Section IV: Cardiac Diseases

HPI: Dyspnea, fatigue, syncope.

PMH: AL (primary) amyloidosis.

FH: Familial amyloidosis.

AC = Amyloid Cardiomyopathy.

SYMP = SYMPtoms of dyspnea, fatigue, and/or syncope.

ECHO = ECHOcardiogram findings of granular sparkling myocardium, thickened left and right ventricular, mitral and aortic valve leaflet thickening.

NCARD-BX = Non-CARDiac tissue and/or (abdominal fat pad, rectum, or kidney) Biopsy positive for amyloid deposits.

IN-NCARD-BX = INconclusive Non-CARDiac tissue Biopsy.

CARD-BX = EndomyoCARDial Biopsy positive for amyloid deposits.

SYMP + ECHO + NCARD-BX = AC

SYMP + ECHO + IN-NCARD-BX + CARD-BX = AC

• – Endomyocardial biopsy is virtually 100% sensitive in amyloid cardiomyopathy as amyloid will be deposited all throughout the heart.

• – In patients with known amyloid deposits in other organs and a history of hypertension, there may be uncertainty as to whether ventricular thickening represents amyloid infiltration or hypertensive heart disease. In such cases, a biopsy may be helpful to determine whether patient has AC.

1. Falk RH. Diagnosis and Management of the Cardiac Amyloidosis. Circulation. 2005;112:2047–2060.

HPI: Chest pain/discomfort precipitated by exercise or at rest lasting average of 10 minutes.

PMH: Hypertension, hyperlipidemia, diabetes.

SH: Alcohol, smoking.

Coronary angiogram: Normal.

Cardiac MRI: Subendocardial perfusion defects.

RF-RED = Risk Factor REDuction: smoking, hypertension, hyperlipidemia, cholesterol, obesity, physical inactivity.

ATEN = ATENolol 100 mg/day for 4 weeks.

AMLO = AMLOdipine 10 mg/day.

NITR = isosorbide monoNITRate 10 mg BID.

CSX = Cardiac Syndrome X.

• – 10–20% of patients with typical angina chest pain have normal coronary angiograms.

1. Fraker TD, et al. 2007 Chronic Angina Focused Update of the ACC/AHA 2002 Guidelines for the Management of Patients with Chronic Stable Angina. J Am Coll Cardiol. 2007;50:2264.

2. Panting JR, et al. Cardiac Syndrome X. N Engl J Med. 2002;346: 1948–1953.

HPI: Sudden onset of sharp chest pain exacerbated by inspiration and relieved by leaning forward.

PMH: Rheumatic heart disease, myocardial infarction, lung cancer, systemic lupus erythematosus.

PSH: Coronary artery bypass graft.

Widespread ST elevation and/or PR depression. Cardiac tamponade (sinus tachycardia, low voltage, or electrical alternans [beat to beat QRS variability]).

Figure 37–1

APC = Patient with Acute PeriCarditis.

CTAMP = Patient with Cardiac TAMPonade.

CT-AD = Connective Tissue or Autoimmune Disease.

RCT = Patient with Recurrent Pericarditis unresponsive to medical therapy.

PEF20 = Pericardial EFfusion > 20 mm present on echocardiogram.

PTN = Suspected Purulent, Tuberculous, or Neoplastic pericarditis.

I-C = Ibuprofen 300 mg Q6 hours and Colchicine 0.5 mg BID.

INEFF I-C = INEFFective response to I-C.

GLC = GLucoCorticoids: Prednisone 1 mg/kg/day. Give a short course with a taper as inflammation improves.

PCDS = Refer patient for PeriCarDiocenteSis.

PCT = Refer patient for PeriCarDiecTomy.

APC = I-C

APC + INEFF I-C = GLC

APC + CT-AD = GLC

APC + CTAMP = PCDS

APC + PEF20 = PCDS

APC + PTN = PCDS

APC + RCT = PCT

• – Aortic dissection is a major contraindication to pericardiocentesis.

• – Relative contraindications to pericardiocentesis include uncorrected coagulopathy, anticoagulant therapy, thrombocytopenia (<50,000/mm³], small, posterior, and loculated effusions.

