CHAPTER 1 Cardiovascular emergencies 16 Acute aortic regurgitation Presentation \200 Sudden, severe aortic regurgitation (AR) presents as cardiogenic shock and acute pulmonary edema. The hemodynamic changes are markedly different from those seen in chronic AR. The pr evious normal-sized LV results in a smaller effective forward \202 ow and higher LVEDP fo r the same degree of AR. Patients are often extremely unstable, tachycardic, and peripheral ly vasoconstricted and often have pulmonary edema. Unlike chronic AR, pulse pressure may be near normal. If available, ask about history of previous valvular heart disease, hypertens ion, features of Marfan \200\231s syndrome (family history), and risk factors for infective endocarditis. Physical signs of severe AR include a quiet aortic closure sound (S2); an ej ection systolic murmur over the aortic valve (turbulent \202 ow); high-pitched and short, early diastolic murmur (AR); quiet S1 (premature closure of the mitral valve). Examine spe ci \201 cally for signs of an underlying cause. Where there is no obvious underlying cause (e.g., acute MI), assume infective endocarditis until proven otherwise. \200 Causes \200 \200 \200 \200 \200 \200 Infective endocarditis Ascending aortic dissection Collagen vascular disorders (e.g., Marfa n \200\231s) Connective tissue diseases (large- and medium-vessel arteritis) Trauma Dehisce nce of a prosthetic valve Diagnosis Diagnosis is based on a combination of clinical features and transthoracic and/or transesophageal ECHO. Management Acute AR is a surgical emergency and all other management measures are only aime d at stabilizing the patient until urgent aortic valve replacement (AVR) can take place. Th e patient \200\231s clinical condition will determine the urgency of surgery (and risk of m ortality). General measures \200 \200 \200 \200 \200 Admit the patient to intensive care unit (ICU). Give oxygen and begin treating any pulmonar y edema with diuretics. Monitor blood gasses; mechanical ventilation may be necessary. Bloo d cultures Serial ECG: watch for developing atrioventricular (AV) block or conduction defec ts in endocarditis. x 3 are essential. ACUTE AORTIC REGURGITATION 17 Speci \201 c measures \200 \200 Every patient must be discussed with a cardiothoracic surgeon. In the context of good syste mic BP, vasodilators such as sodium nitroprusside or hydralazine may temporarily improve fo rward \202 ow and relieve pulmonary edema. Inotropic support may be necessary if the pati ent is hypotensive. However, inotropes are best avoided as any increase in systemic pressur es and peripheral vasoconstriction may worsen AR. All patients with hemodynamic compromise should have immediate or urgent AVR. Infective endocarditis Intra-aortic balloon pump (IABP ) must be avoided, as it will worsen AR. \200 : indications for surgery are given on p. 208. CHAPTER 1 Cardiovascular emergencies 18 Acute mitral regurgitation Presentation \200 Patients most commonly present with acute shortness of breath and severe pulmonary edema. S ymptoms may be less severe, or spontaneously improve as left atrial compliance increases. T here may be a history of previous murmur, angina, or myocardial infarction. The signs are d ifferent from those seen in chronic MR because of the presence of a nondilated and relative ly noncompliant LA. Acute MR results in a large LA systolic pressure wave (v wave) and henc e pulmonary edema. Patients may be acutely ill with tachycardia, hypotension, peripheral va soconstriction, and pulmonary edema, and a pan-systolic murmur of MR. Later in the illness, probably because of sustained high left atrial and pulmonary venous pressures, right heart failure develops. Examine for signs of any underlying conditions. When there is no obvious underlying cause (e.g., acute MI; see Box 1.1), assume the patient has infective endocardi tis until proven otherwise. \200 Diagnosis Diagnosis is based on a combination of clinical features and ECHO. Transthoracic echocardiography (TTE) can be used to readily diagnose and quantify MR. It also provides in formation on LV status (in particular regional wall motion abnormalities that can give rise to MR). TEE can provide speci \201 c information about etiology of valve dysfunc- tion, including papillary muscle rupture and MV lea \202 et (anterior and posterior) structural abnormalit ies. This