Diagnosis and severity \200 Ask about previous BP recordings, previous and current treatment, sympathomimetics, antidep ressants, nonprescription drugs, and recreational drugs. Check the blood pressure yourself, in both arms, after a period of rest and, if possible, on standing. Examine failure, perip heral pulses, renal masses, or focal neurological de \201 cit. Always examine the fundi \200\224dilate if necessary. carefully for clinical evidence of cardiac enlargement or heart All patients should have the following tests: \200 CBC Microangiopathic hemolytic anemia with malignant hypertension Renal impairment and/or dK+ ( diffuse intrarenal ischemia and secondary hyperaldosteronism) Disseminated intravascular co agulation (DIC) with malignant hypertension Cardiac enlargement Aortic contour (dissection? ) Pulmonary edema Protein and red cells casts Chemistries Coagulation screen CXR Urinalysis Other investigations depending on clinical picture and possible etiology include the follow ing: \200 24-hour urine collection Creatinine clearance Free catecholamines, metanephrines or vanilmandellic acid (VMA) LVH, a ortic dissection Size of kidneys and renal artery stenosis Renal artery stenosis Intracrani al bleed Cocaine, amphetamine, others \200 \200 \200 \200 ECHO Renal US and Doppler MR renal angiogram CT/MR brain Drug screen Indications for admission \200 \200 \200 Diastolic blood pressure persistently Retinal hemorrhages, exudates or papilledema Renal im pairment (cid:116)120 mmHg CHAPTER 1 Cardiovascular emergencies 34 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 (abrupt change of >25% in BP will exceed cereb ral BP autoregulation). Initial BP reduction (of 25%) should be achieved over 1 \200\2234 h ours with a less rapid reduction over 24 hours to a diastolic blood pressure (DBP) of 100 m mHg. The only two situations where BP must be lowered rapidly are in the context of aortic dissection and MI. Treatment Most patients who are alert and otherwise well may be treated with oral therapy t o lower BP gradually. First-line treatment should be with a B-blocker (unless contraindicated) with a thiazide diuretic, or a low-dose calcium antagonist. Urgent invasive monitoring (arterial line) prior to drug therapy is indi- cated for patients with the following: \200 \200 Evidence of hypertensive encephalopathy Complications of hypertension (e.g., aortic dissect ion, acute pulmonary edema or renal failure) Treatment of underlying condition (e.g., glome rulonephritis, pheochromocytoma, CREST crisis) Patients with persistent diastolic BP Eclamp sia \200 (cid:116)140 mmHg Sublingual nifedipine must be avoided. Conditions requiring speci \201 c treatment See Box 1.4. Long-term management \200 \200 Investigate as appropriate for an underlying cause. Select a treatment regime that is toler ated 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 (if applicable), giving appropriate dietary advice (cholesterol), and aiming for optimal diabetic control. Monitor long-term control and look for end-organ damage (regular fundoscopy, ECG, blood work). Eve n poor control is better than no control. Box 1.4 Conditions requiring speci \201 c treatment \200 \200 \200 \200 \200 Accelerated and malignant hypertension Hypertensive encephalopathy Eclampsia Pheochromocyto ma Hypertensive patients undergoing anesthesia Drugs for hypertensive emergencies Table 1.4 Drugs for treatment of hypertensive emergencies: IV therapy Onset of action Comments Dosage Drug 2 \200\2235 minutes Drug of choice in suspected pheochromocytoma or aortic dissection. Avoid if there is LVF. M ay be continued orally (see below) Drug of choice in LVF and/or encephalopathy 20 \200\22380 mg IV bolus q10min 20 \200\223200 mg/min by IV infusion, increasing every 15 minutes Labetalol D R U G S Seconds 0.25 \200\22310 g/kg/min IV infusion Nitroprusside Mainly venodilatation. Useful in patients with LVF or angina May provoke angina 2 \200\2235 minutes 1 \200\22310 mg/hr IV infusion Nitroglycerine F O R H Y P E R T E N S I 10 \200\22315 minutes 5 \200\22310 mg IV over 20 minutes 50 \200\223300 g/min IV infusion Hydralazine Short-acting B-blocker also used for SVTs Seconds 500 g/kg/min IV loading dose 50 \200\223200 g/kg/min IV infusion Esmolol HCl Seconds 2 \200\2235 mg IV over 2 \200\2235 minutes prn Phentolamine V E E M E R G E N C E S NB: It is dangerous to reduce the blood pressure quickly. Aim to reduce DBP to 100 \200\223 110 mmHg within 2 \200\2234 hours. Unless there are good reasons to commence IV therapy, al ways use oral medicines. I 3 5 3 6 Table 1.5 Drugs for treatment of hypertensive emergencies: oral therapy C H A P T E R Drug Onset of action