• – Post-pericardiectomy recurrences of pericarditis may occur due to incomplete resection of the pericardium.

• – In pericarditis associated with an acute myocardial infarction, aspirin 650 mg Q6 hours is preferred over ibuprofen.

• – Fever, history of oral anticoagulant therapy, pericarditis associated with trauma, myopericarditis, and a large effusion (>20 mm) are associated with a poor prognosis.

1. Hoit BD. Management of Effusive and Constrictive Pericardial Heart Disease. Circulation. 2002;105;2939–2942.

2. Lange RA. Acute Pericarditis. N Engl J Med. 2004;351:2195–2202.

HPI: Chest pain; tachypnea, dyspnea.

PMH: Malignancy (especially metastatic to thorax), autoimmune disorder, thyroid disorder, uremia, pericarditis, chest trauma, recent thoracotomy, tuberculosis.

Chest x-ray: Enlarged cardiac silhouette, especially if much larger than prior xrays.

Echocardiogram: Best way to rapidly confirm diagnosis as pericardial fluid can be directly visualized and can assess for evidence of tamponade physiology. Also very helpful for treatment planning and during pericardial drainage.

CT chest: Pericardial effusions often appear exaggerated on routine non-gated CT scans due to cardiac motion during acquisition.

CTP = Patient with diagnosis of Cardiac TamPonade on echocardiogram.

REC = Patient with RECurrent pericardial effusion after being drained before.

PCDS = Refer patient for PeriCarDiocenteSis

PW = Refer patient for Pericardial Window or pericardial stripping.

MED-TX = Medical management. While waiting for pericardial drainage it is imperative not to diurese the patient, which will drop preload and can precipitate cardiovascular collapse. Start IV fluids and run continuously until pericardial pressure can be relieved. When pericardial fluid is obtained send diagnostic studies to identify etiology such as culture, cytology, and adenosine deaminase. If pericardial window or stripping is performed a pericardial biopsy can be obtained. A pericardial drain is usually left in place to drain residual fluid and will need to be removed soon to prevent infectious pericarditis.

CTP = PCDS + MED-TX

REC + CTP = PCDS + PW + MED-TX

1. Seferovic MB, et al. Guidelines on the diagnosis and management of pericardial diseases executive summary; The task force on the diagnosis and management of pericardial diseases of the European Society of Cardiology. Eur Heart J. 2004;25:387.

2. Spodick DH. Acute Cardiac Tampondae. N Engl J Med. 2003;349: 684–690.

HPI: Classically sharp, tearing chest pain radiating to the back. Can cause symptoms/signs associated with any of the following due to extension of the dissection: aortic regurgitation, cardiac tamponade, myocardial infarction, stroke, hemorrhagic shock.

PMH: peripheral vascular disease, collagen vascular disease, vasculitis, syphilis, bicuspid aortic valve.

PSH: Aortic valve replacement. Recent CABG or cardiac catheterization.

FH: Marfan's syndrome, Ehlers-Danlos syndrome.

SH: Smoking, cocaine.

Transesophageal echocardiogram (TEE): Can visualize thoracic aorta, aortic root, and aortic valve. Advantage: no radiation and no nephrotoxic contrast required. Can be done at bedside in ICU/CCU if very difficult to transport patient. Disadvantage: cannot visualize abdominal aorta.

CT scan: Can visualize entire aorta. Advantage: Rapid test, available in most emergency departments. Can see entire dissection and what branches are involved. Disadvantage: Radiation and nephrotoxic contrast used.

MRI: Similar to CT in capability but more expensive and takes much longer to acquire images.

SAD = Patient with Suspected Aortic Dissection based on clinical presentation.

HU = Hemodynamically Unstable: hypotension (systolic BP < 90 mm Hg) or evidence of shock (mental status changes or decreased urine output).

HS = Hemodynamically Stable: normotensive, normal mentation, no evidence of shock.

STAB = STABilize: As quickly as possible, determine if hypotension is due to cardiac tamponade, hemorrhagic shock, or acute myocardial infarction and treat.

IMAGE = Obtain diagnostic imaging as soon as possible to confirm diagnosis of AD and type. Can use TEE, CT, or MRI depending on institution strengths and availability.

