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). Examination should be directed at looking for evidence of end-organ damage, even if the pat ient is asymptomatic (heart failure, retinopathy, papilloedema, focal neurology). Hypertensive emergencies \200 Hypertensive emergency with retinopathy/papilloedema \200 Hypertensive encephalopathy \200 Hypertension-induced intracranial hemorrhage/stroke \200 Hypertension with cardiovascular complications: Aortic dissection (see b Aortic dissection: assessment, p. 766) \200 MI \200 Pulmonary oedema (see b Acute pulmonary oedema: assessment, p. 724) Pheochromocytoma \200 Pregnancy-associated hypertensive complications: eclampsia and pre-eclampsia \200 Acute renal insuf \201 ciency Hypertensive emergency secondary to acute withdrawal syndromes (e.g. B -blockers, centrally acting antihypertensives) 756 CHAPTER 17 Cardiovascular emergencies Hypertensive emergencies: management Priorities in management are: 1. con \201 rm the diag nosis and assess the severity 2. identify those patients needing speci \201 c emergency tr eatment 3. plan long-term treatment. Diagnosis and severity \200 Ask about previous BP recordings, previous and current treatm ent, sympathomimetics, antidepressants, non-prescription drugs, recreational drugs. Check the blood pressure yourself, in both arms, after a period of rest and if possible on standing. Monitor the patient \200\231s blood pressure regularly while they are in the emer gency department. Examine carefully for clinical evidence of cardiac enlargement or heart failure, peripheral pulses, renal masses, or focal neurological de \201 cit. Always examine the fundi \200 \224 dilate if necessary. Investigations All patients should have: FBC Microangiopathic haemolytic anemia with malignant hypertension U&E Renal impairment and/or iK + (diffuse intra- renal ischaemia and s hyperaldosteronism) \200 Disseminated intravascular coagulation (DIC) Coagulation screen with malignant hypertension CXR Cardiac enlargement; aortic contour (dissection?); pulmonary oedema Urinalysis Protein and red cells casts Other investigations depending on clinical picture and possible etiology include: 24-h urine collection Creatinine clearance \200 Free catecholamines, metanephrines or vanillyl mandellic acid (VMA) ECHO \200 Renal USS and Doppler \200 MR renal angiogram \200 CT/MR brain \200 Drug screen LVH, aortic dissection \200 Size of kidneys and renal artery stenosis \200 Renal artery stenosis \200 Intracranial bleed \200 Cocaine, amphetamine, others Indications for admission \200 Diastolic blood pressure persistently (cid:116) 120 mmHg \200 Retinal hemorrhages, exudates, or papilloedema \200 Renal impairment HYPERTENSIVE EMERGENCIES: MANAGEMENT 757 Voltage criteria for LVH \200 Tallest R (V 4 \200\223V 6 ) + deepest S (V 1 \200\223V 3 ) > 40 mm \200 Tallest R (V 4 \200\223V 6 ) > 27 mm \200 Deepest S (V 1 \200\223V 3 ) > 30 mm \200 R in aVL > 13 mm \200 R in aVF > 20 mm \200 QRS complex > 0.08 s (2 sm all squares) \200 Abnormal ST depression or T inversion in V 4 \200\223V 6 Treatment principles \200 Rapid reduction in BP is unnecessary, must be avoided, and can be very dangerous. This can result in cerebral and cardiac hypoperfusion (an abrupt change of > 25 % in BP will exceed cerebral BP autoregulation). \200 Initial BP reduction of 25 % should be achieved over 1 \200\2234 hours, with a less rapid reduction over 24 hours to a DBP 100 mmHg. The only two situations where BP must be lowered rapidly are in the context of aortic dissection and MI. Treatment \200 The majority of patients who are alert and otherwise well may be treated with oral therapy to lower BP gradually. First-line treatment should be with a B -blocker (unless contraindicated), with a thiazide diuretic, or a low-dose calcium channel antagonist. Urgent invasive monitoring (arterial line) prior to drug therapy is indicated for patients with: \200 evidence of