Comment There are numerous alternative B-blockers Dosage Atenolol 30 \200\22360 minutes 50 \200\223100 mg po daily 1 C a r d o v a s c u l a r Nimodipine 15 \200\22320 minutes Avoid sublingual use, as the fall in BP is very rapid 10 \200\22320 mg po q8h (q12h if slow release) i Labetalol 30 \200\22360 minutes Use if pheochromocytoma suspected. Safe in pregnancy 100 \200\223400 mg po q12h Hydralazine 20 \200\22340 minutes Safe in pregnancy 10 \200\22350 mg po q8h Minoxidil May cause marked salt and water retention Combine with a loop diuretic (e.g., furosemide 40 \200\223240 mg daily) 30 \200\22360 minutes 5 \200\22310 mg po od e m e r g e n c i e s Sedation is common. Do not stop abruptly as here is a high incidence of rebound hypertensiv e crisis Clonidine 30 \200\22360 minutes 0.2 mg po followed by 0.1 mg hourly max. 30 \200\22360 minutes 0.8 mg total for urgent ther apy, or 0.05 \200\2230.1 mg po q8h increasing every 2 days Note: Aim to reduce DBP to 100 \200\223110 mmHg in 2 \200\2234 hours and normalize BP in 2 \200\2233 days. HYPERTENSIVE EMERGENCY WITH RETINOPATHY 37 Hypertensive emergency with retinopathy (accelerated and malignant hypertension) This is pa rt of a continuum of disorders (see Box 1.5) characterized by hypertension (DBP often >120 mmHg) and acute microvascular damage (seen best in the retina but present in all organs). I t may be dif \201 cult to decide whether the damage in some vascular beds is the cause or effect of hypertension (e.g., an acute glomerulonephritis). Accelerated hypertension (grade 3 retinopathy) may progress to malig- nant hypertension, wi th widespread necrotizing vasculitis of the arterioles (and papilledema). Presentation is commonly with headache or visual loss and varying degrees of confusion. Mor e severe cases present with renal failure, heart failure, microangiopathic hemolytic anemia , and DIC. Management \200 \200 Transfer the patient to the ICU. Insert an arterial line and consider central venous line i f there is evidence of necrotizing vasculitis and DIC. Catheterize the bladder. Monitor neu rological state, ECG, \202 uid balance. Aim to lower the DBP to 100 mmHg or by 15 \200 \22320 mmHg, whichever is higher, over the \201 rst 24 hours. Those patients with early f eatures may be treated successfully with oral therapy (B-blockers, calcium channel blockers \200\224see Table 1.5). Patients with late symptoms or who deteriorate should be given par enteral therapy aiming for more rapid lowering of BP. \200 \200 If there is evidence of pulmonary edema or encephalopathy, give furosemide 40 \200\22380 mg IV. If there is no left ventricular failure (LVF), give a bolus of labetalol followed by a n infusion. For patients with LVF, nitroprusside or hydralazine is preferable. Consult renal team for patients with acute renal failure or evidence of acute glomeruloneph ritis (>2+ proteinuria, red cell casts). Dopamine should be avoided as it may worsen hypert ension. Consider giving an ACE inhibitor. High circulating renin levels may not allow contr ol of hypertension, which in turn causes progressive renal failure. ACE inhibitors will blo ck this vicious circle. There may be marked \201 rst-dose hypotension, so start cautiousl y. Hemolysis and DIC should recover with control of BP. Hypertension in the context of acute stroke or intracranial bleed Stroke or bleed may be th e result of hypertension or vise versa. In the acute setting there is impaired autoregulati on of cerebral blood \202 ow and autonomic function. Small changes in systemic BP may res ult in cata- strophic falls in cerebral blood \202 ow. CHAPTER 1 Cardiovascular emergencies 38 Systemic BP should not be treated unless DBP >130 mmHg and/or there is severe cerebral edema (with clinical manifestations). In most cases, BP tends to settle over 24 \200\22336 hours. If treatment is indi- cated, BP reduction principles must be adhered to and a combination of nitroprusside, labetalol, and calcium channel blockers can be used. Centrally acting agents must be avoided as they caus e sedation. In patients with subarachnoid hemorrhage (SAH), a cerebroselective calcium chan nel blocker, such as nimodipine, is used to decrease cerebral vasospasm. Systemic BP must also be treated if it quali \201 es by principles and/or if it remains el evated after 24 hours. There is no evidence that this reduces further events in the acute p hase. Box 1.5 Hypertensive retinopathy Grade 1 Grade 2 Grade 3 Grade 4 Tortuous retinal arteries, silver wiring Atrioventricular (AV) nicking Flame shaped hemorrh ages and cotton wool exudates Papilledema HYPERTENSIVE ENCEPHALOPATHY 39 Hypertensive encephalopathy This condition is caused by