10 000 solution Minijet ) and repeat if necessary. \200 Dopamine at doses of > 2.5 g/kg/min has a pressor action in addition to direct and indirect inotropic effects and may be used at higher doses (10 \200 \22320 mcg/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 PULMONARY OEDEMA: MANAGEMENT 731 or hydralazine) once the blood pressure is restored (see below). Beware of arrhythmias at t hese doses. Adrenaline infusion may be preferred to high-dose dopamine as an alternative inotrope. Once the blood pressure is restored ( > 100 mmHg), vasodilators such as nitroprusside/hydralazi ne or GTN infusion should be added to counteract the pressor effects. Adrenaline can be com bined with dobutamine and/or a phosphodiesterase inhibitor, especially in the context of a poor ventricle. Intra-aortic balloon counter pulsation should also be used with/without inotropes in the co ntext of a potentially reversible cause for the pulmonary oedema and shock (e.g. ongoing my ocardial ischaemia, VSD, acute MR). Further doses of diuretic may be given. Patients with systolic BP \211 100 mmHg \200 Fu rther doses of diuretic may be given (furosemide 40 \200\22380 mg IV q3 \200\2234h or as a continuous infusion (20 \200\22380 mg/h)). Continue the GTN infusion, increasing the infusion rate every 15 \200\22320 min up to 10 mg /h, titrating against blood pressure (aiming to keep systolic BP 7100 mmHg). Angiotensin-converting enzyme inhibitors (ACE-Is) can be used if BP is adequate and there are no other known contraindications (e.g. RAS, renal failure). Arter iolar vasodilators (nitroprusside or hydralazine) may also be added in or used instead of G TN ( ACE-I) in patients with adequate BP. Arterial pressure should be monitored continuo usly via an arterial line to prevent inadvertent hypotension. Long-term management \200 Unless a contraindication exists, start an ACE-I, increasing th e dose to as near the recommended maximal dose as possible. In the context of LV impairment , ACE-Is have signi \201 cant prognostic bene \201 t. If ACE-Is are contraindicated or not tolerated, consider the use of hydralazine and long-acting oral nitrate in combination. If the patient is already on high doses of diuretics and ACE-Is, consider the addition spir onolactone (25 \200\22350 mg) (NB: monitor renal function and serum potassium). In the context of stable patients (no clinical features of failure) and poor LV function, B \200\223blockers have signi \201 cant mortality and some symptomatic bene \201 t (NB: st art with a very small dose and increase gradually every 2 weeks with regular monitoring). B isoprolol, carvedilol, and metoprolol can all be used. Ensure all arrhythmias are treated. \200 Digoxin can be used for symptomatic improvement. \200 Consider multisite pacing (biventricular) in the context of severe LV dysfunction, broad QRS complex MR on ECHO. Patients in AF, or with poor LV function should be considered for long- term anticoagulation. Patients <60 years with severe irreversible LV dysfunction and debilitating symptoms must be considered for cardiac transplantation. 732 CHAPTER 17 Cardiovascular emergencies Pulmonary oedema: speci \201 c conditions Diastolic LV dysfunction \200 This typically o ccurs in elderly hypertensive patients with LV hypertrophy, where there is impaired relaxation of the ventricle in diastole. There is mark ed hypertension, pulmonary oedema, and normal, or only mild, systolic LV impairment. With tachycardia, diastolic \201 lling time shortens. As the ventricle is \200\230stiff \200\231 in diastole, LA pressure is increased and pulmonary oedema occurs (exacerbated by AF, as \201 lling by atrial systole is lost). Treatment involves control of hypertension with IV nitrates (and/or nitroprusside), calcium-channel blockers (verapamil or nifedipine) and even certain B -bloc kers (e.g. carvedilol, bisoprolol). Fluid overload \200 Standard measures are usually effective. \200 In extreme circumstan ces, venesection may be necessary. \200 Check the patient is not anemic (hemoglobin (Hb) (cid:116) 10 g/dL). Remove 500 mL blood via a cannula in a large vein and repeat if necessa ry. If anemic (e.g. renal failure) and acutely unwell, consider dialysis. Known (or unknown) renal failure \200 Unless the patient is permanently anuric, large dos es of IV furosemide may be required (up to 1 g given at 4 mg/min) in addition to standard t reatment. 