hypertensive encephalopathy \200 complica tions of hypertension (e.g. aortic dissection, acute pulmonary oedema, or renal failure) treatment of underlying condition (e.g. glomerulonephritis, phaeochromocytoma, CREST crisis) persistent diastolic BP (cid:116) 140 mmHg \200 eclampsia. Sublingual nifedipine must be avoided. Conditions requiring speci \201 c treatment \200 Accelerated and malignant hypertension (see b Hypertensive emergency with retinopathy (accelerated and malignant hypertension), p. 762) Hypertensive encephalopathy (see b Hypertensive encephalopathy, p. 764) \200 Eclampsia \200 Phaeochromocytoma \200 Hypertensive patients undergoing a nesthesia 758 CHAPTER 17 Cardiovascular emergencies Long-term management \200 Investigate as appropriate for an underlying causes. \200 Sel ect a treatment regime that is tolerated and effective. Tell the patient why long-term therapy is important. Try to reduce all cardiovascular risk factors by advising the patient to stop smoking, appr opriate dietary advice (cholesterol), and aim for optimal diabetic control. Monitor long-term control and look for end-organ damage (regular fundoscopy, ECG, U&Es). Even poor control is better than no control. This page intentionally left blank 7 6 0 S e e T a b e s D r u g s C H A P T E R Table 17.3 Drugs for the treatment of hypertensive emergencies: IV therapy l Drug Dosage Onset of action Comments 1 7 3 f o r 1 7 . C a r d o v a s c u l a r 2 \200\2235 minutes Drug of choice in suspected phaeochromocytoma or aortic dissection (see b STEMI: additional measures, p. 270). Avoid if there is LV failure (LVF). May be continued orally (see below) Labetalol 20 \200\22380 mg IV bolus q10min 20 \200\223200 mg/min by IV infusion increasing every 15 m inutes ( I V t h e r a p y ) h y p e r t e n s i v e i Seconds Drug of choice in LVF and/or encephalopathy Nitroprusside 0.25 \200\2238 mcg/kg/min IV infusion (see b Pericardial aspiration, p. 814 \200\2236) a n d 1 7 4 . GTN 1 \200\22310 mg/hr IV infusion 2 \200\2235 minutes Mainly venodilatation. Useful in patients with LVF or angina ( o r a l e m e r g e n c i e s t h e r a p y ) . e m e r g e n c i e s Hydralazine 5 \200\22310 mg IV over 20 min 50 \200\223300 mcg/min IV infusion 10 \200\22315 minutes May provoke angina Short acting B -blocker also used for SVTs Esmolol HCl 500 mcg/kg IV loading dose 50 \200\223200 mcg/kg/min IV infusion Seconds Phentolamine 2 \200\2235 mg IV over 2 \200\2235 min prn Seconds NB: it is dangerous to reduce the blood pressure quickly. Aim to reduce the diatolic BP to 100 \200\223110 mmHg within 2 \200\2234 h. Unless there are good reasons to commence IV the rapy, always use oral medicines. Table 17.4 Drugs for the treatment of hypertensive emergencies: oral therapy Drug Dosage Onset of action Comment There are numerous alternative B -blockers \200\224 see British National Formulary (BNF) Atenolol 50 \200\223100 mg PO od 30 \200\22360 minutes D R U G S Nifedipine 10 \200\22320 mg PO q8h (q12h if slow release) 15 \200\22320 minutes Avoid sublingual as the fall in BP is very rapid Labetalol 100 \200\223400 mg PO q12h 30 \200\22360 minutes Use if phaeochromocytoma suspected. Safe in pregnancy F O R Hydralazine 25 \200\22350 mg PO q8h 20 \200\22340 minutes Safe in pregnancy H Y P E R T E N S I Minoxidil 5 \200\22310 mg PO od 30 \200\22360 minutes May cause marked salt and water retention Combine with a loop diuretic (e.g. furosemide 40 \200\223240 mg daily) Clonidine 0.2 mg PO followed by 0.1 mg hourly 30 \200\22360 minutes Sedation common. Do not stop abruptly as here is a high incidence of rebound hypertensive c risis 0.8 mg total for urgent therapy, or 0.05 \200\2230.1 mg PO q8 h increasing every 2 days V E E M E R G E N C E S NB: aim to reduce diastolic BP to 100 \200\223110 mmHg in 2 \200\2234 h and normalize BP in 2 \200\2233 days. I 7 6 1 762 CHAPTER 17 Cardiovascular emergencies Hypertensive emergency with retinopathy (accelerated and malignant hypertension) This is pa rt of a continuum of disorders characterized by hypertension (diastolic BP often > 120 mmHg ) and acute microvascular damage (seen best in the retina but present in all organs). It ma y be dif \201 cult to decide whether the damage in some vascular beds is the cause or effe ct of hyper- tension (e.g. an acute glomerulonephritis). \200 Accelerated hypertension (g rade 3 retinopathy) may progress to malignant hypertension, with widespread necrotizing vasculitis of the arterioles (and papil loedema). Presentation is commonly with headache or visual loss and varying degrees of confusion. Mor e severe cases present with renal failure, heart failure, microangiopathic haemolytic anemi a, and DIC. Management \200 Transfer the patient to medical HDU/ITU. \200 Insert an arterial line a nd consider a central venous line if there is evidence of necrotizing vasculitis and DIC. Catheterize the bladder. Monitor neurological state, ECG, \202 uid balance. \200 Aim to lower the DBP to 100 mmH g or by 15 \200\22320 mmHg, whichever is higher, over the \201 rst 24 hours. Those with early features may be treated successfully with oral therapy ( B -blockers, calc ium-channel blockers \200\224 see b Table 17.4 , p. 761) Patients with late symptoms or who deteriorate should be given parenteral therapy aiming for more rapid lowering of BP. \200 If there is evidence of pul monary oedema or encephalopathy give furosemide 40 \200\22380 mg IV. If there is no LVF, give a bolus of labetalol followed by an infusion. For patients with LV F, nitroprusside or hydralazine are preferable. Consult the renal team for patients with acute renal failure or evidence of acute glomerulonephritis ( > 2 + proteinuria, red cell casts). Dopamine should be avoided as it may worsen hypertension. Consider giving an ACE-I. High circulating renin levels may not allow control of hypertension, which in turn causes progressive renal failure. ACE-Is will block this vicious circle. There may be marked \201 rst-dose hypotension, so start cautiously. Haemolysis and DIC should recover with control of BP. HYPERTENSIVE EMERGENCY WITH RETINOPATHY 763 Hypertension in the context of acute stroke/intracranial bleed \200 Stroke/bleed may be t he result of hypertension, or vise versa. \200 In the acute setting there is impaired aut oregulation of cerebral blood \202 ow and autonomic function. Small changes in systemic B P may result in catastrophic falls in cerebral blood \202 ow. SBP should not be treated unless DBP > 130 mmHg and/or severe cerebral oedema (with clinical manifestations) is present. In most cases, BP tends to settle over 24 \200\22336 hours. If treatment is indicated, the above BP-reduction principles must be adhered to and a combination of nitrop russide, labetalol and calcium-channel blockers can be used. Centrally acting agents must be avoided as they cause sedation. \200 In patients with sub arachnoid hemorrhage (SAH), a cerebroselective calcium-channel blocker, such as nimodipine, is used to decrease cerebral vasospasm. Systemic BP must also be treated, if it quali \201 es the above principles and/or if it remains elevated after 24 hours. There is no evidence that this reduces furthe r events in the acute phase. Hypertensive retinopathy Grade 1 Tortuous retinal arteries, silver wiring Grade 2 AV nipping Grade 3 Flame-shaped hemorrhages and cotton wool exudates Grade 4 Papilloedema 764 CHAPTER 17 Cardiovascular emergencies Hypertensive encephalopathy \200 Hypertensive encephalography is caused by cerebral oedem a s to loss of cerebral autoregulatory function. Usually, there is gradual onset and it may occur in previously normotensive patients at blood pressures as low as 150/100 mmHg. It is rare in patients wit h chronic hypertension, and pressures are also much higher. Symptoms \200 Headache, nausea and vomiting, confusion, grade III and IV hypertensive retinopathy Late