information will be vital for a decision regarding de \201 nitive management. Th e important differential diagnosis is a VSD. TTE and Doppler studies can readily differentiate between the two con- ditions. Alternative ly, if ECHO is not available, pulmonary artery catheter- ization in acute MR will exclude t he presence of a left-to-right shunt and the pulmonary capillary wedge pressure (PCWP) trac e will demonstrate a large v-wave. General measures \200 \200 \200 \200 \200 Admit patient to ICU. Give oxygen and begin treating any pulmonary edema with diuretics. Mo nitor blood gasses; mechanical ventilation may be necessary. Blood cultures If present, MI should be treated in the standard manner. x 3 are essential. Speci \201 c measures Pulmonary edema may be very resistant to treatment. \200 In the presence of good BP, reduction in preload (nitroglycerin infusion) and afterload, es pecially with ACE inhibitors, is important. Systemic vasodilators such as hydralazine (12.5 \200\223100 mg tid) can also be added. ACUTE MITRAL REGURGITATION 19 \200 An IABP will help decrease LVEDP and increase coronary blood \202 ow. Patients may requir e inotropic support. There are multiple combinations and etiologies of MR and hemodynamic s tatus, and local policy and expertise should dictate choice of agent. CPAP and intubation a nd positive-pressure ventilation are extremely useful and must be considered in all severe and/or resistant cases. Hemodynamic disturbance and severe pulmonary edema in the context o f acute MR is a surgical emergency. Infective endocarditis: Post-infarct MR: following resu scitation. Patients who are stabilized may have mitral valve replacement (MVR) deferred bec ause of risks of surgery in the post-infarct patient. Preoperative management should consis t of diuretics and vasodilators, including ACE inhibitors, if tolerated. Opening the infarc t-related artery (angioplasty) may improve acute MR. \200 indications for surgery are given on p. 208. management depends on the patient \200\231s co ndition Box 1.1 Causes of acute mitral regurgitation \200 \200 \200 Infective endocarditis Papillary muscle dysfunction or rupture (post-MI). Rupture of chorda e tendinae (e.g., infection, myxomatous degeneration, systemic lupus erythematosus [SLE]) T rauma (to lea \202 ets, papillary muscle, or chordae) Prosthetic valve malfunction (e.g., secondary to infection) Left atrial myxoma Acute rheumatic fever Collagen vascular disorder s (e.g., Marfan \200\231s) Connective tissue diseases (large- and medium-vessel arteritis) \200 \200 \200 \200 \200 CHAPTER 1 Cardiovascular emergencies 20 Deep vein thrombosis: assessment Presentation \200 Deep vein thrombosis (DVT) is most commonly asymptomatic. Minor leg discomfort or isolated swelling (>65%) in the affected limb are the most common clinical features. Breathlessness or chest pain may be secondary to pulmonary embolism (PE). Signs include erythema and swell ing of the leg, dilated super \201 cial veins, and calf discomfort on dorsi \202 exion of the foot (Homan \200\231s sign). The thrombus may be palpable as a \201 brous cord in th e popliteal fossa. Con \201 rm the presence of swelling (>2 cm) by measuring the limb circ umference 15 cm above and 10 cm below the tibial tuberosity. In all cases of leg swelling, abdominal and rectal (and pelvic in women) examination must be carried out to exclude an ab dominal cause. See Table 1.2 for risk factors for DVT. Investigations \200 of leg veins is Real-time B-mode venous compression ultrasonography largely replacing venog raphy as the initial investigation of choice. It is quick and noninvasive, with sensitivity and speci \201 city of over 90%, and does not carry the risk of contrast allergy or phleb itis. It can simultaneously assess extent of proximal progression of the thrombus, in parti cular, extension into pelvic vessels. D-dimers probability of DVT and a negative D-dimer do es not require further investigation. A positive D-dimer result should be followed by ultra sonography. Venography Consider baseline-investigation blood work. If appropriate, look for an underlying cause. Procoagulant screen : refer to local screening policy and get hematol ogy advice (e.g., prothrombin time [INR] and partial thromboplastin time, C-reactive protei n [CRP], erythrocyte sedimentation rate (ESR), proteins C and S, antithrombin III