MED-TX = Medical management. Goal is to reduced heart rate and blood pressure to reduce shear force that can extend dissection. Admit to intensive care. Pain control with morphine. Keep HR < 60 with IV beta blockade (labetalol 20 mg IV q10 min up to 300 mg max), verapamil second line. Keep SBP 100–120 mm Hg (IV betablockade first line, can add nitroprusside 0.5 mcg/kg/min and titrate up to 3 mcg/kg/min).

AD = Aortic Dissection confirmed by imaging.

CVS = Consult Cardio/Vascular Surgery. Type-A dissections (involves ascending aorta) are a surgical emergency and CVS should be called emergently. Type-B dissections (does not involve ascending aorta) are usually manage medically but may need operation if there is ongoing hemorrhage. Call CVS emergently if patient unstable.

SAD + HU = STAB + IMAGE

SAD + HS = IMAGE + MED-TX

AD + HU = CTS + STAB

AD + HS = CTS + MED-TX

• – Stabilize patients first. Then confirm diagnosis with imaging. Medical management can be started in stable patients while awaiting imaging.

1. Erbel R, et al. Diagnosis and Management of Aortic Dissection: Recommendations of the European Society of Cardiology. Eur Heart J. 2001;22:1642–1681.

2. Nienhaber CA, et al. Aortic Dissection: New Frontiers in Diagnosis and Management. Circulation. 2003;108:628–635.

HPI: Classically sharp, tearing chest pain radiating to the back. Can cause symptoms/signs associated with any of the following due to extension of the dissection: aortic regurgitation, cardiac tamponade, myocardial infarction, stroke, hemorrhagic shock.

PMH: peripheral vascular disease, collagen vascular disease, vasculitis, syphilis, bicuspid aortic valve.

PSH: Aortic valve replacement. Recent CABG or cardiac catheterization.

FH: Marfan's syndrome, Ehlers-Danlos syndrome.

SH: Smoking, cocaine.

X-ray: Mediastinal widening, pleural effusion.

ECHO: Intimal flap, true and false lumen, thrombosis of false lumen, ascending aortic diameter > 5 cm, aortic regurgitation, pericardial effusion.

SA-AD = Stanford type A ascending Aortic Dissection [dissection involving ascending aorta]. This is a surgical emergency and patients are at serious risk as extension of the dissection can compromise the carotid arteries, the coronary arteries, the aortic valve, and the pericardial space.

SB-AD = Stanford type B Aortic Dissection [dissection not involving the descending aorta]. These are usually managed medically unless there is a severe aneurysm with impending rupture or ongoing hemorrhage.

HU = Hemodynamically Unstable: hypotension (systolic BP < 90 mm Hg) or evidence of shock (mental status changes or decreased urine output).

HS = Hemodynamically Stable: normotensive, normal mentation, no evidence of shock.

STAB = STABilize: As quickly as possible, determine if hypotension is due to cardiac tamponade, hemorrhagic shock, or acute myocardial infarction and treat.

MED-TX = Medical management. Goal is to reduced heart rate and blood pressure to reduce shear force that can extend dissection. Admit to intensive care. Pain control with morphine. Keep HR < 60 with IV beta blockade (labetalol 20 mg IV q10 min up to 300 mg max), verapamil second line. Keep SBP 100–120 mm Hg (IV betablockade first line, can add nitroprusside 0.5 mcg/kg/min and titrate up to 3 mcg/kg/min).

CVS = Consult Cardio/Vascular Surgery. Type-A dissections (involves ascending aorta) are a surgical emergency and CVS should be called emergently. Type-B dissections (does not involve ascending aorta) are usually manage medically but may need operation if there is ongoing hemorrhage. Call CVS emergently if patient unstable. If there is a type B dissection and the patient is stable with no evidence of active complication, the patient will still need serial imaging in outpatient follow up to monitor for progression.

SA-AD + HU = STAB + CVS

SA-AD + HS = CVS + MED-TX

SB-AD + HU = STAB + CVS

SB-AD + HS = MED-TX + CVS

• – Do not use medicines that will decrease afterload but not cardiac contractility as this will increase the shear force and can worsen the dissection (ex. hydralazine).