features consist of focal neurological signs, \201 ts, and coma Diagnosis \200 Hypertensive encephalography is a diagnosis of exclusion, and other differ ential diagnosis must be ruled out (e.g. stroke, encephalitis, tumors, bleeding, vasculitis ). History is helpful, particularly of previous seizures, SAH usually being sudden in onset an d strokes being associated with focal neurological de \201 cit. Always exclude hypoglycaemia. \200 Starting hypotensive treatment for hypertension associ ated with a stroke can cause extension of the stroke. An urgent MRI or CT brain must be obtained to rule out some of the differential diagnoses. Management \200 The primary principle of blood pressure control is to reduce DBP by 25 % or reduce DBP to 100 mmHg, whichever is higher, over a period of 1 \200\2232 hours. Transfer the patient to ITU for invasive monitoring (see previous section). Monitor neurological state, ECG, \202 uid balance. \200 Correct electrolyte abnormaliti es (K + , Mg 2 + , Ca 2 + ). \200 Give furosemide 40 \200\22380 mg IV. \200 Nitroprussi de is the \201 rst-line agent, as it is easy to control BP changes, despite its tendency to increase cerebral blood \202 ow. Labetalol and calcium-channel blockers are second-line agents and should be added in if necessary. It is vital to avoid agents with potential sedative action such as B \200\223blockers, clonidine, and methyldopa. In selected patients who are stable and present at the very early stages, oral therapy with a combination of B \200\223blockers and calcium-channel blockers may be suf \201 cient. This page intentionally left blank 766 CHAPTER 17 Cardiovascular emergencies Aortic dissection: assessment Aortic dissection is a surgical/medical emergency and, untrea ted, has a > 90 % one-year mortality. Dissection begins with formation of a tear in the int ima and the force of the blood cleaves the media longitudinally to various lengths. Predisp osing factors are summarized on the next page. Classi \201 cation There are three classi \201 cations as illustrated in Fig. 17.8 b Aort ic dissection: investigations, p. 769 \200\224 DeBakey, Stanford, and descriptive. Dissect ions involving the ascending and/or aortic arch are surgical emergencies and those that are exclusive to the descending aorta are treated medically. Presentation Chest pain: Classically abrupt onset, very severe in nature and most commonly anterior chest pain radiating to the interscapular region. Usually tearing in nature and, u nlike the pain of MI, most severe at its onset. Pain felt maximally in the anterior chest i s associated with ascending aortic dissection, whereas interscapular pain suggests dissecti on of the descending aorta. Patients often use adjectives such as \200\230tearing \200\231 , \200\230ripping \200\231, \200\230sharp \200\231 and \200\230stabbing \200\231 to desc ribe the pain. Sudden death or shock: Usually due to aortic rupture or cardiac tamponade. Congestive cardiac failure: Due to acute aortic incompetence and/or MI. \200 Patients may also present with symptoms and signs of occlusion of one of the branches of the aorta. Examples include: \200 stroke or acute limb ischaemia \200 \224 due to compression or dissection \200 paraplegia with sensory de \201 cits \200 \224 spinal artery occlusion \200 MI \200\224 usually the right coronary artery \200 r enal failure and renovascular hypertension \200 abdominal pain \200\224 coeliac axis or mesenteric artery occlusion. Aortic dissection may be painless. \200 Ask speci \201 cally about history of hypertensi on, previous heart murmurs or aortic valve disease, and previous CXRs that may be useful for comparison. Examination \200 This may be normal. \200 Most patients are hypertensive on presentatio n. Hypotension is more common in dissections of the ascending aorta (20 \200\22325 % ) and may be due to bloo d loss, acute aortic incompetence (which may be accompanied by heart failure), or