levels, f actor VLeiden mutation, auto-Ab screen, immunoglobulins and immunoelectrophoretic strip, an ticardiolipin antibody, Ham test, etc.) Screen for malignancy : ultrasound computed tomo graphy (CT) (abdomen and pelvis), CXR, liver function tests (LFTs), prostate- speci \201 c antigen (PSA), carcinoembryonic antigen (CEA), CA-125, CA-19.9, B-HCG, etc. have a high negative predictive value for DVT. A low clinical \200 \200 \200 : use if results are uncertain and clinical suspicion is high. DEEP VEIN THROMBOSIS: ASSESSMENT 21 Table 1.2 Risk factors for DVT Procoagulant states Congenital Factor VLeiden Antithrombin III de \201 ciency Protein C de \201 ciency Protei n S de \201 ciency Acquired Malignant disease ( 5%) Antiphospholipid syndrome Myeloproliferative disorders Ora l contraceptive pill (especially with Factor VLeiden mutation) Nephrotic syndrome (via rena l AT III losses) Homocystinuria Paroxysmal nocturnal hemoglobinuria Venous stasis Immobility (e.g., long journeys) Pelvic mass Recent surgery Pregnancy or recent childbirth Severe obesity Miscellaneous Hyperviscosity syndromes Previous DVT or PE Family history of DVT/PE CHAPTER 1 Cardiovascular emergencies 22 Deep vein thrombosis: management If there is high clinical suspicion of DVT (the presence o f risk factors and absence of an alternative diagnosis), start empiric anticoagulation with low-molecular-weight heparin (LMWH). This may be stopped if subse- quent investigations ar e negative. Below-knee DVT Thrombi limited to the calf have a lower risk of embolization and may be tre ated with compression stockings and subcutaneous (SC) prophylactic doses of LMWH until the patient is mobile, to deter proximal propagation of thrombus. A brief period of systemic an ticoagulation with LMWH may lessen the pain from below-knee DVT. Above-knee DVT Thrombi within the thigh veins warrant full anticoagulation with LMWH/ unfra ctionated heparin (UFH) and subsequently with 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 allow outpatient treatment. There must be a period of overlap between LMWH/UFH therapy and anticoagulation with warfarin until the INR is within therapeutic ran ge and stable. LMWH are administered primarily as a once-daily subcutaneous (SC) injection, and dosage is determined by patient weight. It may require adjustment for renal dysfunctio n. Warfarin \200 Always anticoagulate with LMWH/UFH before starting warfarin. Protein C (a vitamin K \200 \223dependent anticoagulant) has a shorter half- life than that of the other coagulation fa ctors and levels fall sooner, resulting in a transient procoagulant tendency. If DVT is con \201 rmed, begin warfarin and maintain on LMWH/UFH until INR >2. Anticoagulate (INR 2 \200\2232.5) for 3 months. If there is recurrent DVT or the patient is at high risk of recu rrence, consider lifelong anticoagulation. \200 Thrombolysis This should be considered for recurrent, extensive, proximal venous thrombosis (e.g., femoral or iliac veins), as it is more effective than anti- coagulation alone in pr omoting clot dissolution and produces a better clinical outcome. Catheter-directed thrombolytic therapy (rt-PA or SK) is superior to systemic thrombolysis. One approach is streptokinase (SK) 250,000 U over 30 minutes then 100,000 U every hour for 24 \200\22372 hours. See p. 100 for contraindications to thrombolysis. DEEP VEIN THROMBOSIS: MANAGEMENT 23 Further management Women taking the combined oral contraceptive pill (OCP) should be advise d 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. CHAPTER 1 Cardiovascular emergencies 24 Pulmonary embolism (PE): assessment Symptoms \200 Classically presents with sudden-onset, pleuritic chest pain, associated with breathlessnes s and hemoptysis. Additional symptoms include postural dizziness or syncope. Massive PE may present as cardiac arrest (particularly with electromechanical dissociation) or shock. Pre sentation may be atypical, i.e., unexplained breathlessness or unexplained hypotension or s yncope only. Pulmonary emboli should be suspected in all breathless patients with risk fact ors for DVT or with clinically proven DVT. Recurrent PEs may present with chronic pulmonary hypertension and progressive right heart failure. Signs \200 Examination may reveal tachycardia and tachypnea only. Look for postural hypotension (in th e presence of raised jugular venous pressure [JVP]). Look for signs of raised right heart p ressures and cor pulmonale (raised JVP with prominent a-wave, tricuspid regurgitation, para sternal heave, right ventricular S3, loud pulmonary closure sound with wide splitting of S2 , pulmonary regurgitation). Cyanosis suggests a large PE. Examine for a pleural rub (may be transient) or effusion. Examine lower limbs for obvious thrombophlebitis. Mild fever (>37. 