Spencer C. Knox, MD

Internal Medicine Resident Physician, PGY-3

Category: Cardiovascular (Page 1 of 2)

ACLS Protocols

As a senior internal medicine resident on night float and overnight call, I’m responsible for running to codes and rapid responses.  Rapid responses at my institution are critical patient situations that require urgent bedside attention for things like symptomatic supraventricular tachycardia, new typical chest pain, hemodynamic instability, etc.  Today after work, I wanted to brush up on my ACLS protocol knowledge.  I reviewed the American Heart Association’s protocols, and have attached them here for fellow physicians to reference.

HFpEF Treatment

These patients tend to be very VOLUME SENSITIVE.

  • Daily weight checks – get an accurate bathroom scale.
  • No medications have proven mortality benefit.
  • Treat causes
    • Hypertension – lower the patient’s blood pressure
    • Tachycardia – AV nodal blockade depending on etiology.

 

Bibliography

HFrEF Medical Treatment

Heart Failure with Reduced Ejection Fraction (also known as systolic heart failure) is broken up into two phases of treatment:  the acute (on presentation to the hospital) and chronic (long-term to prevent re-hospitalization).

Acute Exacerbation Treatment
  1. DIURETIC (urinate off all the excess fluid in a volume-overloaded patient)
  2. ACE inhibitor or Angiotensin Receptor Blocker (ARB)
    • contraindicated if symptomatic hypotension (SBP<90 or MAP<65)
  3. After symptoms have improved/resolved, initiate a beta-blocker
    • Metoprolol succinate, carvedilol, bisoprolol all show mortality benefit.
    • A history of COPD is NOT a contraindication to BB therapy.
Long-Term Treatment
  • Chronic therapy is dictates by patient’s FUNCTIONAL status (NY Heart Association Class) and other symptoms of fluid status.
    • I – No limits on physical activity
    • II – Mild limitation of physical activity
    • III – Marked limitation of physical activity
      • IIIA – symptoms with less than ordinary activity
      • IIIB – symptoms with minimal exertion
    • IV – cannot perform physical activity without symptoms.
  • Treatments that reduce mortality and reduce re-hospitalization:
    • ACE inhibitors – can also improve LVEF, ok to use with Creatinine < 3.0
    • Beta-blockers – block chronic neurohormonal activation
    • Aldosterone antagonist (aldactone) – give for NYHA class II, III, and IV
      • Ok to use with Creatinine < 2.5 in men and < 2.0 in women.
    • For black patients with class III/IV – Hydralazine-isosorbide dinitrate
      • Use as supplemental therapy (not replacing other agents).
    • Combination of ACEi and Beta-blocker is best (rather than either alone).
  • Medications to improve symptoms, only:
    • Digoxin – better quality of life and improved exercise tolerance.  Careful with kidney failure patients.
    • Diuretics
    • Vasodilators
    • Inotropic agent(s)
  • Do NOT use CCBs like diltiazem/verapamil – worse outcomes in patients with heart failure.

Bibliography
ACP MKSAP 17:  Cardiovascular Medicine, pp. 32-34

Heart Failure Pathophysiology and Diagnosis

Pathophysiology
  • In an average healthy person, normal LV ejection fraction (LVEF):  >50%
  • Roughly 50% of those with heart failure have reduced left ventricular (LV) function (HFrEF)
    • Heart cannot squeeze/contract properly, and then progressively dilates.
  • The other 50% have preserved (normal contraction) LV function (HFpEF)
    • Cannot relax properly, leading to high diastolic (filling) pressures.
  • New heart failure – work patient up for ischemic disease (CAD) and ACS
    • Coronary Artery Disease causes 67% of heart failure!  #1 cause of heart failure
  • Symptomatic hypotension and kidney failure can be due to cardiac output failure.  Organs simply do not have sufficient blood to perfuse and stay alive.
  • Etiology of HFrEF
    • Hypertension
    • CAD
    • Myocarditis
    • Drugs – cyclophosphamide, doxorubicin, trastuzumab
    • Toxins – EtOH, cocaine, cobalt/lead, amphetamines
    • Systemic disease – hypo- or hyperthyroidism, HIV, SLE, Neuromuscular disease (Duchenne & Becker muscular dystrophy), scleroderma
    • Idiopathic (unknown cause)
  • Etiology of HFpEF
    • Hypertension
    • CAD
    • Infiltrative – amyloidosis & hemochromatosis (check ferritin)
Diagnosis
  • Clinical signs and symptoms
    • Shortness of breath either with exertion or at rest
    • Orthopnea (shortness of breath lying flat on one’s back)
    • Paroxysmal nocturnal dyspnea (sudden bouts of shortness of breath and cough during the night/sleep hours)
    • Peripheral edema (swelling of feet/legs)
    • Decompensated signs/symptoms
      • More pillows at nighttime
      • Can’t walk up as many stairs before getting short of breath
      • Increased belly size, anorexia, nausea (gut edema)
  • Patients must weigh themselves daily, call the office if interval change.
  • History and physical
  • Paroxysmal nocturnal dyspnea leads to >2x increase in likelihood of HF
  • S3 confers 11x greater chance of HF.
  • If no dyspnea on exertion or crackles on lung exam, HF less likely.
  • BNP level – use when cause not clear.  If elevated, dyspnea is due to heart failure!  If not, consider other lungs as cause.
    • BNP level increases with age and bad kidneys
    • BNP level decreases with high BMI.
  • 12-lead EKG
    • Rule out MI, tachycardia, LV hypertrophy
  • CXR
  • Labs – BMP, CBC, UA, LFTs, lipid panel, TSH
Workup to Find A Cause
  • Must think of Ischemia first –
    • Serial EKGs and troponin levels to evaluate for NSTEMI/STEMI.
    • Routine investigation via stress or cath no longer part of routine workup for new HF patients.
    • However, if chest pain/pressure and/or risk factors are present –> proceed to cardiac cath.
  • Echocardiogram is most important test in HF.
    • “Wall motion abnormalities” is a clue to CAD or MI.
    • Assesses valvular anatomy and function
    • Left ventricular end-diastolic dimension:  can aid in telling how chronic the condition is and prognosis.
      • If DILATED w/acute symptoms –> chronic disease process.
      • If small LV –> better shot at recovery.
  • Cardiac magnetic resonance (CMR)
    • Looks for wall motion abnormalities, perfusion, and VIABILITY of tissue.
    • If thinking fibrosis, infiltration (amyloid/sarcoid), or iron deposition.

Bibliography
ACP MKSAP 17:  Cardiovascular Medicine, pp. 32-34

Atrial Flutter

  • More organized, saw-tooth type pattern seen on standard 12-lead EKG.
    • Negative flutter waves in inferior leads
    • Positive flutter waves in V1
    • Typical Flutter = counterclockwise reentry around tricuspid annulus.
  • Rate is ~250/min; noted as 2:1 or 4:1 for its atrial rate and the ratio of electrical conduction down the AV node.
  • Atrial Flutter is often seen in patients diagnosed with concomitant Atrial Fibrillation (Fib-Flutter).
Management
  • Similar to AFib – think CHA2DS2-VASc for stroke prevention.
  • Benefit of Rate vs. rhythm control is the same.
  • CAN require larger doses of AV nodal blockers (CCBs or BBs).
  • Catheter ablation for typical flutter is generally preferred (high success rate).

Bibliography
ACP MKSAP 17:  Cardiovascular Medicine, pp. 58

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