tamponade (distended neck veins, tachycardia, pulsus paradoxus). Pseudohypotension may be seen if \202 ow to either or both subclavian arteries is compromised. Look for unequal blood pressure in the arms and document the prese nce of peripheral pulses carefully. Absent or changing pulses suggests extension of the dis section. Auscultation may reveal aortic valve regurgitation and, occasionally, a pericardial frictio n rub. Descending aortic dissections may rupture or leak into the left pleural space, and t he effusion results in dullness in the left base. AORTIC DISSECTION: ASSESSMENT 767 Neurologic de \201 cits may be due to carotid artery dissection or compression (hemiplegia) or spinal artery occlusion (paraplegia with sensory loss). Conditions associated with aortic dissection \200 Hypertension \200 Connective tissue d isorders Smoking, dyslipidaemia, cocaine/crack \200 Marfan syndrome a \200 Ehlers \200\223Danlos syndrome \200 Bicuspid aortic valve \200 Coarctaion \200 Giant cell arteritis \200 Takayasu arteritis \200 Beh et \200\231s disease \200 Syphllis \200 Car accident \200 Falls Hereditary vascular disorders Vascular in \202 ammation Deceleration trauma Chest trauma \200 Pregnancy \200 Iatrogenic Catheterization \200 Cardiac surgery a Marfan syndrome (arm span > height, pubis to sole > pubis to vertex, depressed sternum, s coliosis, high arched palate, upward lens dislocation, thoracic aortic dilation/aortic regu rgitation, increased urinary hydroxyprolene (some). Differential diagnosis \200 The chest pain may be mistaken for acute MI and acute MI may complicate aortic dissection. Always look for other signs of dissection (see above), as thr ombolysis will be fatal. Severe chest pain and collapse may also be due to pulmonary embolism, spontaneous pneumotho rax, acute pancreatitis, and penetrating duodenal ulcer. Pulse de \201 cits without backache should suggest other diagnoses: atherosclerotic periph eral vascular disease, arterial embolism, Takayasu arteritis, etc. Acute cardiac tamponade with chest pain is also seen in acute viral or idiopathic pericarditis, and acute MI with external rupture. 768 CHAPTER 17 Cardiovascular emergencies Aortic dissection: investigations General \200 ECG may be normal or non-speci \201 c (LV H, ST/T abnormalities). Look speci \201 cally for evidence of acute MI (inferior MI is seen if the dissection compromis es the right coronary artery ostium). CXR may appear normal, but with hindsight is almost always abnormal. Look for widened upper mediastinum, haziness or enlargement of the aortic knuckle, irregular aortic contour, sepa ration ( > 5 mm) of intimal calcium from outer aortic contour, displacement of the trachea to the right, enlarged cardiac silhouette (pericardial effusion), pleural effusion (usually on left). Compare with previous \201 lms if available. Bloods: Base FBC, U&E, cardiac enzyme as well as cross match. A novel monoclonal antibody a ssay to smooth muscle myosin heavy chains can accurately differentiate an acute dissection from a MI. Diagnostic \200 Echocardiography: Transthoracic ECHO may be useful in diagnosing aortic r oot dilatation, aortic regurgitation, and pericardial effusion/ tamponade. TOE is the inves tigation of choice as it allows better evaluation of both the ascending aorta and descendin g aorta, may identify the origin of the intimal tear, allows evaluation of the origins of t he coronary arteries in relation to the dissection \202 ap, and provides information on a ortic insuf \201 ciency. It is not good at imaging the distal ascending aorta and proximal arch. MRI angiography is the gold standard for diagnosing aortic dissection. It has all the posit ive features of TOE and, in particular, also provides accurate information on all segments of the ascending/arch/descending aorta, entry/exit sites, and branch vessels. Images can be displayed in multiple views as well as reconstructed in three