• – Type-A dissections (involves ascending aorta) are a surgical emergency and CVS should be called emergently.

1. Erbel R, et al. Diagnosis and Management of Aortic Dissection. Eur Heart J. 2001;22:1642–1648.

HPI: LVT detected on echocardiogram.

PMH: Myocardial infarction, coronary artery disease, AFIB, dilated cardiomyopathy, ischemic stroke.

PSH: Alcohol, smoking.

ECHO: Direct visualization of intracardiac thrombus (sensitivity improved with echocontrast), regional or global wall motion abnormalities, left ventricular aneurysm.

Cardiac MRI: Very sensitive and specific for chronic LV thrombus.

LVT = Left Ventricular Thrombus detected (ex. on echocardiogram.)

LV-SC = Left Ventricular Structural Change: severe hypokinesis/akinesis/dyskinesis of the left ventricle (especially near apex). Left ventricular aneurysm formation.

AC = AntiCoagulation: Must ensure there is no significant contraindication to anticoagulation before initiating. Can use warfarin initiated at 5 mg/day and titrated to target INR of 2.0–3.0. Anticoagulate patients for a minimum of 3 months. If there is no increased risk of bleeding, continue anticoagulation for life.

FOLLOW = Follow up: obtain a repeat echocardiogram in 3–6 months to assess for resolution or evolution of the thrombus.

LVT = AC + FOLLOW

LVT + LV-SC = AC + FOLLOW

• – Anticoagulation appears to reduce the incidence of embolization even if thrombus remains on repeat echocardiogram.

1. Antman EM, et al. 2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients with ST-Elevation Myocardial Infarction. J Am Coll Cardiol. 2008;51;210–247.

HPI: Dyspnea, cough, fatigue, chest discomfort, orthopnea, hemoptysis, abdominal pain, arrhythmias, thromboembolism, asymptomatic LV dysfunction.

FH: PPCM.

PPCM = PeriPartum CardioMyopathy.

CF = Development of Cardiac Failure in the last month of pregnancy or within 5 months of delivery.

ABS-IC = ABSence of an Identifiable Cause for the cardiac failure, and high suspicion of nonischemic cardiomyopathy.

ABS-RHD = ABSence of Recognizable Heart Disease prior to the last month of pregnancy.

LVSD = Left Ventricular Systolic Dysfunction (LVEF <45%).

Once a patient is diagnosed with PPCM, treatment should be begun to alleviate symptoms of heart failure.

Treatment:

Safe drugs = Digoxin, nitrates, hydralazine, heparin, diuretics, beta-blockers. Taken till LV EF normalizes.

Unsafe drugs = ACEI, nitroprusside, coumadin, amiodarone.

• – Risk factors for PPCM are multiparity, advanced maternal age, multifetal pregnancy, preeclampsia, and gestational hypertension.

• – Subsequent pregnancy can lead to persistent depression of LVEF, CHF, and even death.

1. Pearson GD, et al. Peripartum Cardiomyopathy. JAMA. 2000;283(9): 1183–1188.

HPI: Discomfort and pain in calf, recent immobilization for prolonged period of time.

PMH: Obesity, antithrombin deficiency, protein C or S deficiency, Factor V Leiden mutation.

PSH: Recent hospitalization for surgery.

DVT = Deep Vein Thrombosis.

NO-DVT = NO Deep Vein Thrombosis.

CLIN = CLINical findings: patient complaining of discomfort and pain in calf, or physical exam findings of pain, tenderness, and swelling in leg.

COMP-US = COMPression UltraSonography with findings of: abnormal compressibility of vein; abnormal Doppler color flow; presence of echogenic band.

INCON = INCONclusive.

VENO-POS = VENOgraphy POSitive for DVT.

VENO-NEG = VENOgraphy NEGative for DVT.

CLIN + COMP-US = DVT

CLIN + INCON[COMP-US] + VENO-POS = DVT

CLIN + INCON[COMP-US] + VENO-NEG = NO-DVT

1. Jaff MR, et al. Management of Massive and Submassive Pulmonary Embolism, Iliofemoral Deep Venous Thrombosis, and Chronic Thromboembolic Pulmonary Hypertension. Circulation. 2011;123:1788–1830.

