Rosen & Barkin's 5-Minute Emergency Medicine Consult (127 page)

Record rhythm strips for analysis

• Oxygen administered via 100% nonrebreather
  
• Intubation as needed
  
• IV access
  
• Advanced cardiac life support drugs as per usual protocol (especially for bradycardia)
  
• Defibrillation: Avoid placing paddles over generator.
  
• Transcutaneous pacemaker in hemodynamically unstable patients with pacemaker failure
  

• Pacemaker failure:
  
  • Transcutaneous pacemaker
    
  • Temporary transvenous pacemaker:
    
    • Obtain central IV access with a Cordis introducer (right IJ preferred)
      
    • Perform the procedure under fluoroscopy if possible.
      
    • Set the pulse generator to asynchronous mode.
      
    • Turn the output dial all the way up.
      
    • Advance the catheter through the central venous access Cordis until you see a QRS complex on the monitor.
      
    • Check the femoral pulse.
      
    • If you have a pulse and see a QRS complex, the pacer is “capturing.”
      
    • Slowly turn the output dial down until you lose the QRS complex (capture threshold).
      
    • Turn the output dial up to 2 or 3 times the capture threshold.
      
    • Continuous EKG monitoring facilitates correct placement.
      
• Treat hyperkalemia (see “Hyperkalemia”).
  
• Runaway pacemaker:
  
  • AV node blocking or reprogramming
    
  • In extreme situation, may need to disconnect lead from generator surgically
    

Adenosine: 6 mg IV bolus

FOLLOW-UP

• Permanent pacemaker failure or malfunction
  
• Suspicion of infection involving pacemaker components
  

• Asymptomatic pacemaker malfunction
  
• A cardiologist has interrogated the pacemaker
  

Refer to cardiologist and/or pacemaker clinic

• Always consider pacemaker failure in evaluation of cardiac decompensation, bradycardia, or syncope.
  
• Utilize pacemaker magnet to evaluate function.
  

• Cardall TY, Brady WJ, Chan TC, et al. Permanent cardiac pacemakers: Issues relevant to the emergency physician, parts I and II.
  J Emerg Med
  . 1999;17:479–489, 697–709.
  
• Griffin J, Smithline H, Cook J. Runaway pacemaker: A case report and review.
  J Emerg Med
  . 2000;19:177–181.
  
• McMullan J, Valento M, Attari M, et al. Care of the pacemaker/implantable cardioverter defibrillator patient in the ED.
  Am J Emerg Med.
  2007;25(7):812–822.
  
• Scher DL. Troubleshooting pacemakers and implantable cardioverter-defibrillators.
  Curr Opin Cardiol
  . 2004;19:36–46.
  
• Stone KR, McPherson CA. Assessment and management of patients with pacemakers and implantable defibrillators.
  Crit Care Med
  . 2004;32:155–165.
  

CODES

• V45.01 Cardiac pacemaker in situ
  
• V53.31 Fitting and adjustment of cardiac pacemaker
  
• 996.61 Infection and inflammatory reaction due to cardiac device, implant, and graft
  

BASICS

• Cardiac testing is indicated for emergency patients at risk for heart failure (HF) or acute coronary syndrome (ACS).
  
• These pathologies may be thought of as a spectrum: Unstable angina can evolve into MI, which in turn can cause HF:
  
  • ∼20% of ED malpractice claims are due to missed diagnosis of ACS.
    
  • ∼2% of patients with ACS are inappropriately discharged from an ED.
    
  • History, physical exam, and ECG are the critical elements in working up chest pain and ACS/HF.
    
  • History, physical, and ECG nevertheless miss 1–4% of all heart attacks.
    
  • Additional tools include imaging modalities and blood tests (e.g., cardiac biomarkers).
    

ACS is caused by atherosclerotic narrowing of coronary vessels or by coronary vasospasm.

In the pregnant patient with chest pain and ischemic changes on ECG, also consider spontaneous coronary artery dissection.

DIAGNOSIS

• Anginal symptoms usually are produced by bodily stresses, including exertional and emotional events, and relieved by rest.
  
• ACS is less likely when chest pain is sharp, stabbing, pleuritic, or reproducible with palpation.
  
• Ischemia is still diagnosed in 13% of pleuritic chest pain and in 7% of chest pain reproducible with palpation.
  
• Nitroglycerin may relieve cardiac ischemia, but can also relieve pain in GI and aortic pathology.
  
• A “GI cocktail” of lidocaine and Maalox, or a proton-pump inhibitor such as omeprazole, may relieve GI pathology, but can also relieve cardiac ischemia.
  