dimensions. However, there a re a number of disadvantages, including (1) the availability of service out of hours and co st; (2) the presence of metallic valves or pacemakers may preclude the patient from having an MRI; (3) monitoring of unstable patients in the scanner can be dif \201 cult and unsafe . Spiral (helical) CT with contrast allows three-dimensional display of all segments of the a orta and adjacent structures. True and false lumen are identi \201 ed by differential cont rast \202 ow; the entry and exit site of the intimal \202 ap can be seen, as well as pl eural and pericardial \202 uid. However, it cannot demonstrate disruption of the aortic v alve, which may be associated with ascending aortic dissection. Angiography using the femoral or axillary approach may demonstrate altered \202 ow in the two lumens, aortic valve incompetence, and involvement of the bran ches and the site of the intimal tear. It is invasive and associated with a higher risk of complications in an already high-risk patient. It has largely been superseded by CT/MRI and TOE. AORTIC DISSECTION: INVESTIGATIONS 769 Selecting a diagnostic modality \200 Con \201 rm or refute a diagnosis of dissection. \200 Is the dissection con \201 ned to the descending aorta or does it involve the ascending/arch? Identify the extent, sites of entry and exit, and presence and absence of thrombus. Aim to see whether there is aortic regurgitation, coronary involvement, or pericardial effusions. Selecting a diagnostic modality \200 Where available, TOE should be the \201 rst-line i nvestigation. It is safe and can provide all the information necessary to take the patient to the operating theater. If TOE is not available, or if it fails to provide the necessary information, a spiral cont rast CT should be performed. \200 MRI should generally be reserved for follow-up images. \200 Angiography is rarely used, but is of value if other modalities have failed to provide a diagnosis, and/or extensive information is needed on branch vessels. Type III Type I Type II DeBakey classification Stanford classification Type A Type B Fig. 17.8 Clari \201 cation of aortic dissection. 770 CHAPTER 17 Cardiovascular emergencies Aortic dissection: management Stabilize the patient \200 If the diagnosis is suspected, t ransfer the patient to an area where full resuscitation facilities are readily available. Secure venous access with large-bore cannulae (e.g. gray Ven \202 on). \200 Take blood f or FBC, U&Es, and cross match (10 units). \200 When the diagnosis is con \201 rmed, or i n cases with cardiovascular complications, transfer to ITU , insert an arterial line (radial unless the subclavian arte ry is compromised when a femoral line is preferred), central venous line , and urinary cath eter. Immediate measures should be taken to correct blood pressure (see below). Give adequate analgesia (diamorphine 2.5 \200\22310 mg IV and metoclopramide 10 mg IV). Plan the de \201 nitive treatment This depends on the type of dissection (see Fig. 17.8 b Aortic dissection: investigations, p. 769) and its effects on the patient. General principl es are: \200 patients with involvement of the ascending aorta should have emergency surgical repair and BP control patients with dissection limited to the descending aorta are managed initially medically, with aggressive BP control. However, this may change in the near future, with encouraging data emerging from deployment of endovascular stent-grafts. Indications and principles for surgery \200 Involvement of the ascending aorta \200 Ext ernal rupture (haemopericardium, haemothorax, effusions) \200 Arterial compromise (limb i schaemia, renal failure, stroke) \200 Contraindications to medical therapy (AR, LVF) \200 Progression (continued pain, expansion of haematoma on further imaging, loss of pulse s, pericardial rub, or aortic insuf \201 ciency) The aim of surgical therapy is to replace the ascending aorta, thereby