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 be 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. Generally, transfusion is unnecessary with Hb > 9 g/dL unless there is a risk of an acute b leed. Treatment of pulmonary oedema will result in haemoconcentration and a \200\230rise \200\231 in the Hb. If the anemia is thought to be exacerbating pulmonary oedema, ensure that an adequate diuresis is obtained prior to transfusion. Give slow transfusion (3 \200\2234 h per unit) of packed cells, with IV furosemide 20 \200\22340 mg before each uni t. PULMONARY OEDEMA: SPECIFIC CONDITIONS 733 Hypoproteinaemia \200 The critical left atrial (LA) pressure at which hydrostatic pulmona ry oedema occurs is in \202 uenced by the serum albumin and approximates to serum albumin con centration (g/L) x 0.57. Treatment involves diuretics, cautious albumin replacement, spironolactone (if there is secondary hyperaldosteronism), and treatment of the underlying cause for hypoproteinaemia. 734 CHAPTER 17 Cardiovascular emergencies Acute aortic regurgitation Presentation \200 Sudden, severe aortic regurgitation (AR) pre sents as cardiogenic shock and acute pulmonary oedema. The haemodynamic changes are markedly different from those seen in chronic AR. The previous normal-sized LV results in a smaller effective forward \202 ow and higher LVEDP for the same degree of AR. Patients are often extremely unwell, tachycardic, peripherally shut down, and frequently ha ve pulmonary oedema. Unlike chronic AR, pulse pressure may be near normal. If available, ask for a history of previous valvular heart disease, hypertension, features of Marfan syndrome, and risk factors for infective endocarditis. Physical signs of severe AR include a quiet aortic closure sound (S 2 ); an ejection systol ic murmur over the aortic valve (turbulent \202 ow); high- pitched and short, early diast olic murmur (AR); quiet S 1 (premature closure of the mitral valve (MV)). Examine speci \201 cally for signs of an underlying cause (see b Aortic regurgitation, p. 170). Where there is no obvious underlying cause (e.g. acute MI), assume infective endocarditis until proven otherwise. Causes \200 Infective endocarditis \200 Ascending aortic dissection \200 Collagen vas cular disorders (e.g. Marfan) \200 Connective tissue diseases (large and medium vessel ar teritis) \200 Trauma \200 Dehiscence of a prosthetic valve. Diagnosis Diagnosis is based on a combination of clinical features and transthoracic and/or transoesophageal 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 replace- ment (AVR) can take place. The patient \200\231s clinical condition will determine the urgency of surgery (and mortali ty). Liaise immediately with local cardiologists. General measures (see b Pulmonary oedema: management, p. 728) \200 Admit the patient to intensive care or medical HDU. \200 Give oxygen, and begin treating any pulmonary ooedema with diuretics. Monitor blood gasses; mechanical ventilation may be necessary. \200 Blood cultures x3 are essential. \200 Serial ECG: watch for developing AV block or conduction defects. ACUTE AORTIC REGURGITATION 735 Speci \201 c measures \200 Every patient must be discussed with the regional cardiothora cic center. In the context of good systemic BP, vasodilators such as sodium nitroprusside or hydralazine may temporarily improve forward \202 ow and relieve pulmonar y oedema. Inotropic support may be necessary if the patient is hypotensive. However, inotropes are be st avoided, as any increase in systemic pressures may worsen AR. All patients with haemodynamic compromise should have immediate or urgent AVR. Infective endocarditis: indications for surgery are given on b Surgery for endocarditis, p. 202. Use of an intra-aortic balloon pump (IABP) must be avoided, as it will worsen AR. 736 CHAPTER 17 Cardiovascular emergencies Acute mitral regurgitation Presentation \200 Patients most commonly present with acute br eathlessness and severe pulmonary oedema. Symptoms may be less severe, or spontaneously imp rove as left atrial compliance increases. There may be a history of previous murmur, angina , or MI. The signs are different from those seen in chronic mitral regurgitation (MR) because of the presence of a non-dilated, and relatively non- compliant LA. Acute MR results in a large L A systolic pressure wave ( \200\230v \200\231 wave), and hence pulmonary oedema. Patients may be acutely unwell with tachycardia, hypotension, peripheral vasoconstriction and pulmonary oedema, and a pansystolic 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. \200 The important differential diagnosis is a VSD. Transthoracic ECHO and Doppler studies can readily differentiate between the two conditions. Alternatively, if ECHO not available, pulmonary artery catheterization in acut e MR will exclude the presence of a left-to-right shunt, and the PCWP trace will demonstrat e a large \200\230v \200\231 wave. Where there is no obvious underlying cause (e.g. acute MI), assume the patient has infective endocarditis until proven otherwise. Diagnosis Diagnosis is based on a combination of clinical features and ECHO. Transthoracic ECHO can readily diagnose and quantify MR. It