cerebral edema secondary to loss of cerebral autoregulatory function. It is usually gradual in onset and may occur in previously normotensive patients at blood p ressures as low as 150/100 mmHg. It is rare in patients with chronic hypertension and press ures are also much higher. Symptoms \200 Headache, nausea and vomiting, confusion, grade III and IV hypertensive retinopathy. Late f eatures consist of focal neurological signs, seizures, and coma. Diagnosis This is a diagnosis of exclusion and other diagnoses must be ruled out (e.g., str oke, 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 def- icit. Always exclude hypoglycemia. Starting hypotensive treatment for hypertension associated with a stroke can cause extension of the stroke. An urgent MRI or CT brain must be obtained to rule out some of the other diagnoses. Management The primary principle of blood pressure control is to reduce DBP by 25% or reduc e DBP to 100 mmHg, whichever is higher, over a period of 1 \200\2232 hours. \200 \200 \200 \200 \200 Transfer the patient to the ICU for invasive monitoring Monitor neurological state, ECG, \202 uid balance. Correct electrolyte abnormalities (K Give furosemide 40 \200\22380 mg IV. Nitroprusside is the \201 rst-line agent as it is easy to control BP changes, despite it s tendency to increase cerebral blood \202 ow. Labetalol and calcium channel blockers suc h as nicardipine are second- line agents and should be added in if necessary. It is vital t o avoid agents with potential sedative action such as B-blockers, clonidine, and methyldopa . In selected patients who are stable, oral therapy with a combination of B-blockers and ca lcium blockers may be suf \201 cient. +, Mg2+, Ca2+). CHAPTER 1 Cardiovascular emergencies 40 Aortic dissection: assessment Aortic dissection is a surgical and medical emergency; untrea ted it has a >90% 1-year mortality rate. Dissection begins with formation of a tear in the intima and the force of the blood cleaves the media longitudinally to various lengths. Pred isposing factors are summarized in Box 1.6. Classi \201 cation There are three classi \201 cations, illustrated in Figure 1.5 \200 \224DeBakey, Stanford, and descriptive. Dissections involving the ascending aorta and/or ao rtic arch are surgical emergencies and ones limited to the descending aorta are treated med ically. Presentation \200 Chest pain classically has abrupt onset, is very severe in nature, and most commonly is anterior chest pain radiating to the interscapular region. Usually it is t earing in nature and, unlike the pain of myocardial infarction, most severe at its onset. P ain felt maximally in the anterior chest is associated with ascending aortic dissection, wh ereas interscapular pain suggests dissection of the descending aorta. Patients often use ad jectives such as tearing, ripping, sharp, and stabbing to describe the pain. Sudden death t amponade. Congestive cardiac failure myocardial infarction. or shock: is usually due to aortic rupture or cardiac is due to acute aortic incompetence and/or Box 1.6 Conditions associated with aortic dissection \200 \200 Hypertension Connective tissue disorders Smoking, dyslipidemia, cocaine/crack Marfan \200\231s syndrome* Ehlers \200\223Danlos syndr ome Bicuspid aortic valve Coarctaion Giant cell arteritis Takayasu arteritis Beh et \200 \231s disease Syphilis Car accident Falls Hereditary vascular disorders Vascular in \202 ammation Deceleration trauma \200 \200 Chest trauma Pregnancy Iatrogenic Catheterization Cardiac surgery Marfan \200\231s syndrome: arm span > height, pubis to sole > pubis to vertex, depressed st ernum, scoliosis, high arched palate, upward lens dislocation, thoracic aortic dilation/aor tic regurgitation, increased urinary hydroxyprolene. AORTIC DISSECTION: ASSESSMENT 41 Type II Type III Type I DeBakey classification Stanford classification Type A Type B Figure 1.5 Classi \201 cation of aortic dissection. Patients may also present with symptoms and signs of occlusion of one of the branches of th e aorta. Examples include: \200 \200 \200 \200 \200 Stroke or acute limb ischemia \200\224due to compression or dissection Paraplegia with sens ory de \201 cits \200\224spinal artery occlusion Myocardial infarction \200\224usually the right coronary artery Renal failure and renovascular hypertension Abdominal pain \200\224c eliac axis or mesenteric artery occlusion Aortic dissection may be painless. Ask speci \201 cally about history of hypertension, previous heart mur- murs, or aortic va lve disease and previous CXR that may be useful for comparison. Examination This may be normal. Most patients are hypertensive on presentation. Hypotension