5 C) may be present. There may be signs of coexisting COPD. \200 \200 \200 Causes Most frequently PE is secondary to DVT (leg >> arm). Other causes \200 \200 \200 \200 \200 \200 \200 \200 Rarely secondary to right ventricular thrombus (post-MI) Septic emboli (e.g., tricuspid end ocarditis) Fat embolism (post-fracture) Air embolism (venous lines, diving) Amniotic \202 uid Parasites Neoplastic cells Foreign materials (e.g., venous catheters) Prognostic features The prognosis in patients with pulmonary emboli varies greatly and is a ssociated in part with any underlying condition. Generally worse prog- nosis is associated with larger PE; poor prognostic indicators include the following: \200 \200 \200 Hypotension Hypoxia ECG changes (other than nonspeci \201 c T-wave changes) PULMONARY EMBOLISM: INVESTIGATIONS 25 Pulmonary embolism: investigations General investigations \200 ABG Normal ABG does not exclude a PE. dPaO2 is invariable with larger PEs. Other changes includ e mild respiratory alkalosis and dPaCO2 (due to tachypnea) and metabolic acidosis (secondar y to shock). Commonly shows sinus tachycardia nonspeci \201 c ST- and T-wave changes in the anterior chest leads. The classical changes of acute cor pulmonale such as S1Q3T3, rig ht axis deviation, or right bundle branch block (RBBB) are only seen with massive PE. Less common \201 ndings include AF. May be normal; a near-normal chest \201 lm in the contex t of severe respiratory compromise is highly suggestive of a PE. Less commonly may show foc al pulmonary oligemia (Westermark \200\231s sign), a raised hemidiaphragm, small pleural ef fusion, wedge-shaped pleural shadow, subsegmental atelectasis, or dilated proximal pulmonar y arteries. There is no speci \201 c test. Mildly elevated CK, troponin, BNP may be seen. Insensitive for diagnosis but can exclude other causes of hypotension and raised right-side d pressures (e.g., tamponade, RV infarction). In PE may show RV dila- tation and global hyp okinesia (with sparing of apex [McConnell \200\231s sign]) and pulmonary artery dilation, a nd Doppler may show tricuspid/pulmonary regurgitation, allowing estimation of RV systolic p ressure. Rarely, the thrombus in the pulmonary artery may be visible. ECG CXR Blood tests ECHO Speci \201 c investigations D-dimer \200 \200 \200 A highly sensitive but nonspeci \201 c test. Useful in ruling out PE in patients with low probability. Results can be affected by advancing age, pregnancy, trauma, surgery, malignan cy, and in \202 ammatory states. Ventilation/perfusion (V/Q) lung scanning A perfusion lung scan (with IV technetium-99-labe led albumin) can be con- sidered in suspected cases of PE, especially if there is a contrai ndication to giving contrast. A ventilation scan (inhaled xenon-133) in conjunction increas es the speci \201 city by assessing whether the defects in the ventila- tion and perfusion scans \200\234match \200\235 or \200\234mismatch. \200\235 Pre-existing lung disease mak es interpretation dif \201 cult. A normal perfusion scan rules out signi \201 cant-sized PE. Abnormal scans are reported as 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 another cause for the patient \200\231s symptoms. CHAPTER 1 Cardiovascular emergencies 26 Box 1.2 Investigations for an underlying cause for PE \200 \200 Ultrasound of deep veins of legs Ultrasound of abdomen and pelvis (? occult malignancy, pel vic mass, lymphadenopathy) CT of abdomen/pelvis Screen for inherited procoagulant tendency ( thrombin III, factor VLeiden, etc.) Autoimmune screen (anticardiolipin antibody, antinucl ear antibody [ANA]) Biopsy of suspicious lymph nodes or masses \200 e.g., proteins C, S, anti If clinical suspicion of PE is high and the scan is of low or medium prob- ability, alternative investigations are required. CT pulmonary angiography (CTPA) This is the recommended initial lung imaging modality in pa tients with PE as long as there are no contraindications. \200 