2. Hirsch J, et al. Management of Deep Vein Thrombosis and Pulmonary Embolism. Circulation. 1996;93:2212–2245.

3. Bates SM, et al. Treatment of Deep-Vein Thrombosis. N Engl J Med. 2004;351:268–277.

HPI: Discomfort and pain in calf.

PMH: Obesity, antithrombin deficiency, protein C or S deficiency, Factor V Leiden mutation.

PSH: Recent hospitalization for surgery.

DVT = Deep Venous Thrombosis.

APDVT/APE = Acute Proximal DVT or Acute Pulmonary Embolism.

HIT = Heparin Induced Thrombocytopenia (suspected or proven).

ENOX = ENOXaparin 1 mg/kg every 12 hours subcutaneously, maximum of 180 mg/day. APTT goal of 1.5 times upper limit of normal (45 seconds). Continue for minimum of 5 days, and/or discontinue when INR is >=2.0 for at least 24 hours (target INR is 2.0–3.0).

UNFH = UNFractionated Heparin 80 U/kg bolus followed by a continuous infusion, initially at 18 U/kg/hr (dose adjust to goal APTT 1.5–2.3 times control (46–70 seconds). Continue for minimum of 5 days, and/or discontinue when INR is >=2.0 for at least 24 hours (target INR is 2.0–3.0).

FOND = FONDaparinux subcutaneous injection once daily: 5 mg for patients 50 kg weight, 7.5 mg for 50–100, and 10 mg for >100 kg. Discontinue when INR is within therapeutic range of 2–3.

COUM = COUMadin initiated at 5 mg/day, and titrated for target INR of 2.0–3.0. Continue for 3 months (in patients with first-episode of DVT related to a major reversible risk factor), 6 months (patients with recurrent or unprovoked DVT).

DTI = Direct Thrombin Inhibitor (see chapter on DTI).

CI-AC = ContraIndication to AntiCoagulation (active bleeding; platelet count <20000/mm³; neurosurgery, ocular surgery or intracranial bleeding within past 10 days).

INEFF-AC = If AntiCoagulation with ENOX,UNFH or FOND and COUM is INEFFective.

IVCF = Refer patient for Inferior Vena Cava Filter placement.

DVT = ENOX + COUM or

• UNFH + COUM or

• FOND + COUM

DVT + HIT = DTI + COUM

APDVT/APE + CI-AC = IVCF

APDVT/APE + INEFF-AC = IVCF

1. Jaff MR, et al. Management of Massive and Submassive Pulmonary Embolism, Iliofemoral Deep Venous Thrombosis, and Chronic Thromboembolic Pulmonary Hypertension. Circulation. 2011;123:1788–1830.

2. Bates SM, et al. Treatment of Deep-Vein Thrombosis. N Engl J Med. 2004;351:268–277.

3. Kahn SR, et al. Therapy for Venous Thromboembolic Disease. Chest. 2008;133:454S–545S.

HPI: Dyspnea, chest pain, cough, hemoptysis, recent trauma/surgery, smoking, pregnancy, hormone contraceptive/therapy

Labs: PT/PTT, Troponin, BNP, creatinine, d-dimer

PMH: Obesity, hypercoaguable state, history of DVT or PE, malignancy

Resp: Hypoxia, tachypnea, hemoptysis.

CV: Tachycardia, hypotension.

Ext: Leg swelling.

ECG: RV strain, S1T3Q3, sinus tachycardia, Q in III, aVF, right axis deviation, RBBB.

Echocardiogram: Right ventricular dysfunction and akinesia.

V/Q scan: Perfusion defect.

CT angiogram: Filling defect, RV dilation.

PE = Pulmonary Embolism

NO-PE = Insufficient evidence to make the diagnosis of PE.