is more common in dissections of the ascending aorta (20% \200\22325%) and may be due to b lood loss, acute aortic incompetence (which may be accompanied by heart failure), or tampon ade (distended neck veins, tachycardia, pulsus paradoxus). Pseudohypotension may be seen if \202 ow to either or both subclavian arteries is comprom ised. Look for unequal blood pressure in the arms and document the presence of peripheral p ulses carefully. Absent or changing pulses suggest extension of the dissection. Auscultation may reveal aortic valve regurgitation and occasionally a pericardial friction rub. Descending aortic dissections may rupture or leak into the left pleural space, and the effusion results in dullness in the left base. Neurological de \201 cits may be due to carotid artery dissection or com- pression (hemipl egia) or spinal artery occlusion (paraplegia with sensory loss). CHAPTER 1 Cardiovascular emergencies 42 Box 1.7 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 Presentation, p. 40), as thrombolysis will be fatal. Severe chest pain and collapse may also be due to pulmonary embolism, spontaneous pneumothorax, acute pancreatitis, and penetrating duodenal ulcer. Pulse de \201 cits with out backache should suggest other diagnoses: atherosclerotic peripheral vascular disease, a rterial embolism, Takayasu \200\231s arteritis, etc. Acute cardiac tamponade with chest pai n is also seen in acute viral or idiopathic pericarditis and acute myocardial infarction wi th external rupture. AORTIC DISSECTION: INVESTIGATIONS 43 Aortic dissection: investigations General ECG may be normal or nonspeci \201 c (LVH, ST/T abnormalities). Look spe- ci \201 cally for evidence of acute MI (inferior MI is seen if t he dissection com- promises the right coronary artery ostium). CXR may appear normal. Look for widened upper mediastinum, hazi- ness or enlargement of the aortic knuckle, irregular aortic contour, separ- ation (>5 mm) of intimal calcium from out er aortic contour, displacement of trachea to the right, enlarged cardiac silhouette (peric ardial effusion), pleural effusion (usually on left). Compare with previous \201 lms if a vailable. Bloods: Base-line CBC, chemistries, cardiac enzymes as well as cross- match. A no vel monoclonal antibody assay to smooth muscle myosin heavy chains can accurately different iate an acute dissection from an MI. Diagnostic Echocardiography Transthoracic echocardiogram (TTE) may be useful in diagnosing aortic root dilatation, aortic regurgitation, and pericardial effusion/tamponade. Transesophageal echocardiogram (TEE) is the investigation of choice, as it allows better ev aluation of both ascending aorta and descending aorta, may identify the origin of intimal t ear, allows evaluation of the origins of the coronary arteries in relation to the dissectio n \202 ap, and provides infor- mation on aortic insuf \201 ciency. It is not good at ima ging the distal ascending aorta and proximal arch. MRI angiography This is the gold standard for diagnosing aortic dissection. It has all the positive features of TEE and in particular also provides accurate informa- tion on all segm ents of 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 are a number of disadvantages: 1) availability of service after hours and co st; 2) presence of metallic valves or pacemakers may preclude patients from having an MRI; 3) monitoring of unstable patients in the scanner can be dif \201 cult and unsafe. Spiral (helical) CT with contrast This allows three-dimensional display of all segments of the aorta and adja- cent structures. True and false lumen are identi \201 ed by differenti al contrast \202 ow, and entry and exit sites of intimal \202 ap can be seen as well as pleural and pericardial \202 uid. However, it cannot demonstrate disruption of the aortic valve, which may be associated with ascending aortic dissection. It requires the use of iodinate contrast CHAPTER 1 Cardiovascular emergencies 44 Angiography Angiography using the femoral or axillary approach may demonstrate altered \202 ow in the two lumens, aortic valve incompetence, and involve- ment of the branches and the site of the intimal tear. It is invasive and asso- ciated with a higher risk of compli cations in an already high-risk patient. It has largely been superseded by CT/MRI and TEE. Selecting a diagnostic modality (see Box 1.8) \200 \200 Con \201 rm or refute a diagnosis of dissection. Is the dissection con \201 ned to the de scending aorta or does it involve the ascending/arch? Identify the extent, sites of entry a nd exit, and presence and absence of thrombus. See whether there is aortic regurgitation, c oronary involvement, or