It allows direct visualization of emboli as well as other potential parenchymal disease, wh ich may provide alternative explanation for symptoms. Sensitivity and speci \201 city are high (>90%) for lobar pulmonary arteries but not so high for segmental and subsegmental pul monary arteries. A patient with a positive CTPA does not require further investigation. A p atient with a negative CTPA in the context of a high or intermediate probability of a PE sh ould undergo further investigation. \200 Evaluation of leg veins with ultrasound This is not very reliable. Almost half of patients with PE do not have evi- dence of a DVT and thus a negative result cannot rule out a PE. Ultrasound is a useful second-line investigation as an adjunct to a CTPA/ VQ scan. Outcome studies have demonstrated that it would be safe not to anti- coagulate patients wit h a negative CTPA and lower limb ultrasound who have an intermediate or low probability of a PE. Pulmonary angiography This is the gold-standard investigation. It is indicated in patients in whom diagnosis of embolism cannot be established by noninvasive means. Look for sharp cu toff of vessels or obvious \201 lling defects. It is an invasive inves- tigation and can be associated with 0.5% mortality. If there is an obvious \201 lling defect, the catheter or a guide wire passed through the catheter may be used to disrupt the thrombus. After angiography, the catheter may be used to give thrombolytics directly into the affected pulmonary artery (see below). The contrast can cause systemic vasodilatation and hemodynamic collapse in hypotensive patients. MR pulmonary angiography Results are comparable to those of pulmonary angiography in prelim inary studies. It can simultaneously assess ventricular function. PULMONARY EMBOLISM: MANAGEMENT 27 Pulmonary embolism: management 1. Stabilize the patient \200 Unless an alternative diagnosis is made, the patient should be treated as for a pulmonary e mbolus 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 resuscitat ion facilities are available. Obtain venous access and start IV \202 uids (crystalloid or colloid). Give maximal inspired oxygen via facemask to correct hypoxia. Mechanical ventila tion may be necessary if the patient is tiring (beware of cardiovascular collapse when seda tion is given for ET intubation). Give LMWH or UFH to all patients with high or intermediat e risk of PE until diagnosis is con \201 rmed. Meta-analysis of multiple trials has shown LMWH to be superior to UFH with a reduction in mortality and bleeding complications. For do ses, consult local formulary. If there is evidence of hemodynamic instability (systemic hyp otension, features of right heart failure) or cardiac arrest, patients will bene \201 t fr om thrombolysis with recombinant tissue plasminogen activator (rtPA) or streptokinase (see Table 1.3; same doses used for treatment of STEMI [see p. 100]). Local delivery of thrombol ytics to the site of thrombus via a PA catheter may also be considered. \200 2. Analgesia \200 \200 Patients may respond to oral nonsteroidal anti-in \202 ammatory drugs. Opiate analgesia sh ould be used with caution. The vasodilatation caused by these drugs may precipitate or wors en hypotension. Give small doses (1 \200\2232 mg morphine IV) slowly. Hypotension should re spond to IV colloid. Avoid IM injections (anticoagulation and possible thrombolysis). 3. Anticoagulation Patients with a positive diagnosis must undergo anticoagulation with war - farin. There should be a period of overlap with LMWH/UFH until INR values are therapeutic . Target INR is 2 \200\2233 for most cases. Standard duration of anticoagulation is as foll ows: 3 months for temporary risk factor 3 months for \201 rst idiopathic cases At least 6 months for other cases With recurrent events and underlying predisposition to thromboembol ic events (e.g., antiphospholipid antibody syndrome) lifelong anticoagulation may be needed (as well as higher target INR >3). \200 \200 \200 Table 1.3 Dosage of thrombolytic agents for pulmonary embolus rtPA 100 mg over 2 hours or 0.6 mg/kg over 15 minutes (maximum of 50 mg) followed by heparin Streptokinase 250,000 U over 30 minutes followed by 100,000 U/hr infusion for 24 hours Contraindications for thrombolysis are identical to those for STEMI (p. 100). CHAPTER 1 Cardiovascular emergencies 28 Cardiac arrest (also see p. 5) Massive PE may present as cardiac arrest with electromechani cal dissoci- ation (EMD). Exclude the other causes of EMD. 