Modified Wells Criteria: Clinical symptoms of DVT (3 points), Other diagnoses less likely than PE (3 points), Heart rate >100 (1.5 points), Immobilization ≥3 days or surgery in previous four weeks (1.5 points), Previous DVT/PE (1.5 points), Hemoptysis (1 point), Malignancy (1 point)

W-UNLIKELY = Wells Score = < 4

W-LIKELY = Wells Score > 4. Must obtain further testing such as CT Angiogram to affirm or exclude PE.

DD-NEG = D-Dimer level < 500 ng/mL

DD-POS = D-Dimer level > 500 ng/mL

CTA-NEG = CT Angio NEGative for PE. Like any test, a CT angiogram is not 100% sensitive and specific. Rarely the test is non-diagnostic or the clinical suspicion is still too high to exclude PE, and a pulmonary angiogram can be done.

CTA-POS = CT Angiogram POSitive for PE.

W-UNLIKELY + DD-NEG = NO-PE (no further testing)

W-LIKELY + DD-NEG/POS + CTA-POS = PE

W-LIKELY + DD-NEG/POS + CTA-NEG = NO-PE

1. Torbicki A, et al. Guidelines on the Diagnosis and Management of Acute Pulmonary Embolism: The Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC). Eur Heart J. 2008;29:2276–2315.

2. Goldhaber SZ, Visani L, De Rosa M. Acute Pulmonary Embolism: Clinical Outcomes in the International Cooperative Pulmonary Embolism Registry (ICOPER). Lancet. 1999;353:1386–1389.

HPI: SOB, chest pain, cough, hemoptysis, age >50, recent trauma/surgery, smoking, pregnancy.

Labs: PT/PTT, troponin, BNP, creatinine, D-dimer.

PMH: Obesity, antithrombin deficiency, protein C/S deficiency, Factor V Leiden mutation, presence or history of DVT, malignancy, hormone contraceptive/therapy.

PSH: Recent hospitalization for surgery, prolonged immobilization.

Resp: Hypoxia, tachypnea, hemoptysis.

CV: Tachycardia, hypotension.

Ext: Leg swelling.

ECG: RV strain, S1T3Q3, sinus tachycardia, Q in III, aVF, right axis deviation, RBBB.

Echocardiogram: Right ventricular dysfunction, akinesia, RVSP >40 mm Hg.

V/Q scan: Perfusion defect.

CT angiogram: Filling defect, RV dilation.

PE = Patient diagnosed with acute Pulmonary Embolism.

HEP = Unfractionated IV HEParin (bolus of 80 U/kg followed by continuous infusion dosed at 18 U/kg/hr with dose adjustment).

ENOX = ENOXaparin 1 mg/kg every 12 hours subcutaneously, maximum of 180 mg/day. APTT goal of 1.5 times upper limit of normal (45 seconds). Discontinue when INR is therapeutic range of 2–3 if bridging with Coumadin.

COUM = COUMadin 5 mg/day with target INR of 2–3. Continue for 3–6 months for first PE, lifetime for second PE with INR 2.5–3.5.

THROM = THROMbolysis for massive PE with hemodynamic compromise or RV dysfunction (streptokinase 250,000-IU IV bolus followed by100,000-IU/hr infusion for 12–24 hours or alteplase 100 mg IV infusion over 2 hours).

UNSTABLE = Hypotension, shock, SBP <90 mm Hg, drop of 40 mm Hg, respiratory distress.

CI-THROM = ContraIndication to THROMbolysis.

INEFF-THROM = INEFFective THROMbolysis.

CI-AC = ContraIndication to AntiCoagulation (active bleeding; platelet count <20,000/mm³; neurosurgery, ocular surgery, or intracranial bleeding within past 10 days).

INEFF-AC = If AntiCoagulation with ENOX and COUM is INEFFective or recurrent PE.

IVCF = Refer patient for Inferior Vena Cava Filter placement.

SURG = Refer patient for SURGical embolectomy/endarterectomy.

PE = ENOX/HEP + COUM

PE + CI-AC = IVCF

PE + INEFF-AC = IVCF

PE + UNSTABLE = THROM

PE + UNSTABLE + CI-THROM = SURG

In patients with PE, prompt diagnosis and treatment are essential to prevent cardiorespiratory failure and sudden cardiac death.

An abnormal D-dimer level at the end of therapy may signal the need of continue treatment in patients with first PE. If untreated, mortality is as high as 26%.