pericardial effusions. Rule out other causes of symptoms. Box 1.8 Selecting a diagnostic modality \200 Where available, TEE should be the \201 rst-line investigation. It is safe and can provid e all the information necessary to take the patient to the operating room. If TEE is not av ailable or if it fails to provide the necessary information, a spiral contrast CT should be performed. MRI should generally be reserved for follow-up images. Angiography is rarely us ed but is of value if other modalities have failed to provide a diagnosis and/or extensive information is needed on branch vessels. \200 AORTIC DISSECTION: MANAGEMENT 45 Aortic dissection: management Stabilize the patient \200 If the diagnosis is suspected, transfer the patient to an area where full resuscitation fac ilities are readily available. Secure Take blood When the diagnosis is con \201 rmed or in cases with cardiovascular complications, transfer to ICU, insert an arterial line (radial unless the subclavian artery is compromised when a femoral line is preferred), central veno us line, and urinary catheter. Immediate measures should be taken to correct blood pressure (see below). Give adequate analgesia (morphine 2.5 \200\22310 mg IV and metoclopramide 10 mg IV). \200 \200 venous access with large-bore cannulas. for CBC, chemistries, and cross-match (10 units). Plan de \201 nitive treatment This depends on the type of dissection (see Fig. 1.5) and it s effects on the patient. General principles are as follows: \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 blood pressure control. However, this may change in the near future with emerging encouraging data from deployment of endovascular stent-grafts. Indications and principles for surgery \200 \200 \200 \200 \200 Involvement of the ascending aorta External rupture (hemopericardium, hemothorax, effusions ) Arterial compromise (limb ischemia, renal failure, stroke) Contraindications to medical t herapy (AR, CHF) Progression (continued pain, expansion of hematoma on further imaging, los s of pulses, 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 \200 \231s), when it is replaced. Indications and principles for medical management Medical therapy is the treatment of choic e for the following: \200 \200 \200 Uncomplicated type B dissection. Stable isolated arch dissection. Chronic (>2 weeks duratio n) stable type B dissection. In all but those patients who are hypotensive, initial management is aimed at reducing syst emic blood pressure and myocardial contractility. The goal is to stop spread of the intramu ral hematoma and to prevent rupture. The best guide is control of pain. Strict bed rest in a quiet room is essential. CHAPTER 1 Cardiovascular emergencies 46 Control blood pressure Reduce systolic BP to 100 \200\223120 mmHg. \200 B-blocker (if no contraindications) aiming to reduce the Start on IV heart rate to 60 \200\22370/min (see Table 1.6). Once this is achieved, if bloo d pressure remains high, add a vasodilator such as sodium nitroprusside (see Table 1.6). Va sodilators in the absence of B-blockade may increase myocardial contractility and the rate of rise of pressure (dP/dt). Theoretically this may promote extension of the dissection. Fu rther antihypertensive therapy may be necessary and other conventional agents such as calci um channel blockers, B-blockers, and ACE inhibitors can be used. In patients with aortic re gurgitation and congestive cardiac failure, myocardial depressants should not be given. Aim to control blood pressure with vasodilators only. Hypotension This may be due to hemorrhage or cardiac tamponade. \200 Resuscitate with rapid IV volume (ideally colloid or blood, but crystalloid may be used als o). A central venous or pulmonary artery wedge catheter (Swan \200\223Ganz) may be used to monitor the wedge pressure and guide \202 uid replacement. If there are signs of aortic r egurgitation or tamponade, arrange for an urgent ECHO and discuss with the surgeons. Table 1.6 Medical therapy of aortic dissection B-Blockade (aim for HR <60 \200\22370/min) Labetalol 20 \200\22380 mg slow IV injection over 10 minutes, then 20 \200\223200 mg/hr IV, increasin g every 15 minutes 100 \200\223400 mg po q12h Atenolol 5 \200\22310 mg slow IV injection then 50 mg po after 15 minutes and at 12 hours, then 100 mg po daily Propranolol 0.5 mg IV (test dose), then 1 mg every 2 \200\2235 minutes up to max 10 mg; repeat every 2 \200\2233 hours 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 g/kg/min IV infusion Hydralazine 5 \200\22310 mg IV over 20 minutes 50 \200\223300 g/min IV infusion 25 \200\22350 mg po q 8h Nitroglycerin 1 \200\22310 mg/hr IV infusion Amlodipine 