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 wors ened by \202 uid overload. \200 Insert an internal jugular sheath prior to anticoagulation. This can be used for access lat er if necessary. Give thrombolysis if there are no contraindications. If hypotensive give I V \202 uids. If hypotension persists, invasive monitoring and/or inotropic support is req uired. The JVP is a poor indicator of the left-sided \201 lling pressures in such cases. Adrenaline is the inotrope of choice. Femorofemoral cardiopulmonary bypass may be used to s upport the circulation until thrombolysis or surgical embolectomy can be performed. Pulmona ry angiography in a hypotensive patient is hazardous as the contrast may cause systemic vas odilatation and cardiovascular collapse. \200 \200 Pulmonary embolectomy In patients who have contraindications to thrombolysis and are in sho ck requiring inotropic support, there may be a role for embolectomy if appropriate skills a re on site. This can be performed percutaneously in the catheterization labora- tory using a number of devices or surgically on cardiopulmonary bypass Percutaneous procedures may be combined wit h peripheral or central thrombolysis. Seek specialist advice early. Best results are obtained before onset of cardiogenic shock. Radiological con \201 rmation of the extent and site of embolism is prefer- able before thoracotomy. Mortality is 25% \200\22330%. Inferior vena cava (IVC) \201 lter There is little evidence that use of an IVC \201 lte r improves short- or long- term mortality rates. Filters are positioned percutaneously and, if possible, patients must remain anticoagulated to prevent further thrombus formation. Most IVC \201 lters are positioned infrarenally ( bird \200\231s nest \201 lter) but can also be supra- renal (Green \201 eld \201 lter) . Indications for IVC \201 lter use include the following: Anticoagulation contraindicated \200\224e.g., active bleeding, heparin-induced thrombocytopenia, planned intensive chemothe rapy. Anticoagulation failure despite adequate therapy. Prophylaxis in high-risk patients \200\224e.g., progressive venous thrombosis, severe pulmonary hypertension, extensive traum a. \200 FAT EMBOLISM 29 Fat embolism This is commonly seen in patients with major trauma. There is embol- ization o f fat and microaggregates of platelets, red blood cells (RBCs), and \201 brin in systemic and pulmonary circulation. Pulmonary damage may result directly from the emboli (infarctio n) or from chemical pneumonitis and ARDS. Clinical features There may be a history of fractures followed (24 \200\22348 hours later) by breathlessness, cough, hemoptysis, confusion, and rash. Examination reveals fever (38 \200\22339 C), widespread petechial rash (25% \200\22350%), cyanosis, and tachypnea. There may be scattered rales in the chest, although examination ma y be normal. Changes in mental state may be the \201 rst sign with confusion, drowsiness, seizures, and coma. Examine the eyes for conjunctival and retinal hemorrhages; occasionall y fat globules may be seen in the retinal vessels. Severe fat embolism may present as shock. Investigations \200 ABG Hypoxia and a respiratory alkalosis (with low PaCO2) as for thromboembolic PE Thrombocytope nia, acute intravascular hemolysis Disseminated intravascular coagulation Renal failure, hy poglycemia \200 \200 CBC Coagulation Chemistries and glucose 2+ Ca Urine ECG \200 \200 May be low Microscopy for fat and dipstick for hemoglobin. Usually nonspeci \201 c (sinus tachycardia; occasionally signs of right heart strain) Usually lags behind the clinical cou rse. There may be patchy, bilateral, air space opaci \201 cation. Effusions are rare Consi der if there is a possibility of head injury with expanding subdural or epidural bleed CXR CT head Differential diagnosis This includes pulmonary thromboembolism, other causes of ARDS, septi c shock, hypovolemia, cardiac or pulmonary contusion, head injury, aspir- ation pneumonia, and transfusion reaction. Management \200 Treat respiratory failure. Give oxygen (maximal via face mask; CPAP and mechanical ventilat ion if necessary). Ensure adequate circulating volume and cardiac output. Central venous pr essure (CVP) is not a good guide to left-sided \201 lling pressures, and a PA catheter (S wan \200\223Ganz) may be used to guide \202 uid replacement. Try to keep PCWP 15 \200\223 18 mmHg and give diuretics if necessary. Use inotropes to support circulation as required. CHAPTER 1 Cardiovascular emergencies 30 Aspirin, heparin, and Dextran 40 (500 mL over 4 \200\2236 hours) are of some bene \201 t i n the acute stages but may exacerbate bleeding from sites of trauma. High-dose steroids (me thylprednisolone 30 mg/kg q8h for 3 doses) have been shown to improve hypoxemia,1 but stero ids are probably most effective if given prophylactically. 