pre- venting retrogr ade dissection and cardiac tamponade (the main cause of death). The aortic valve may need r econstruction and resuspension unless it is structurally abnormal (bicuspid or Marfan), whe re it is replaced. Indications and principles for medical management Medical therapy is the treatment of choic e for: \200 uncomplicated type B dissection \200 stable isolated arch dissection \200 chronic ( > 2 weeks \200\231 duration) stable type B dissection. In all but those patients who are hypotensive, initial management is aimed at reducing systemic blood pressure and m yocardial contractility. The goal is to stop spread of the intramural haematoma and to prev ent rupture. The best guide is control of pain. Strict bed rest in a quiet room is essentia l. AORTIC DISSECTION: MANAGEMENT 771 Control blood pressure Reduce systolic BP to 100 \200\223120 mmHg. \200 Start on IV B -bl ocker (if no contraindications), aiming to reduce the heart rate to 60 \200\22370/min (see box, b p.772). Once this is achieved, if blood pressure remains high, add a vasodilator such as sodium nit roprusside (see box opposite). Vasodilators in the absence of B-blockade may increase myoca rdial contractility and the rate of rise of pressure (d P /d t ). Theoretically, this may p romote extension of the dissection. Further antihypertensive therapy may be necessary, and other conventional agents such as calcium-channel blockers, B -blockers, and ACE-Is can be used. In patients with aortic regurgitation and congestive cardiac failure, myocardial depressants should not be given. Aim to control BP with vasodilators only. Hypotension may be due to hemorrhage or cardiac tamponade. \200 Resuscitate with rapid in travenous volume (ideally colloid or blood, but crystalloid may be used also). A pulmonary artery wedge catheter (Swan \200\223Ganz) sh ould be used to monitor the wedge pressure and guide \202 uid replacement. If there are signs of aortic regurgitation or tamponade, arrange for an urgent ECHO and discuss with the surgeons. Emerging indications and principles for interventional therapy There are increasing reports and short case series demonstrating favorable outcome (prognostic as well as symptomatic) data on using endovascular stent-grafts in management of primarily type B and also, to a le sser extent, type A aortic dissections. On the basis of the current evidence, endovascular stent-grafts should be considered to sea l the entry to false lumen and to enlarge compressed true lumen in the following situations : \200 unstable type B dissection \200 malperfusion syndrome (proximal aortic stent-gra ft and/or distal fenestration/stenting of branch arteries) routine management of type B dissection (under evaluation). Cardiac tamponade: If the patie nt is relatively stable, pericardiocentesis may precipitate haemodynamic collapse and shoul d be avoided. The patient should be transferred to the operating theater for direct repair as urgently as possible. In the context of tamponade and EMD or marked hypotension, pericar diocentesis is warranted. Long-term treatment must involve strict BP control. 772 CHAPTER 17 Cardiovascular emergencies Prognosis \200 The mortality for untreated aortic dissection is roughly 20 \200\22330 % a t 24 hours and 65 \200\22375 % at 2 weeks. For dissections con \201 ned to the descending aorta, short-term survival is better (up to 80 % ) but 730 \200\22350 % will have progression of dissection despite aggressive medical therapy, and require surgery. Operative mortality is of the order of 10 \200\22325 % and depends on the condition of the patient preoperatively. Postoperative 5-year actuarial survival of up to 7 5 % may be expected. Medical therapy of aortic dissection B-blockade (aim for heart rate (HR)<60 \200\22370/min) Labetalol 20 \200\22380 mg slow IV injection over 10 min then 20 \200\223200 mg/h IV, increasing ever y 15 min 100 \200\223400 mg PO q12h Atenolol 5 \200\22310 