If the patient has contraindication to LMWH (kidney failure) then admission to hospital is needed for bridging with IV unfractionated heparin.

• – Low-molecular-weight heparin may reduce bleeding compared to unfractionated heparin in patients with PE. It also has a lower risk of heparin-induced thrombocytopenia as well as a greater bioavailability when given by subcutaneous injection.

• – Avoid Coumadin in pregnant patients.

1. Bates SM, et al. Treatment of Deep-Vein Thrombosis. N Engl J Med 2004;351:268–277.

2. Kahn SR, et al. Therapy for Venous Thromboembolic Disease. Chest. 2008;133:454S–545S. Goldhaber SZ. Pulmonary embolism. Lancet. 2004;363(9417):1295.

3. Barritt DW, Jordan SC. Anticoagulant Drugs in the Treatment of Pulmonary Embolism: A Controlled Trial. Lancet. 1960;1(7138): 1309–1312.

4. Torbicki A, et al. Guidelines on the Diagnosis and Management of Acute Pulmonary Embolism: The Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC). Eur Heart J. 2008;29:2276–2315.

HPI: Palpitations, headache, sweating, generalized weakness.

PMH: Von Hippel–Lindau syndrome (hemangioblastoma of brain and spine, retinal angioma, tumors of the middle ear), neurofibromatosis type 1 (café au lait spots, axillary and inguinal freckling, and iris hamartomas), hyperparathyroidism, medullary thyroid cancer.

FH: Multiple endocrine neoplasia type 2A (medullary thyroid cancer, pheochromocytoma, parathyroid hyperplasia).

PHEO = Patient has PHEOchromocytoma.

PHEO-SYMP = Triad of SYMPtoms of palpitations, headache, and sweating.

URIN-POS = 24-hour URINary catecholamine and metanephrine test is POSitive (norepinephrine > 170 mcg/24 hr, epinephrine > 5 mcg/24 hr, dopamine > 700 mcg/24 hr, or metanephrine > 400 mcg/24 hr).

• – Tricyclic antidepressants most commonly interfere with interpretation of 24-hour urinary catecholamine and metanephrine testing and should be tapered and discontinued for at least 2 weeks prior to diagnostic testing.

1. Young WF Jr. Pheochromocytoma: 1926–1993. In Trends in Endocrinology and Metabolism, Vol. 4, p. 122. Elsevier Science, Inc.; 1993.

2. Pacak K, et al. Recent Advances in Genetics, Diagnosis, Localization, and Treatment of Pheochromocytoma. Ann Intern Med. 2001;134(4): 315–329.

ECHO: LVH, tachycardia-induced cardiomyopathy, wall motion abnormalities, dilated cardiomyopathy.

CT scan with contrast.

T2-weighted MRI.

MIBG scintigraphy.

PET scan.

U-HTN = Uncontrolled HyperTensioN.

I-HTN = Inadequately controlled BP despite labetolol or contraindication to labetolol.

PT = Poor Tolerance to standard medications.

S = Surgery (definitive treatment of choice).

METS = Metastatic lesions, surgery not an option.

A-HTN = Acute HyperTensive crisis.

LAB = LABetalol 40–80 mg IV q10 minutes.

NIC = Nicardipie 5 mg/hr and titrate 2.5 mg/hr q5–15 min prn.

MET = Metyrosine 250 mg QID PO.

PRES = Preoperative preparation via blood PRESsure control (phenoxybenzamine 10 mg x 1 week) and salt load (5000 mg daily) to prevent post-surgical hypotension.

ALPHA = ALPHA blockers—prazosin 1 mg TID max 15 mg.

IV-MEDS = Sodium nitroprusside 0.25 mcg/kg/min and titrate, nicardipine, phentolamine bolus (1–5 mg).

U-HTN = LAB

I-HTN = NIC

I-HTN + PT = MET

S = PRES

METS = ALPHA

A-HTN = IV-MEDS

• – Suspect pheochromocytoma if hypertension is resistant to traditional medications.

• – The classic triad is headache, sweating, tachycardia.

Avoid beta blockers (may worsen blood pressure).