1 Lindeque BG, Schoeman HS, Dommisse GF, Boeyens MC, Vlok AL (1987). Fat embolism and the f at embolism syndrome. A double-blind therapeutic study. J Bone Joint Surg, 69:128 \200\2231 31. HYPERTENSIVE EMERGENCIES 31 Hypertensive emergencies Hypertensive crisis Hypertensive crisis is de \201 ned as a sever e elevation in BP (SBP >200 mmHg, DBP >120 mmHg). Rate of change in BP is important. A rapi d rise is poorly tolerated and leads to end-organ damage, whereas a gradual rise in a patie nt with existent poor BP control is better tolerated. Hypertensive crises are classi \201 ed as follows: 1. Hypertensive emergency, where a high BP is complicated by acute target organ dysfunction (see Box 1.3) and includes Hypertensive emergency with retinopathy in BP (classically DBP >140 mmHg) with retinal hemorrhages and exudates (previously called accelerated hypertension), and Hypertensive emergency with papilledema papilledema (previo usly called malignant hypertension). \200\224there is marked elevation with a similarly high BP and 2. Hypertensive urgency, where there is a similar rise in BP but without target organ damage. Conditions presenting as hypertensive emergency \200 \200 Essential hypertension. Renovascular hypertension renal artery occlusion. Renal parenchymal disease: acute glomerulonephritis, vasculitis, scleroderma. Endocrine disorders: pheochrom ocytoma, Cushing \200\231s syndrome, primary hyperaldosteronism, thyrotoxicosis, heperparat hyroidism, acromegaly, adrenal carcinoma. Eclampsia and pre-eclampsia. Vasculitis. Drugs: p resence of cocaine, amphetamines, MAOI interactions, or cyclosporine, or withdrawal of B-bl ocker or clonidine. Autonomic hyperactivity in the presence of spinal cord injury. Coarctat ion of the aorta. : atheroma, \201 bromuscular dysplasia, acute \200 \200 \200 Presentation Occasionally there are minimal nonspeci \201 c symptoms such as mild head- ac he and nosebleed. A small group of patients present with symptoms resulting from BP-induced microvascular damage: \200 Neurological symptoms: severe headache, nausea, vomiting, visual loss, focal neurological d e \201 cits, seizures, confusion, intracerebral hemorrhage, coma (see below) Chest pain (h ypertensive heart disease, MI, or aortic dissection) and congestive cardiac failure Symptom s of renal failure: renal impairment may be chronic (secondary to long-standing hypertensio n) or acute (from the necrotizing vasculitis of malignant hypertension) CHAPTER 1 Cardiovascular emergencies 32 Patients may present with hypertension as one manifestation of an under- lying \200\234dis ease \200\235 (renovascular hypertension, chronic renal failure, CREST syndrome, pheochromo cytoma, pregnancy). Examination should be directed at looking for evidence of end-organ damage even if the pati ent is asymptomatic (heart or renal failure, retinop- athy, papilledema, focal neurological symptoms). Box 1.3 Hypertensive emergencies \200 \200 \200 \200 Hypertensive emergency with retinopathy/papilledema Hypertensive encephalopathy Hypertensio n-induced intracranial hemorrhage/stroke Hypertension with cardiovascular complications: \200 Aortic dissection \200 MI \200 Pulmonary edema Pheochromocytoma Pregnancy-associa ted hypertensive complications \200 Acute renal insuf \201 ciency Hypertensive emergency secondary to acute withdrawal syndromes (e.g., B-blockers, centrally acting antihypertensi ves) \200 Eclampsia and pre-eclampsia \200 HYPERTENSIVE EMERGENCIES: MANAGEMENT 33 Hypertensive emergencies: management Priorities in management are as follows: 1. Con \201 rm the diagnosis and assess the severity. 2. Identify those patients needing speci \201 c emergency treatment. 3. Plan long-term treatment. 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.