also pro- vides information on LV status (in particular, regional wall motion abnor- malities, which can give rise to MR). TOE can provi de speci \201 c information about the etiology of valve dysfunction, including papillary m uscle rupture and MV lea \202 et (anterior and posterior) structural abnormalities. This i nformation will be vital for a decision regarding de \201 nitive management. General measu res (see b Pulmonary oedema: management, p. 728) \200 Admit the patient to intensive care or medical HDU. \200 Give oxygen, and begin treating any pulmonary oedema with diuretics . \200 Monitor blood gasses; mechanical ventilation may be necessary. \200 Blood cultur es x3 are essential. \200 If present, MI should be treated in the standard manner. Speci \201 c measures \200 Pulmonary oedema may be very resistant to treatment. \200 I n the presence of good BP, reduction in preload (GTN infusion and afterload especially with ACE-Is important. Systemic vasodilators such as hydralazine (12.5 \200\223100 mg tds) can also be added in. An IABP will help decrease LVEDP and increase coronary blood \202 ow. ACUTE MITRAL REGURGITATION 737 Patients may require inotropic support. There are multiple combinations and etiology of MR, and haemodynamic status, and local policy/ expertise should dictate cho ice of agent. CPAP and intubation and positive pressure ventilation are extremely useful and must be cons idered in all severe and/or resistant cases. \200 Haemodynamic disturbance and severe pul monary oedema in the context of acute MR is a surgical emergency. Infective endocarditis: indications for surgery are given on b Surgery for endocarditis, p. 202. Post-infarct MR: management depends upon the patient \200\231s condition following resuscit ation. Patients who are stabilized may have mitral valve replacement (MVR) deferred because of the risks of surgery in the post-infarct patient. Their preoperative management should consist of diuretics and vasodilators, including ACE-Is if tolerated. Advise patients regar ding endocarditis prophylaxis. Causes of acute mitral regurgitation \200 Infective endocarditis \200 Papillary muscle dysfunction or rupture (post MI, see b Ventricular septal defect post-MI, p. 278) Rupture of chordae tendinae (e.g. infection, myxomatous degeneration, systemic lupus eryhtematosus (SLE)) \200 Trauma (to lea \202 ets, papillar y muscle, or chordae) \200 Prosthetic valve malfunction (e.g. secondary to infection) \200 Left atrial myxoma \200 Acute rheumatic fever \200 Collagen vascular disorders (e .g. Marfan) \200 Connective tissue diseases (large and medium vessel arteritis) 738 CHAPTER 17 Cardiovascular emergencies Deep vein thrombosis: assessment Presentation \200 Deep vein thrombosis (DVT) is most com monly asymptomatic. Minor leg discomfort or isolated swelling ( > 65 % ) in the affected li mb are the most common clinical features. Breathlessness or chest pain may be secondary to pulmonary embolism (PE). Signs include erythema and swelling of the leg, dilated super \201 cial veins, and calf di scomfort on dorsi \202 exion of the foot (Homan \200\231s sign). The thrombus may be palpa ble as a \201 brous cord in the popliteal fossa. Con \201 rm the presence of swelling ( > 2 cm) by measuring the limb circumference 15 cm above and 10 cm below the tibial tuberosi ty. \200 In all cases of leg swelling, abdominal and rectal (and pelvic in women) examination must be carried out to exclude an abdominal cause. Risk factors for DVT Procoagulant states Congenital Acquired Malignant disease (75 % ) Factor V Leiden Antithrombin III de \201 ciency Antiphospholipid syndrome Protein C de \201 ciency Myeloproliferative disorders Protein S de \201 ciency Oral contraceptive pill (especially with factor V Leiden mutation) Nephrotic syndrome (via renal antithrombin (AT)III losses) Homocystinuria Paroxysmal nocturnal haemoglobinuria Venous stasis Immobility (e.g. long journeys) Recent surgery Pelvic mass Pregnancy or recent childbirth Severe obesity Miscellaneous Hyperviscosity syndromes Previous DVT or PE Family history of DVT/PE DEEP VEIN THROMBOSIS: ASSESSMENT 739 Investigations \200 Venous compression ultrasonography of the leg veins has largely repla ced venography as the investigation of choice. It is quick and non-invasive, with sensitivi ty and speci \201 city of over 90 % , and does not carry the risk of contrast allergy or p hlebitis. It can simultaneously assess the extent of proximal progression of the thrombus, in particular extension into pelvic vessels. D-dimers have a high negative predictive value for DVT. A low clinical probability of DVT a nd a negative D-dimer does not require further investigation. A positive D-dimer result sho uld be followed by ultrasonography. Venography : use if results are uncertain and