Rosen & Barkin's 5-Minute Emergency Medicine Consult (321 page)

• Pulmonic stenosis:
  
  • Systolic crescendo–decrescendo ejection murmur at left upper sternal border
    
  • Severe lesions may have a thrill
    
  • Widely split S
    ₂
    
  • Dyspnea with exertion in serious cases
    
  • May have signs of right heart failure
    
• Pulmonic regurgitation:
  
  • High-pitched, early, decrescendo diastolic murmur
    
  • Widely split S
    ₂
    
  • Associated with Graham Steell murmur of pulmonary HTN (high-pitched early diastolic murmur)
    
  • May have signs of right heart failure
    
• Atrial septal defect:
  
  • Systolic ejection murmur in secundum defect
    
  • Secundum associated with pulmonary HTN
    
  • Wide fixed S
    ₂
    
  • No murmur in PFO
    
• Patent ductus arteriosus:
  
  • Continuous machinery murmur at upper left sternal border with systolic thrill
    
  • Cyanosis
    
  • Bounding peripheral pulses
    
  • Tachypnea
    
• Coarctation of the aorta:
  
  • Continuous or late systolic murmur
    
  • Possible aortic click related to bicuspid valve
    
  • Difference between upper and lower extremity pulses
    
• Hypertrophic cardiomyopathy/idiopathic hypertrophic subaortic stenosis:
  
  • Systolic, harsh, crescendo–decrescendo murmur at left sternal border
    
  • Increased intensity with Valsalva
    
  • Dyspnea
    
  • Chest pain
    
  • Exertional syncope
    
  • Sudden death
    

• Auscultation of heart and lung sounds
  
• Evaluation of pulses, peripheral perfusion, and edema
  

For more details, see Valvular Heart Disease, Mitral Valve Prolapse, Congenital Heart Disease, Patent Ductus Arteriosus, Pericarditis, and Pericardial Effusion/Tamponade.

• EKG
  
• CXR
  
• Echo:
  
  • Evaluate valves, chambers, flow
    
• CT:
  
  • Rule out aortic dissection
    

Acute regurgitant lesions: Cardiac catheterization

See Etiology.

TREATMENT

• IV fluids:
  
  • Patients with critical aortic stenosis are very sensitive to fluid shifts.
    
• Oxygen as appropriate
  

• Oxygen
  
• IV access
  
• Cardiac monitor
  
• Treat symptoms (CHF, dysrhythmias)
  
• Exercise care with fluids and medications in aortic stenosis
  

For more details, see Endocarditis, Valvular Heart Disease, Mitral Valve Prolapse, Congenital Heart Disease, Patent Ductus Arteriosus, Pericarditis, and Pericardial Effusion/Tamponade.

• Digoxin: 0.5 mg IV, then 0.25 mg IV 6 and 12 hr later
  
• Diltiazem (Cardizem):
  
  • 0.25 mg/kg (17.5 mg for 70 kg person) IV over 2 min
    
  • May rebolus after 15 min with 0.35 mg/kg IV
    
  • Start drip at 5–15 mg/hr
    
• Furosemide (Lasix):
  
  • 20–80 mg IV; may increase dose if necessary
    
  • Max. of 600 mg per 24 hr
    
• Heparin:
  
  • 80 U/kg bolus IV, then drip at 18 U/kg/hr
    
  • Monitor partial thromboplastin time
    
• Metoprolol (Lopressor): 5 mg IV q5–15 min for 3 doses, as tolerated
  
• Nitroglycerin:
  
  • 10–20 μg/min IV
    
  • Titrate to effect
    
  • Max. 300 μg/min
    
• Nitroprusside:
  
  • 0.3 μg/kg/min IV
    
  • Titrate to effect
    
  • Max. 10 μg/kg/min
    
  • Protect bag from light
    
  • Thiocyanate toxicity from prolonged use
    
• Propranolol (Inderal):
  
  • 1--3 mg IV q2--5min up to max 5 mg
    
  • No additional doses for 4 hrs after reaching max dose or desired response
    

FOLLOW-UP

• Signs of cardiac ischemia
  
• Syncope or near syncope
  
• Pulmonary edema
  
• Hemodynamic instability
  
• Endocarditis
  
• Arrhythmia
  

• Asymptomatic
  
• Hemodynamically stable
  

Patients with new murmurs should be referred to their caregiver or a cardiologist.

• Patients should always inform their medical and dental caregivers that they have a heart murmur.
  
• To avoid an infection of the lining of the heart, antibiotics may be needed before procedures such as teeth cleaning.
  

Patients with new heart murmurs and fever need to be assessed for endocarditis.

• Bonow RO, Carabello BA, Chatterjee K, et al. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease.
  Circulation
  . 2006;114:e84–e231.
  
• Frank JE, Jacobe KM. Evaluation and management of heart murmurs in children.
  Am Fam Physician.
  2011;84:793–800.
  
• Nishimura RA, Carabello BA, Faxon DP, et al. ACC/AHA 2008 Guideline update on valvular heart disease: Focused update on infective endocarditis.
  Circulation.
  2008;118:887–896.
  
• www.blaufuss.org/tutorial/
  
• www.easyauscultation.com/heart-sounds.aspx
  

CODES

• 394.0 Mitral stenosis
  
• 424.1 Aortic valve disorders
  
• 785.2 Undiagnosed cardiac murmurs
  

BASICS

• HELLP syndrome:
  H
  emolysis
  E
  levated
  L
  iver enzymes,
  L
  ow
  P
  latelets
  
• Continuum with severe preeclampsia as most patients will be hypertensive
  
• Liver involvement is hallmark:
  
  • Other organs may be involved (e.g., brain, kidneys, lungs)
    
• HELLP syndrome divided into 3 groups, representing severity of the disease; severity is directly related to the platelet count:
  
  • Class 1: Most severe form; platelet nadir <50,000 platelets/μL
    
  • Class 2: Less severe; platelet nadir between 50,000 and 100,000 platelets/μL
    
  • Class 3: Least severe; platelet nadir between 100,000 and 150,000 platelets/μL
    
• Most maternal deaths occur with class 1
  
• Increased mortality rate is associated with hepatic hemorrhage or CNS or vascular insult to the cardiopulmonary or renal systems
  
• Incidence: 0.2% of all pregnancies
  
• 12–18% have normal BP
  
• Occurs in 20% of pregnancies with severe preeclampsia or eclampsia
  
• At diagnosis:
  
  • 52% preterm
    
  • 18% term
    
  • 32% postpartum
    

Frequently white, multiparous, older

Infant mortality is greater in women with HELLP

• Unclear, but vasospasm is the basis:
  
  • Fetal-placental debris is released into maternal circulation, causing systemic inflammatory response
    
  • Vascular constriction causes resistance to blood flow and HTN
    
  • Vasospasm probably damages vessels directly
    
  • Angiotensin II causes endothelial cells to contract
    
  • Endothelial cell is damaged and interendothelial cell leaks are the result
    
• Small-vessel leaks:
  
  • Platelets and fibrinogen get deposited in the subendothelium
    
  • Fibrin deposition develops in severe cases
    
• Vascular changes and local tissue hypoxia lead to hemorrhage, necrosis, and end-organ damage
  

DIAGNOSIS