 in cardiac arrest 316 intravenous 208 preloading 213 protocol 367 377 Cardiovascular Emergencies in tachycardia 235, 243, 270 amnesia 285 and syncope 290 amoxicillin 101 anaesthesia 207, 268 analgesia... 2.3 2.7 70 1.1 1.6 2.1 2.6 80 1.2 1.8 2.4 3.0 4 5 6 7 8 9 10 15 20 2.6 3.0 3.8 4.5 5.3 6.0 6.8 7.5 11.3 15 3.2 3.6 4.5 5.4 6.3 7.2 8.1 9.0 13.5 18 3.2 3.7 4.2 5.3 6.3 7.4 8.4 9.5 10. 5 15.8 21 3.6 4.2 4.8 6.0 7.2 8.4 9.6 10. 8 12.0 18.0 24 90 1.4 2.0 2.7 3.4 4.1 4.7 5.4 6.8 8.1 9.5 10. 8 12.2 13.5 20.3 27 100 1.5 2.3 3.0 3.8 4.5 5.3 6.0 7.5 9.0 10. 5 12.0 13.5 15.0 22.5 30 (Figures within the table are... quickly 50 mg in 10 ml over 1 minute If necessary repeat at 5 minute intervals Infusion 500 mg (100 ml) in 500 ml 5% dextrose Commence infusion at 120 mg/hr Titrate to keep systolic BP at approximately 100 mmHg Lidocaine (lignocaine) Administration: Route Any IV access by slow injection – too rapid may cause fitting Bolus Usually 50 100 mg A further 50–l00 mg can be given Infusion Lidocaine (lignocaine)... minutes to total of 10 mg Bretylium Administration: Route Any IV access Bolus 5 mg/kg (undiluted) If no response after 5 minutes, increase to 10 mg/kg Maximum dose 40 mg/kg or 500 mg plus 40 ml 5% dextrose or 0.9% N saline (stable for up to 24 hours) Infuse over 8–30 minutes up to a total dose of 5 10 mg/kg Infusion 1–2 mg/min or 5 10 mg/kg over 15–30 minutes every 6 hours 367 Cardiovascular Emergencies Dalteparin... 8.6 10. 1 11.5 13.0 14.4 18 5.0 5.9 6.7 7.6 8.4 10. 1 11.8 13.4 15.1 16.8 21 5.8 6.7 7.7 8.6 9.6 11.5 13.4 15.4 17.3 19.2 24 14 16 18 20 25 90 2.2 3.2 4.3 5.4 6.5 7.6 8.6 9.7 10. 8 13.0 15.1 17.3 19.4 21.6 27 100 2.4 3.6 4.8 6.0 7.2 8.4 9.6 10. 8 12.0 14.4 16.8 19.2 21.6 24.0 30 (Figures within the table are expressed in ml/hr) Appendix 369 Cardiovascular Emergencies 370 Dopamine Administration: Route... 95, 113–14 nitroprusside see sodium nitroprusside non-Q wave infarction 32–3, 37, 38, 62 management 96 revascularisation 91 non-specific chest pain 21 non-ST elevation infarction 32 non-VT/VF 312, 314–15 reversible causes 315, 323 noradrenaline (norepinephrine) 145, 374 nuclear perfusion scanning 91, 130 OASIS-2 trial 87 obstructive airways disease 105 , 219 occlusion coronary arteries 44, 132 intermittent... 2 50 1.5 3.0 6.0 60 1.8 3.6 70 2.1 80 micrograms/kg/min 3 4 5 6 9.0 12.0 15.0 18.0 7.2 10. 8 14.4 18.0 21.6 4.2 8.4 12.6 16.8 21.0 25.2 2.4 4.8 9.6 14.4 19.2 24.0 28.8 90 2.7 5.4 10. 8 16.2 21.6 27.0 32.4 100 3.0 6.0 12.0 18.0 24.0 30.0 36.0 375 Appendix (Figures within table are expressed in ml/hr) Cardiovascular Emergencies Tirofiban Administration: Route: IV Infusion: Rmove 50 ml from a 250 ml container... 80–83 9500 >83 368 10 000 Dobutamine Administration: Route Any IV access – ideally should be given centrally Infusion 250 mg in 50 ml 5% dextrose Usual range ϭ2.5 10 micrograms/kg/min Dose (micrograms/kg/min) Weight (kg) 2 3 4 5 6 7 50 1.2 1.8 2.4 3.0 3.6 60 1.4 2.2 2.9 3.6 4.3 70 1.7 2.5 3.4 4.2 80 1.9 2.9 3.8 4.8 8 9 10 12 4.2 4.8 5.4 6.0 7.2 8.4 9.6 10. 8 12 15 5.0 5.8 6.5 7.2 8.6 10. 1 11.5 13.0 14.4... arrest 326 in cardiac arrest 316 comparative efficacy 210 maintenance 210 in polymorphic VT 275 anticoagulation 192, 213, 214–5, 218 after DC cardioversion 356 antithrombotic therapy 214 in aortic dissection 169 378 long-term 190–1 and syncope 295 anti-emesis in aortic dissection 161 in myocardial infarction 52 antiplatelet therapy 83–5, 93 second-line 83 sites of action 84 antithrombin therapy direct . patients with VSDs will demonstrate the characteristic “step-up” between the RA and RV samples. Cardiovascular Emergencies 352 1318 BMJ Cardio Emergencies 29/5/01 3:52 pm Page 352 Table 14.2 Normal. Cardiol 2000;86:348–50. 13 Pinski SL, Sgarbossa EB, Ching E, Trohman RG. A comparison of 50-J versus 100 -J shocks for direct-current cardioversion of atrial flutter. Am Heart J 1999;137:439–42. 14 Sutton. 6500 58–62 7000 63–66 7500 67–69 8000 70–74 8500 75–79 9000 80–83 9500 >83 10 000 Cardiovascular Emergencies 368 1318 BMJ Cardio Emergencies 29/5/01 3:52 pm Page 368 Appendix 369 Dobutamine Administration: Route Any