clinical suspicion is high. \200 Consider b aseline investigations (FBC, U&Es, ECG, CXR, urinalysis, and pulse oximetry ( ABG)) on all patients. \200 If appropriate, look for an underlying ca use: coagulation screen \200 pro-coagulant screen: refer to local screening policy and get hematology advice (e.g. C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), pro teins C and S, ATIII levels, factor V Leiden mutation, auto-antibody (Ab) screen, immunoglo bulins and immunoelectrophoretic strip, anticardiolipin antibody, Ham test, etc.) screen for malignancy: ultrasound computed tomography (CT) (abdomen and pelvis), CXR, li ver function tests (LFTs), prostate- speci \201 c antigen (PSA), carcinoembryonic antigen (CEA), CA-125, CA-19.9, B-HCG (human chorionic gonadotrophin), etc. 740 CHAPTER 17 Cardiovascular emergencies Deep vein thrombosis: management \200 If there is a high clinical suspicion of DVT (the p resence of risk factors and absence of an alternative diagnosis), start empiric anticoagula tion with low molecular weight heparin (LMWH). This may be stopped if subsequent investigat ions are negative . Below-knee DVT : thrombi limited to the calf have a lower risk of embolization and may be treated with compression stockings and subcutaneous prophylactic do ses of LMWH until mobile, to deter proximal propagation of thrombus. A brief period of syst emic anticoagulation with LMWH may lessen the pain from below-knee DVT. Above-knee DVT : thrombi within the thigh veins warrant full anticoagulation with LMWH/unfractionated heparin (UFH), and subsequently warfarin. Anticoagulation Heparin \200 LMWHs have now superceded UFH for management of both DVT and PE. They require no monitoring on a daily basis and also allow outpatient treatment. There must be a period of overlap between LMWH/UFH therapy and anticoagulation with warfari n until INR is within the therapeutic range and stable. LMWH is administered primarily as once-daily SC injection, and dosage is determined by patient weight. Warfarin \200 Always anticoagulate with LMWH/UFH before starting warfarin. Protein C (a vitamin K-dependent anticoagulant) has a shorter half-life than the other coag ulation factors and levels fall more quickly, resulting in a transient procoagulant tendenc y. If DVT is con \201 rmed, commence warfarin and maintain on LMWH/UFH until INR > 2. Anticoagulate (INR 2 \200\2232.5) for 3 months. \200 If there is recurrent DVT, or the pa tient is at high-risk of recurrence, consider lifelong anticoagulation. Thrombolysis \200 This should be considered for recurrent, extensive, proximal venous thr ombosis (e.g. femoral or iliac veins), as it is more effective than anticoagulation alone i n promoting clot dissolution, and produces a better clinical outcome. Catheter-directed thrombolytic therapy (recombinant tissue plasminogen activator (rt-PA) or streptokinase (SK)) is superior to systemic thrombolysis. One approach is streptokinase 250 000 U over 30 min then 100 000 U every hour for 24 \200\22372 hours (see data sheet). See b STEMI: reperfusion therapy (thro mbolysis), p. 264 for contraindications to thrombolysis. DEEP VEIN THROMBOSIS: MANAGEMENT 741 Further management \200 Women taking the combined oral contraceptive pill (OCP) should be advised to stop this. If there are contraindications to anticoagulation, consider the insertion of a caval \201 lter to prevent PE. All patients should be treated with thigh-high compression stockings to try to reduce symptomatic venous distension when mobilizing. See Fig 17.6. Suspected DVT Wells score \200\223 pre test probability LRR/D-Dimer level Low probability, score <1 Moderate and high probability, score 1 to >3 Await D-Dimer, no USS or LMWH Give LMWH Abnormal D-Dimer Normal D-Dimer Arrange USS Normal USS Clot on USS Discharge to GP with letter Provide with shaped tubigrip and A&E RC at least 1 week on Tues or Thurs Refer to outpatient DVT team Notes 1. Patients who are pregnant or who have previously had a DVT should be in the modera te to high group. 2. Patients who attend after hours should return to the CDU the following morning for a scan. Not all need LMWH. Fig. 17.6 DVT management algorithm. Reproduced with permission from Ramrakha P, Moore K and Sam, M (2010). Oxford Handbook of Acute Medicine , 3rd ed. Oxford: Oxford University Press . A&E RC = ; CDU = ; GP = general practitioner; LRR = ; USS = ultrasound scan . 