5 \200\22310 mg po qd AORTIC DISSECTION: MANAGEMENT 47 Emerging indications and principles for interventional therapy There are increasing reports and short case series demonstrating favorable outcome (prognostic as well as symptomatic) data for use of endovascular stent-grafts in management of primarily type B and, to a lesse r extent, type A aortic dissections. On the basis of the current evidence, endovascular stent-grafts should be considered to sea l 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-graft and/or distal fenestration/stenting of branch arteries) Patients with high-risk type B diss ections who represent high surgical risk Routine management of type B dissection (under eva luation) Cardiac tamponade: if the patient is relatively stable, pericardiocentesis may precipitate hemodynamic collapse and should be avoided. The patient should be transferred to the operat ing room for direct repair as urgently as possible. In the context of tamponade and EMD or marked hypoten- sion, pericardiocentesis is warranted. Long-term treatment must involve strict blood pressure control. Prognosis The mortality rate for untreated aortic dissection is roughly 20% \200\22330% at 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 30% \200\22350% will have progression of dissection des- pite aggressive medical therapy and will 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 75% may be expecte d. CHAPTER 1 Cardiovascular emergencies 48 Acute pericarditis: assessment Presentation \200 Typically presents as central chest pain \200\224often pleuritic \200\224relieved by sittin g forward and can be associated with breathlessness. Other symptoms (e.g., fever, cough, ar thralgia, rash, faintness or dizziness secondary to pain/iHR) may re \202 ect the underlyi ng disease. A pericardial friction rub is pathognomonic. This may be positional and transie nt and may be confused with the murmur of TR or MR. Venous pressure rises if an effusion de velops. Look for signs of cardiac tamponade (p. 51). Causes of acute pericarditis are listed in Box 1.9. Investigations ECG \200 \200 May be normal in up to 10%. Saddle-shaped ST-segment elevation T inversion (usually late st ages) and PR-segment depression (opposite to p-wave polarity). Minimal lead involvement con sidered typical includes I, II, aVL, aVF, and V3 \200\223V6. ST segment is always depressed in aVR, frequently depressed or isoelectric in V1, and sometimes depressed in V2. It may b e dif \201 cult to distinguish from acute MI. Features suggesting pericarditis are the fol lowing: \200 \200 \200 \200 Early repolarization (a normal variant) may be mistaken for pericarditis. In the former; ST elevation occurs in precordial and rarely in V6 or the limb leads and is unlikely to show ST depression in V1 or PR segment depression. (concave upward), with variable Concave ST elevation (vs. convex) All leads involved (vs. a territory, e.g., inferior) Fail ure of usual ST evolution and no Q waves No AV block, bundle branch block (BBB), or QT prol ongation Box 1.9 Causes of acute pericarditis \200 \200 \200 \200 \200 \200 \200 Idiopathic Infection (viral, bacterial, tuberculosis [TB], and fungal) Acute MI Dressler \200\231s syndrome, postcardiotomy syndrome Malignancy (e.g., breast, bronchus, lymphoma) U remia Autoimmune disease (e.g., SLE, rheumatoid arthritis [RA], Wegner \200\231s, scleroder ma, polyarteritis nodosa [PAN]) Granulomatous diseases (e.g., sarcoid) Hypothyroidism Drugs (hydralazine, procainamide, isoniazid) Trauma (chest trauma, iatrogenic) Radiotherapy \200 \200 \200 \200 ACUTE PERICARDITIS: ASSESSMENT 49 \200 ECG is usually not helpful in diagnosing pericarditis post-MI. The voltage drops as an effu sion develops and in tamponade there is electrical alternans best seen in QRS complexes. ECHO \200 \200 May demonstrate a pericardial collection Useful to monitor LV function in case of deteriora tion due to associated myopericarditis We recommend that every patient have an ECHO prior t o discharge to assess LV function. Other Other investigations depend on the suspected etiology. All patients should have \200 \200 \200 CBC and biochemical pro \201 le ESR and CRP (levels rise proportionate to intensity of dis ease) Serial cardiac enzymes (CK, CK-MB, troponin) \200\224elevations indicate subpericardi al myocarditis CXR (heart size, pulmonary edema, infection) Echocardiogram: evaluate size, hemodynamic consequences of any effusion \200 Where appropriate \200 \200 \200 \200 \200 \200 \200 Viral titers (acute +2 weeks later) and obtain infectious disease opinion Blood cultures Au toantibody screen (RF, ANA, anti-DNA, complement levels) Thyroid function