mg slow IV injection then 50 mg PO after 15 min and at 12 h, then 100 mg PO da ily Propranolol 0.5 mg IV (test dose), then 1 mg every 2 \200\2235 min up to max 10 mg; repeat every 2 \200 \2233 h 10 \200\22340 mg PO 3 \200\2234 times daily When HR 60 \200\22370 /min, (or if B -blocker contraindicated), add Nitroprusside 0.25 \200\22310 mcg/kg/min IV infusion Hydralazine 5 \200\22310 mg IV over 20 minutes 50 \200\223300 mcg/min IV infusion 25 \200\22350 mg PO q 8h GTN 1 \200\22310 mg/h IV infusion Amlodipine 5 \200\22310 mg PO od This page intentionally left blank 774 CHAPTER 17 Cardiovascular emergencies Acute pericarditis: assessment Presentation \200 Typically presents as central chest pain \200\224 often pleuritic \200\224 relieved by sitting forward and can be associated with breathlessness. Other symptoms (e.g. fever, cough, arthralgia, rash, faintness/dizziness secondary to pain/iHR) may re \202 ect the underlying disease. A pericardial friction rub is pathognomonic. This may be positional and transient and may b e confused with the murmur of triscuspid regurgitation (TR) or MR. Venous pressure rises if an effusion develops. Look for signs of cardiac tamponade (see b Cardiac tamponade: presentation, p. 778). Investigations May be normal in up to 10 % . \200 \200\230Saddle-shaped \200\231 ST-segment elevation ( concave upwards), ECG with variable T inversion (usually late stages) and PR-segment depression (opposite to P-wa ve polarity). Minimal lead involvement to be considered typical includes I, II, aVL, aVF an d V 3 \200\223V 6 . ST-segement is always depressed in aVR, frequently depressed or isoelectric in V 1 , and sometimes depressed in V 2 . \200 May be dif \201 cult to di stinguish from acute MI. Features suggesting pericarditis are: \200 concave ST elevation (vs. convex) \200 all leads invo lved (vs. a territory e.g. inferior) \200 failure of usual ST evolution and no Q waves \200 no AV block, BBB, or QT prolongation. Early repolarization (a normal variant) may be mistaken for pericarditis. In the former, ST elevation occurs in precordial and, rarely, in V 6 or the limb leads, and is unlikely to s how ST depression in V 1 or PR segment depression. Usually not helpful in diagnosing pericarditis post-MI. \200 The voltage drops as an effu sion develops, and in tamponade there is electrical alternans, best seen in QRS complexes. May demonstrate a pericardial collection. \200 Useful to monitor LV function in case of d eterioration due ECHO to associated myopericarditis. We recommend every patient has an ECHO prior to discharge to assess LV function. Other investigations depend on the suspected etiology. ACUTE PERICARDITIS: ASSESSMENT 775 All patients should have: \200 FBC and biochemical pro \201 le \200 ESR and CRP (level s rise proportionate to intensity of disease) \200 serial cardiac enzymes (CK, CK-MB, tro ponin) \200\224 elevations indicate subpericardial myocarditis CXR (heart size, pulmonary oedema, infection). And, where appropriate: \200 viral titres (acute + 2 weeks later) \200\224 and obtain virology opinion \200 blood cultures \200 autoantibody screen (rheumatoid factor (RF), ANA, anti-DNA, complement levels) thyroid function tests (TFTs) \200 fungal precipitins (if immunosuppressed), iMantoux tes t \200 sputum culture and cytology \200 diagnostic pericardial tap (culture, cytology). Causes of acute pericarditis \200 Idiopathic \200 Infection (viral, bacterial, tubercul osis (TB), and fungal) \200 Acute MI \200 Dressler \200\231s syndrome, post-cardiotomy syndrome \200 Malignancy (e.g. breast, bronchus, lymphoma) \200 Uraemia \200 Autoimmu ne disease (e.g. SLE, rheumatoid arthritis (RA), Wegner \200\231s, scleroderma, polyarteritis nodosa (PAN)) Granulomatous diseases (e.g. sarcoid) \200 Hypothyroidism \200 Drugs (hydralazine, proc ainamide, isoniazid) \200 Trauma (chest trauma, iatrogenic) \200 Radiotherapy 776 CHAPTER 17 Cardiovascular emergencies