• Anginal symptoms often last <20 min but >5 min
  
• AMI and UA should be considered if symptoms last >20 min.
  

Often unremarkable

EKG:

• Per ACC/AHA guidelines, a 12-lead ECG should be performed on a patient with chest pain within 10 min of arrival to the ED:
  
  • A single ECG will miss ∼50% AMI.
    
  • Hyperacute T-waves (tall, broad-based, especially in anterior leads) may be the earliest and only sign of AMI.
    
  • During an MI, the ECG may evolve. Continuous ECG monitoring can identify an additional 16% of acute MIs not seen on initial ECGs. Absent continuous monitoring, consider a repeat EKG 15–60 min after the initial ECG.
    
  • New ST-segment changes or T-wave inversions are suspicious for ischemia.
    
  • ST depressions of 1 mm are characteristic of ischemia; or, could be reciprocal changes, so check other leads.
    
  • STEMI: ST-elevation of >1–2 mm in ≥2 contiguous leads.
    
  • New left bundle branch block (LBBB) is suggestive of AMI:
    
    • Old LBBB makes diagnosing AMI difficult: Apply Sgarbossa criteria: AMI is likely if LBBB and >1 mm ST-elevation concordant with QRS, or ST depression >1 mm in leads V1, V2, or V3.
      
    • Current ACCF/AHA guidelines advise that LBBB “not known to be old” in isolation is not diagnostic of AMI, and should be further evaluated with serum biomarkers and immediate cardiac consultation for consideration of echocardiography and invasive angiography.
      
• Additional-lead EKGs: Standard 12 leads often miss infarcts in the posterior, right, and high lateral walls.
  
  • Right-sided EKG:
    
    • Move lead V4 to the right side of chest, midclavicular line, 5th intercostal space, and repeat EKG, to capture infarct in right ventricle.
      
    • A right-sided EKG is often performed in the setting of a STEMI in inferior leads (II, III, aVF) to diagnose a right ventricular (RV) infarct.
      
  • Posterior EKG:
    
    • Leads V7, V8, V9 are placed posterior thorax along 5th intercostal space: V7 at posterior axillary line, V8 at inferior angle of scapula, V9 paraspinal.
      
    • Performed in setting of inferior or lateral wall MI; or if ST depression in V1–V3. May identify a lateral or left circumflex infarct.
      
• EKG may be helpful in diagnosing other etiologies of chest pain:
  
  • Pericarditis is suggested by diffuse ST-elevations followed by T-wave inversions and P-R depression.
    
  • Pulmonary embolism is suggested by unexplained tachycardia, signs of right heart strain (RVH, RBBB, “p” pulmonale), new-onset atrial fibrillation, or rarely with S1, Q3, T3 pattern.
    

• Cardiac biomarkers:
  
  • Indicated if the history is suspicious for ACS.
    
  • Should not be elevated in stable angina and may be normal in unstable angina.
    
• Troponin T and I: Starts to rise 2–3 hr after onset of chest pain of ACS and peaks in 8–12 hr. Remains elevated 7–14 days:
  
  • A single troponin has low sensitivity for ACS (1 study of low-risk chest pain in patients with negative initial troponin: 2.3% rate of AMI and 1% rate of death at 30 days).
    
  • Timing of biomarker testing is critical: ACEP endorses with “moderate clinical certainty” that a single negative troponin can rule out AMI if drawn 8–12 hr after onset of symptoms. However, uncertainty in time of symptom onset, unreliable history, and possibility of preinfarction angina complicates utilizing single troponin.
    
  • Newer, more sensitive assays may in the future eliminate the need for a 2nd troponin.
    
  • Minor troponin elevations may occur with renal failure, structural heart disease, CHF (acute or chronic), cardiac pacing, pulmonary embolism, sepsis, stroke.
    
  • Lack of standardization between assays (particularly with troponin I) means values from 1 lab cannot always be simply compared to values from another.
    
• CK/CK-Mb: Less sensitive than troponin, rises more slowly. Little gained by using both CK-Mb and troponin assays. Obtain CK-Mb if
  
  • Renal failure is present (Tn less accurate)
    
  • Recent prior infarct
    
• Myoglobin: Rises faster than standard troponin assays and thus able to detect AMI sooner, but max. sensitivity is 70%.
  
• B-type natriuretic peptide (BNP):
  
  • Release and synthesis activated by diastolic ventricular stretch.
    
  • Useful for detecting HF.
    
  • A cutoff of >100 pg/mL diagnosed HF with a sensitivity of 90% and specificity of 76%.
    
  • Unclear significance of elevated BNP in setting of ACS.