Caution salt load in patients with CHF/renal failure.

1. Gifford RW Jr. Management of Hypertensive Crises. JAMA. 1991; 266–829.

2. Kassin TA, Clarke DD, Mi VQ, et al. Catecholamine-Induced Cardiomyopathy. Endocr Pract. 2008;14:1137.

Patient with recent infection presents with fever, viral prodromes, chest pain, joint pain, myalgias, fatigue, dyspnea palpitations, or heart failure.

Establish characteristics of chest pain, presence of sick contacts, cardiac toxic medications/drugs, cardiac history, family history of cardiac disease.

Fever, signs of diminished cardiac output, tachycardia, weak pulses, cool extremities, muffled heart sounds, presence of S3, JVD, and edema.

Ongoing myocardial inflammation may result in dilated cardiomyopathy, restrictive CMP, or acute LV failure without LV dilatation.

Diffuse T wave inversions and ST segment elevations.

Severe changes could have bundle branch, high-degree AV blocks, and Q waves.

CXR: Cardiomegaly, pulmonary effusion.

Echocardiogram evaluates LVEF, chamber size (presence of left ventricular dilation), wall motion abnormalities, increased LV EDV, presence of effusions.

Cardiac MRI reveals inflammation, delayed contrast enhancement, following gadolinium infusion and increased T2 signals.

MYO-U = Uncomplicated Myocarditis.

MYO-C = Myocarditis with cardiac dysfunction.

MYO-S = Myocarditis with severe dysfunction and morbidity.

ST = Supportive Therapy (for uncomplicated conditions: symptomatic therapy, best rest, pain control, NSAIDs).

MT = Medical Therapy (if cardiac dysfunction is present, use ACEI, inotropes (milrinone), digoxin, diuretics, IVIG, steroids, carvedilol).

UNRES-MT = Patient UNRESponsive to Medical Therapy.

EMBX = EndoMyocardial Biopsy.

AVT = AntiViral Therapy (antiviral therapy with ribavirin/interferon alpha immunosuppressive therapy with corticosteroids, cyclosporine, azathioprine).

UNRES-AVT = Patient UNRESponsive to AntiViral Therapy.

MYO-U = ST

MYO-C = MT

MOC-C + UNRES-MT = EMBX

MYO-S = AVT

MYO-S + UNRES-AVT = EMBX

• – Myocarditis can cause mild disease with self-resolution, chest pain, heart failure, arrhythmias, and sudden cardiac death.

• – Common causes are virus (coxsackie, parvoirus, EBV, CMV, adenovirus), bacteria (Borrelia, Brucella, Rickettsia, Haemophilus), protozoa (trypanosome), fungal (Aspergillus) hypersensitivity to drugs, autoimmune reactions, and toxins.

• – Routine use of immunosuppressive therapy is not recommended in myocarditis.

• – Endomyocardial biopsy is recommended in patients with acute deterioration of cardiac function of unknown etiology who are unresponsive to medical therapy. Transcriptomic biomarkers from a single endomyocardial biopsy can improve the clinical detection of patients with inflammatory diseases of the heart. This approach advances the clinical management and treatment of cardiac disorders with highly variable outcome.

• – 20% of sudden cardiac deaths are from myocarditis.

• – Complete recovery of ventricular function is seen is as much as 50% of patients.

• – Most causes/etiologies are not found; definite diagnosis requires heart muscle biopsy.

• – Place patient on telemetry/electrocardiographic monitoring. Check CBC, blood cultures, cardiac enzymes (CKMB, troponin I), LDH, serial ECG, Echo, ESR/CRP, IgM serology of viruses and cultures, LFTs, anti-alpha myosin autoantibodies, anti-cardiac IgG.

1. Mahrholdt H, et al. Presentation, Patterns of Myocardial Damage, and Clinical Course of Viral Myocarditis. Circulation. 2006;114:1581.

2. Gerzen P, et al. Acute Myocarditis. A Follow-up Study. Br Heart J. 1972;34:575.

3. Heidecker B, et al. Transcriptomic Biomarkers for the Accurate Diagnosis of Myocarditis. Circulation. 2011;123:1174–1184.