742 CHAPTER 17 Cardiovascular emergencies Pulmonary embolism: assessment Symptoms \200 PE classically presents with sudden-onset, p leuritic chest pain, associated with breathlessness and haemoptysis. Additional symptoms include postural dizzin ess or syncope. Massive PE may present as cardiac arrest (particularly with electromechanical dissociation) or shock. Presentation may be atypical, i.e. unexplained breathlessness or unexplained hypotension, or syncope only. Pulmonary emboli should be suspected in all breathless patients with risk factors for DVT o r with clinically proven DVT (see b Deep vein thrombosis: assessment, p. 738). Recurrent PEs may present with chronic pulmonary hypertension and progressive right heart failure. Signs \200 Examination may reveal tachycardia and tachypnoea only. Look for postural hypotension (in the presence of raised jugular venous pressure (JVP)). Look for signs of raised right heart pressures and cor pulmonale (raised JVP with prominent \200\230a \200\231 wave, tricuspid regurgitation, parasternal heave, right ventricular (R V) S 3 , loud pulmonary closure sound with wide splitting of S 2 , pulmonary regurgitation) . Cyanosis suggests a large pulmonary embolism. \200 Examine for a pleural rub (may be tran sient) or effusion. \200 Examine the lower limbs for obvious thrombophlebitis. \200 Mil d fever ( > 37.5 C) may be present. There may be signs of co-existing COPD. Causes PE is most frequently secondary to DVT (leg > > arm; see b Deep vein thrombosis: ass essment, p. 738). Other causes \200 Rarely secondary to right ventricular thrombus (post-MI) \200 Septic emboli (e.g. tricuspid endocarditis) \200 Fat embolism (post fracture) \200 Air embolis m (venous lines, diving) \200 Amniotic \202 uid \200 Parasites \200 Neoplastic cell s \200 Foreign materials (e.g. venous catheters). Prognostic features The prognosis in patients with pulmonary emboli varies greatly, associa ted in part with any underlying condition. Generally, worse prognosis is asso- ciated with larger PE; poor prognostic indicators include: \200 hypotension \200 hypoxia \200 ECG changes (other than non-speci \201 c T-wave changes). This page intentionally left blank 744 CHAPTER 17 Cardiovascular emergencies Pulmonary embolism: investigations See Fig. 17.7 . General investigations ABG Normal ABG does not exclude a PE. \200 dP a O 2 (partial pressure of oxygen in arterial b lood) is invariable with larger PEs. Other changes include mild respiratory alkalosis and d P a CO 2 (partial pressure of carbon dioxide in arterial blood; due to tachypnoea), and met abolic acidosis (s to shock). ECG Commonly shows sinus tachycardia non-speci \201 c ST- and T-wave changes in the anterio r chest leads. The classical changes of acute cor pulmonale such as S 1 Q 3 T 3 , right-axi s deviation, or right bundle branch block (RBBB) are only seen with massive PE. Less common \201 ndings include AF. CXR May be normal, and a near-normal chest \201 lm in the context of severe respiratory compr omise is highly suggestive of a PE. Less commonly, CXR may show focal pulmonary oligaemia ( Westermark \200\231s sign ), a raised hemidiaphragm, small pleural effusion, wedge- shaped shadows based on the pleura, subsegmental atelectasis, or dilated proximal pulmonary arter ies. \200 There is no speci \201 c test. FBC may show neutrophil leucocytosis; mildly el evated CK, troponin, and bilirubin may be seen. Blood tests ECHO/TOE Are insensitive for diagnosis but can exclude other causes of hypotension and raised right-sided pressures (e.g. tamponade, RV infarction ). In PE they will show RV dilatation and global hypokinesia (with sparing of apex ( McConn ell \200\231s sign )), pulmonary artery dilatation and Doppler may show tricuspid/ pulmonar y regurgitation allowing estimation of RV systolic pressure. Rarely, the thrombus in the pu lmonary artery may be visible. Speci \201 c investigations D-dimer \200 A highly sensitive, but non-speci \201 c test. \200 Useful in ruling out PE in patients with low or intermediate probability. \200 Re sults can be affected by advancing age, pregnancy, trauma, surgery, malignancy, and in \202 ammatory states. Ventilation/perfusion (V/Q) lung scanning A perfusion lung scan (with IV technetium-99-labe led albumin) should be performed in all suspected cases of PE. A ventilation scan (inhaled xenon-133) in conjunction increases the speci \201 city by assessing whether PULMONARY EMBOLISM: INVESTIGATIONS 745 the defects in the ventilation and perfusion scans \200\230match \200\231 or \200\230mism atch \200\231. Pre-existing lung disease makes interpretation dif \201 cult. \200 A norm al perfusion scan rules out signi \201 cant-sized PE. \200 Abnormal scans are reported a s low, medium, or high probability: a high-probability scan is strongly associated with a PE, but there is a signi \201 cant minority of false positives a low-probability scan with a low clinical suspicion of PE should prompt a search for anoth er cause for the patient \200\231s symptoms. Investigations for an underlying cause for PEs \200 Ultrasound scan (USS) of deep veins o f the legs \200 USS abdomen and pelvis (?occult malignancy/pelvic mass) \200 CT