tests Fungal prec ipitins (if immunosuppressed), Sputum culture and cytology Diagnostic pericardial tap (cult ure, cytology) iPPD CHAPTER 1 Cardiovascular emergencies 50 Acute pericarditis: management General measures \200 Admit? This depends on the clinical picture. We recommend admission of most patients for ob servation for complications, especially effusions, tamponade, and myocarditis. Patients sho uld be discharged when pain free. Bed rest Analgesia: increases coronary \202 ow (200 \200\223800 mg qid). Aspirin is an alternative (650 mg q6h po). Indomethacin should be avoi ded in adults as it reduces coronary \202 ow and has marked side effects. Use proton pump inhibitor (PPI) (lansoprazole 30 mg od) to minimize gastrointestinal (GI) side effects. Op ioid analgesia may be required. Colchicine used as monotherapy or in addition to NSAIDs may help reduce pain acutely and prevent recurrence. Steroids (e.g., prednisolone 40 \200\2236 0 mg po qd for up to 2 weeks, tapering down when pain decreases). Use in conjunction with N SAID and taper steroids \201 rst before stopping NSAID. It is also of value if pericardit is is secondary to autoimmune disorders. Colchicine: monotherpay or in conjunction with NSA IDs it may help to reduce pain acutely and prevent relapses (1 mg/day divided doses). Stop if patient develops diarrhea, nausea (1 mg stat, 500 g q6h for 48 hours). Pericardiocente sis should be considered for signi \201 cant effusion or if there are signs of tamponade ( p. 75), diagnostically if persistent or recurrent effusion. Antibiotics should be discontin ued (risk of hemopericardium). Oral anticoagulants Patients should be given IV UFH if absol utely necessary, which is easier to reverse (IV protamine) if complications arise. \200 NSAIDs are the mainstay. Ibuprofen is well tolerated and may be used if the pain does not decrease within 48 hours There is evidence to support that either used as \200 should be given only if bacterial infection is suspected. CARDIAC TAMPONADE: PRESENTATION 51 Cardiac tamponade: presentation Cardiac tamponade occurs when a pericardial effusion causes hemo- dynamically signi \201 cant cardiac compression. The presentation depends on the sp eed with which \202 uid accumulates within the pericardium. Acute tamponade may occur with 100 \200\223200 mL in a relatively restricted pericardial sac. Chronic pericardial collections may contain up to 1000 mL of \202 uid with- out clinical tamponade. Causes Acute tamponade \200 Cardiac trauma \200 Iatrogenic \200 \200 \200 Aortic dissection Spontaneous bleed \200 Anticoagulation \200 Uremia \200 Thrombocytopenia C ardiac rupture post-MI Subacute tamponade \200 Malignant disease \200 Idiopathic pericarditis \200 Uremia \200 Infections \200 Bacterial \200 Radiation Hypothyroidism Postpericardiotomy SLE Ot her autoimmune disease Post-cardiac surgery Post-cardiac catheterization Post-pacing/EP study \200 Tuberculosis \200 \200 \200 \200 Presentation Patients commonly present with either cardiac arrest (commonly electrical mech anical dissociation) or hypotension, confusion, stupor, and shock. Patients who develop cardiac tamponade slowly are usually acutely unwell, but not in extremis. Their main symptoms include the following: \200 \200 \200 Shortness of breath, leading to air hunger at rest. There may be a preceding history of che st discomfort. Symptoms resulting from compression of adjacent structures by a large effusi on (i.e., dysphagia, cough, hoarseness, or hiccough). There may be symptoms due to the unde rlying cause. Insidious development may present with complications of tamponade, including renal failure, liver and/or mesenteric ischemia, and abdominal plethora. \200 Important physical signs Most physical \201 ndings are nonspeci \201 c and include the f ollowing: \200 \200 \200 Tachycardia (except in hypothyroidism and uremia). Hypotension ( shock) with postural hyp otension. Raised JVP (often >10 cm) with a prominent systolic absent diastolic y descent (s ee Box 1.10). If the JVP is visible and either remains static or rises with inspiration, it indicates concomitant pericardial constriction (Kussmaul \200\231s sign). Auscultation may reveal diminished heart sounds. Pericardial rub may be present and suggests a small perica rdial collection. x descent and CHAPTER 1 Cardiovascular emergencies 52 Look for pulsus paradoxus (a decrease in the palpable pulse and SBP of >10 mmHg on inspirat ion). This may be so marked that the pulse and Korotkoff sounds may be completely lost duri ng inspiration. This can be measured using a BP cuff 1 or arterial catheter if in situ alre ady. Other conditions that can cause a pulsus paradoxus