abdomen /pelvis \200 Screen for inherited procoagulant tendency (e.g. protein C, S, AT III, factor V Leiden, etc.) Autoimmune screen (anticardiolipin antibody, antinuclear antibody (ANA)) Biopsy of suspicious lymph nodes/masses if the clinical suspicion of PE is high and the scan is of low or medium probability, alter native investigations are required. CT pulmonary angiography (CTPA) \200 This is the recommended initial lung imaging modalit y in patients with non- massive PE. Allows direct visualization of emboli as well as other potential parenchymal disease, which may allow an alternative explanation for symptoms. Sensitivity and speci \201 city are high ( > 90 % ) for lobar pulmonary arteries but not s o high for segmental and subsegmental pulmonary arteries. \200 A patient with a positive CTPA does not require further investigation. \200 A patient with a negative CTPA in the c ontext of a high/intermediate probability of a PE should undergo further investigation. Evaluation of leg veins with USS \200 Not very reliable. Almost half of patients with PE do not have evidence of a DVT and therefore a negative result cannot rule out a PE. \200 Useful second-line in vestigation as an adjunct to CTPA/VQ scan. \200 Outcome studies have demonstrated that it would be safe not to anticoagulate patients with a negative CTPA, and to use lower-limb USS for those with an in termediate/low probability of a PE. Pulmonary angiography \200 Is the \200\230gold standard \200\231 investigation. \200 I t is indicated in patients in whom diagnosis of embolism cannot be established by non-invasive means. Look for sharp cut-off of vessels or obvious \201 llin g defects. Invasive investigation and can be associated with 0.5 % mortality. \200 If there is an ob vious \201 lling defect, the catheter or a guide wire passed through the catheter may be used to disobliterate the thrombus. 746 CHAPTER 17 Cardiovascular emergencies After angiography, the catheter may be used to give thrombolysis directly into the affected pulmonary artery (see later). The contrast can cause systemic vasodilatation and haemodynamic collapse in hypotensive patients. MR pulmonary angiography \200 Results are comparable to pulmonary angiography in prelimin ary studies. It can simultaneously assess ventricular function. Suspected PE Monitored area O2, iv fluids, analgesia ABG, ECG, CXR, bloods High or intermediate risk of PE Low risk of PE Treat as out-patient or in A&E US lower limb D-dimer Admit LMWH (UFH) Negative Positive V/Q or CTPA Discharge Results do not confirm clinical suspicion Results confirm clinical suspicion Positive for PE Negative for PE } US Lower Limb D-DIMER V/Q or CTPA (which ever not performed) Pulmonary angiogram +ve \206\222 Treat Anti-coagulate with warfarin Discharge Fig. 17.7 Proposed pathway for investigation of patients with suspected PE. Reproduced with permission from Ramrakha P, Moore K, and Sam M (2010). Oxford Handbook of Acute Medicine . 3rd ed. Oxford: Oxford University Press. This page intentionally left blank 748 CHAPTER 17 Cardiovascular emergencies Pulmonary embolism: management 1. Stabilize the patient \200 Unless an alternative diagno sis is made, the patient should be treated as for a pulmonary embolus until this can be excluded. Monitor cardiac rhythm, pulse, BP, and respiration rate every 15 minutes with continuous pulse oximetry and cardiac monitor. Ensure full resuscitation facilities ar e available. Obtain venous access and start IV \202 uids (crystalloid or colloid). \200 Give maximal inspired oxygen via face mask to correct hypoxia. Mechanical ventilation may be necessary if the patient is tiring (beware of cardiovascular collapse when sedation is given for endotracheal intubation). Give LMWH or UFH to all patients with high or intermediate risk of PE until diagnosis is co n \201 rmed. Meta-analysis of multiple trials has shown LMWH to be superior to UFH, with a reduction in mortality and bleeding complications. For doses consult local formulary. If there is evidence of haemodynamic instability (systemic hypotension, features of right h eart failure) or cardiac arrest, patients may bene \201 t from thrombolysis with rt-PA or SK (same doses as used for treatment of STEMI (see b STEMI: reperfusion therapy (thrombolys is), p. 264). 2. Analgesia \200 Patients may respond to oral non-steroidal anti-in \202 ammatory drugs (NSAIDs). Opiate analgesia should be used with caution. The vasodilatation caused by these drugs may precipitate or worsen hypotension. Give small doses (1 \200\2232 mg diamorphine IV) slowly. Hypotension should respond to IV colloid. Avoid IM injections (anticoagulation and possible thrombolysis). 3. Investigations with view to a de \201 nite diagnosis See previous section. 