include acute hypotension, obstruct ive airways disease, and pulmonary embolus. Other physical signs include cool extremities (ears, nose), tachypnea, hep- atomegaly, and signs of underlying cause of the pericardial effusion. Box 1.10 Causes of hypotension with a raised JVP \200 \200 \200 \200 \200 \200 \200 \200 \200 Cardiac tamponade Constrictive pericarditis Restrictive cardiomyopathy Severe biventricular failure Right ventricular infarction Pulmonary embolism Tension pneumothorax Acute severe asthma Malignant superior vena cava (SVC) obstruction and sepsis (e.g., lymphoma) 1 Teaching point: To establish presence of pulsus paradoxus noninvasively, in \202 ate BP cuff to 15 mmHg above highest systolic pressure. De \202 ate cuff gradually until \201 r st beats are heard and hold pressure at that level concentrating on disappearance and reapp earance of sounds with respiration (bump-bump, silence-silence, bump-bump, where noise re \202 ects expiration). Continue to de \202 ate slowly, paying attention to the same patter n until all beats are audible. The difference between the initial and \201 nal pressure s hould be >10 mmHg when paradox is present. CARDIAC TAMPONADE: MANAGEMENT 53 Cardiac tamponade: management Tamponade should be suspected in patients with hypotension, e levated venous pressure, falling BP, iHR and iRR (with clear chest), and pulsus paradoxus, especially if predisposing factors are present. Investigations \200 CXR: the heart size may be normal (e.g., in acute hemopericardium following cardiac trauma) . With slower accumulation of pericardial \202 uid (>250 mL) the cardiac silhouette will enlarge with a globular appearance. The size of the effusion is unrelated to its hemodynami c signi \201 cance. Look for signs of pulmonary edema. ECG and variable ST-segment changes . With large effusions, electrical alternans may be present with beat-to-beat variation in the QRS morphology possibly resulting form the movement of the heart within the pericardial effusion. Echocardiography diagnosis of tamponade is a clinical one. ECHO signs highly sug gestive of tamponade include 1) chamber collapse during diastole (RA, RV, RV out \202 ow t ract), 2) marked variation in transvalvular \202 ow, and 3) dilated IVC with little or no diameter change on respiration. usually shows a sinus tachycardia, with low-voltage complexes con \201 rms presence of a pericardial effusion. The If available, examine the central venous pressure trace for the characteris- tic exaggerate d x descent and absent y descent. Management Following con \201 rmation of the diagnosis: \200 While preparing for drainage of the pericardial \202 uid, the patient \200\231s circulati on may temporarily be supported by loading with IV colloid (500 \200\2231000 mL stat) and s tarting inotropes (i.e., adrenaline). The effusion should be urgently drained (see p. 75 fo r pericardio- centesis), guided by ECHO or \202 uoroscopy. In the event of circulatory co llapse, drainage must happen immediately without imaging. Surgical drainage is indicated if the effusion is secondary to trauma. Avoid intubation and positive pressure ventilation as this reduces CO. In patients with cardiac arrest, chest compression has little or no value , as there is no room for additional \201 lling. Uremic patients will also need dialysis. The cause of the effusion should be established (see p. 309). Pericardial \202 uid shoul d be sent for cytology, microbiology including TB, virology, and, if appropriate, Hb, gluco se, and amylase. \200 \200 \200 Further management is of the underlying cause. CHAPTER 1 Cardiovascular emergencies 54 Special cases Recurrent pericardial effusion In some cases, pericardial effusion recurs. Th is requires either a change in the treatment of the underlying cause or a formal surgical d rainage pro- cedure such as a surgical pericardial window or pericardiectomy. Low-pressure tamponade This is seen in the setting of dehydration. The JVP is not raised, r ight atrial pressure is normal, and tamponade occurs even with small volumes of pericardial \202 uid. \200 \200 The patient may respond well to IV \202 uids. If there is a signi \201 cant pericardial collection, this should be drained. CENTRAL LINE INSERTION 55 Practical procedures Central line insertion Check list of required materials \200 Sterile dressing pack and gloves \200 10 mL and 5 mL syringe (21G) and (25G) needles \200 Loca l anesthetic (e.g., 2% lidocaine) \200 Central line (e.g., 16G long Abbocath \200 Salin e \202 ush \200 Silk suture and needle \200 No 11 scalpel blade \200 Sterile occlus ive dressing (e.g., Tegaderm or Seldinger catheter) ) Risks \200 \200 \200 \200 \200 \200 