4. Anticoagulate \200 Patients with a positive diagnosis must undergo anticoagulation wit h warfarin. There should be period of overlap with LMWH/UFH until INR values are therapeuti c. Target INR is 2 \200\2233 for most cases. Standard duration of anticoagulation is: \200 4 \200\2236 weeks for temporary risk factor \200 3 months \201 rst idiopathic cases \200 at least 6 months for other cases \200 with recurrent events and underlying predisposition to thromboembolic events (e.g. antiphospholipid antibody syndrome), lifelong anticoagulation m ay be needed (as well as higher target INR > 3). PULMONARY EMBOLISM: MANAGEMENT 749 Dosage of thrombolytic agents for pulmonary embolus Alteplase (rt-PA) 100 mg over 2 h or 0.6 mg/kg over 15 min (maximum of 50 mg) followed by heparin. Streptokinase 250 000 U over 30 min followed by 100 000 U/h infusion for 24 h NB: contraindications for thrombolysis are identical to ones for STEMI (see b STEMI: reperf usion therapy (thrombolysis), p. 264). Cardiac arrest (also see b Adult advanced life support, p. 712) \200 Massive PE may prese nt as cardiac arrest with electromechanical dissociation (EMD). Exclude the other causes of EMD (see b Universal treatment algorithm, p. 716). Chest compressions may help break up the thrombus and allow it to progress more distally, thereby restoring some cardiac output. If clinical suspicion of PE is high and there is no absolute contraindication to thrombolysis, give rt-PA (similar in dose to STEMI with a maximum of 50 mg (see b STEMI: reperfusion therapy (thrombolysis), p. 264) followed by heparin). If cardiac output returns, consider pulmonary angiography or inserting a PA catheter to try to mechanically disrupt the embolus. Hypotension The acute increase in pulmonary vascular resistance results in right ven- tricu lar dilatation and pressure overload, which mechanically impairs LV \201 lling and functi on. Patients require a higher than normal right-sided \201 lling pressure, but may be wor sened by \202 uid overload. \200 Insert an internal jugular sheath prior to anticoagula tion. This can be used for access, later if necessary. If hypotensive, give colloid (e.g. 500 mL Haemacell stat). \200 If hypotension persist s, invasive monitoring and/or inotropic support is required. The JVP is a poor indicator of the left-sided \201 lling pressures in such cases. Adrenaline is the inotrope of choice. Femoro-femoral cardiopulmonary bypass may be used to support the circulation until thrombol ysis or surgical embolectomy can be performed. Pulmonary angiography in a hypotensive patient is hazardous, as the contrast may cause systemic vasodilatation and cardiovascular collapse. Pulmonary embolectomy \200 In patients who have contraindications to thrombolysis and are in shock requiring inotropic support, there may be a role for embolectomy if appropriate s kills are on site. This can be performed percutaneously in the catheterization laboratory, using a number of devices, or surgically on cardiopulmonary bypass. Percutaneous procedures may be combined with peripheral or central thrombolysis. Seek specialist advice early. The best results are obtained before onset of cardiogenic shock. 750 CHAPTER 17 Cardiovascular emergencies Radiological con \201 rmation of the extent and site of embolism is preferable before thoracotomy. Mortality is 725 \200\22330 % . Inferior vena cava (IVC) \201 lter \200 Infrequently used, as there is little to sugges t improved short- or long-term mortality. Filters are positioned percutaneously and, if possible, patients must remain anticoagulated to prevent further thrombus formation. \200 Most are positioned infra-renally (bird \200 \231s nest \201 lter), but can also be supra-renal (Green \201 eld \201 lter). Indications for IVC \201 lter use include: anticoagulation contraindicated: e.g. active bleeding, heparin- induced thrombocytopenia, p lanned intensive chemotherapy anticoagulation failure despite adequate therapy \200 prophylaxis in high-risk patients: e.g. progressive venous thrombosis, severe pulmonary hypertension. This page intentionally left blank 752 CHAPTER 17 Cardiovascular emergencies Fat embolism Commonly seen in patients with major trauma. There is embolization of fat and micro-aggregates of platelets, red blood cells, and \201 brin in the sys- temic and pulmo nary circulation. Pulmonary damage may result directly from the emboli (infarction) or by a chemical pneumonitis and ARDS. Clinical features \200 There may be a history of fractures followed (24 \200\22348 h late r) by breathlessness, cough, haemoptysis, confusion, and rash. Examination reveals fever (38 \200\22339 * C), widespread petechial rash (25 \200\22350 % ) , cyanosis, and tachypnoea. There may be scattered crepitations in the chest, though examin ation may be normal. Changes in mental state may be the \201 rst sign, with confusion, dr owsiness, seizures, and coma. Examine the eyes for conjunctival and retinal hemorrhages; oc casionally, fat globules may be seen in the retinal vessels. Severe fat embolism may presen t as shock. Investigations \200 ABG Hypoxia and a respiratory alkalosis (with low P a CO 2 ) as for thromboembolic PE \200 Thrombocytopenia, acute intravascular FBC haemolysis Coagulation \200 U&Es and glucose \200 Ca 2 + \200 Urine \200 ECG Disseminated intravascular coagulation \200 Renal failure, hypoglycaemia \200 May be lo w \200 Microscopy for fat and dipstick for hemoglobin \200 Usually non-speci \201 c (s inus tachycardia; occasionally signs of right heart strain) CXR Usually lags behind the clinical course. There may be patchy, bilateral, air space opaci \201 cation. Effusions are rare CT head Consider if there is a possibility of head injury with expanding subdural or epidural bleed Differential diagnosis \200 Pulmonary thromboembolism, other causes of ARDS, septic shock , hypovolaemia, cardiac or pulmonary contusion, head injury, aspiration pneumonia, transfusio n reaction. Management \200 Treat respiratory failure. Give oxygen (maximal via face mask; CPAP and mechanical ventilation if necessary). Ensure adequate circulating volume and cardiac output. Central venous pressure (CVP) is not a good guide to left-sided \201 lling pressures, and a PA catheter (Swan \200\223Ganz) s hould be used to guide \202 uid replacement. Try to keep PCWP at 12 \200\22315 mmHg and g ive diuretics if necessary. Use inotropes to support circulation as required. FAT EMBOLISM 753 Aspirin, heparin and dextran 40 (500 mL over 4 \200\2236 h) are of some bene \201 t in the acute stages, but may exacerbate bleeding from sites of trauma. High-dose steroids (methylprednisolone 30 mg/kg q8 h for 3 doses) have been shown to improv e hypoxaemia, 1 but steroids are probably most effective if given prophylactically. 1 Lindeque B, Schoeman H, Dommisse G, Boeyens MC, Vlok AL (1987). Fat embolism and the fat embolism syndrome. J Bone Joint Surg 69: 128 \200\22331. 754 CHAPTER 17 Cardiovascular emergencies Hypertensive emergencies Hypertensive crisis Hypertensive crisis is de \201 ned as a sever e elevation in blood pressure (systolic blood pressure (SBP) > 200 mmHg, diastolic blood pr essure (DBP) > 120 mmHg). The rate of change in BP is important. A rapid rise is poorly tol erated and leads to end-organ damage, whereas a gradual rise in a patient with existent poo r BP control is tolerated better. Hypertensive crisis are classi \201 ed as: 1 . hypertens ive emergency, where a high BP is complicated by acute target organ dysfunction (see b Hype rtensive emergencies, p. 754) and includes: \200 hypertensive emergency with retinopathy where there is marked elevation in BP (classically DBP > 40 mmHg) with retinal hemorrhages and exudates (previous ly called accelerated hypertension), and hypertensive emergency with papilloedema with a similarly high BP and papilloedema (previously called malignant hypertension). 2 . hypertensive urgency, where there is a similar rise in BP, but without target organ dam age. Conditions that present as hypertensive emergency \200 Essential hypertension \200 Reno vascular hypertension: atheroma, \201 bromuscular dysplasia, acute renal occlusion Renal parenchymal disease: acute glomerulonephritis, vasculitis, scleroderma. Endocrine disorders: phaeochromocytoma, Cushing \200\231s syndrome, primary hyperaldosteron ism, thyrotoxicosis, hyperparathyroidism, acromegaly, adrenal carcinoma Eclampsia and pre-eclampsia \200 Vasculitis \200 Drugs: cocaine, amphetamines, monoamin e oxidase inhibitor (MAOI) interactions, ciclosporin, B -blocker, and clonidine withdrawal \200 Autonomic hyperactiv ity in the presence of spinal cord injury \200 Coarctation of the aorta Presentation \200 Occasionally there are minimal non-speci \201 c symptoms such as mild headache and nose bleed. A small group of patients present with symptoms resulting from BP-induced microvascular damage: \200 neurological symptoms: severe headache, nausea, vom iting, visual loss, focal neurological de \201 cits, \201 ts, confusion, intracerebral hemorrhage, com a (see later) chest pain (hypertensive heart disease, MI, or aortic dissection) and congestive cardiac failure symptoms of renal failure: renal impairment may be chronic (secondary to longstanding hyper tension) or acute (from the necrotizing vasculitis of malignant hypertension). HYPERTENSIVE EMERGENCIES 755 Patients may present with hypertension as one manifestation of an underlying \200\230disease \200\231 (renovascular hypertension, chronic renal failure, CRE ST syndrome (calcinosis, Raynaud phenomenon, oesophageal dysmotility, sclerodactyly, and te langiectasia), phaeochromocytoma, pregnancy).