Heart failure is the inability of the myocardium to adequately meet the demands of the body.
Ischemi heart dz = CHF
- Orthopnia
- Pulse
- RR
- (+) JVD
- BL Peripheral Edema
- (+)
Rales/bibasilar crackles

(-) (+)
(+) Response
(-) Response
Long-Term Management:
- BB (most beneficial with verly low EF)
- -Statin
- Spironolactone
- Dobutamine
(+) Response
(-) Response

Systolic VS Diastolic Dysfunction (Overview)
Systolic dysfunction: Diastolic dysfunction:
- Usually from ischemic heart disease and myocardial cell death
- Impaired contractility
- Ejection fraction (EF) < 40%
- Output is dependent on resistance to emptying the ventricle (afterload).
- Usually from chronic HTN and left ventricular hypertrophy
- Impaired relaxation and ventricular filling
- Normal ejection fraction with elevate proBNP
- Output is dependent on filling of the ventricle (preload)
• Preload reduction
  – Diuretics, nitrates (Hydralazine/isosorbide)

• Afterload reduction
  – ACEI, ARB, nitrates (Hydralazine/isosorbide)

• Sympathetic blockade
  – ß-blockers (Only 3 have sufficient data: Metoprolol succinate XL, Carvedilol, Bisoprolol)

• Aldosterone-antagonist therapy
  – Spironolactone, eplerenone (Inspra)- Improve EF  in systolic HF

• Increase Contractions
  – Digoxin

Verapamil, due to its negative inotropic effect, is associated with worsening heart failure and an increased risk of adverse cardiovascular events.
• BB (Only 3 have sufficient data: Metoprolol succinate XL, Carvedilol, Bisoprolol)

• Nondihydropyridine CCB (Diltiazem)

• Diuretic

If rapid atrial fibrillation/flutter = digoxin is indicated for rate control.


  • Fatigue, weakness, memory problems, Mild dyspnea to marked respiratory distress (depending on severity), Left heart failure
  • Dyspnea, Orthopnea, Paroxysmal nocturnal dyspnea
  • Right heart failure, Abdominal distention or pain, Leg swelling


  • Diaphoresis, tachycardia, HTN: From sympathetic activation
  • Tachypnea, rales, and/or “cardiac” wheezes
  • S3 and S4 gallop
  • Underlying or associated right heart failure
  • Hepatic enlargement, Peripheral edema, Jugular venous distention, Hepatojugular reflex
  • End stage = severe hypoxia and ventilatory failure with mental status change and terminal dysrhythmias
  • Look for evidence of underlying cause/event: infection, PE, valvular disease.


  • Noncardiogenic pulmonary edema in which capillary membrane permeability is compromised (infection, ARDS, drug reaction)
  • Pneumonia
  • Asthma
  • COPD
  • PE

Causes of Heart Failure and Pulmonary Edema

Common Causes of Heart Failure and Pulmonary Edema
Myocardial ischemia: acute and chronic
  Valvular dysfunction
  Aortic valve disease
  Aortic stenosis
  Aortic insufficiency
  Aortic dissection
  Infectious endocarditis
  Mitral valve disease
  Mitral stenosis
  Mitral regurgitation
  Papillary muscle dysfunction or rupture
  Ruptured chordae tendineae
  Infectious endocarditis
  Prosthetic valve malfunction
Other causes of left ventricular outflow obstruction
  Supravalvular aortic stenosis
  Membranous subvalvular aortic stenosis
  Hypertrophic cardiomyopathy
Acquired cardiomyopathy
  Toxic: alcohol, cocaine, doxorubicin
  Metabolic: thyrotoxicosis, myxedema
Myocarditis: radiation, infection
Constrictive pericarditis
Cardiac tamponade
Systemic hypertension
  Cardiac dysrhythmias

DDx for Heart Failure

Differential Diagnoses for Heart Failure
Dyspneic states
  Asthma exacerbation
  Chronic obstructive pulmonary disease exacerbation
  Pleural effusion
  Pneumonia or other pulmonary infection
  Pulmonary embolus
  Physical deconditioning or obesity
Fluid retentive states
  Dependent edema or deep vein thrombosis
  Liver failure or cirrhosis
  Portal vein thrombosis
  Renal failure or nephrotic syndrome
Impaired cardiac output states
  Acute myocardial infarction
  Acute valvular insufficiency
  Drug overdose/effect
  Pericardial tamponade
  Tension hydro- or pneumothorax
High output states
  Thyroid dysfunction

Heart Failure with Normal EF

Heart Failure with Normal Ejection Fraction
Primary valvular disease
High metabolic demand (high output states)
Arteriovenous fistulae
Restrictive heart disease (e.g., amyloidosis, sarcoidosis, hemochromatosis)
Pericardial constriction
Episodic left ventricular systolic dysfunction
Severe hypertension,
Chronic pulmonary disease with right heart failure
Atrial myxoma

Precipitants of Acute Heart Failure

Precipitants of an Acute Heart Failure Syndrome
  Excess salt*
  Medication noncompliance*
Cardiac causes
  New arrhythmia
  Rapid atrial fibrillation*
  Acute coronary syndrome or acute myocardial infarction*
  Uncontrolled hypertension
  Use of calcium channel blocker, β-blocker, or NSAIDs
  Inappropriate therapy reduction
  Antiarrhythmic agents within 48 h
Noncardiac causes
  Exacerbation of comorbidity (e.g., chronic obstructive pulmonary disease)
  Pulmonary embolus
Volume overload
  Renal failure (especially missed dialysis)*
* = Very common



ECG Look for LVH, ischemia, dysrhythmias.
Upright chest radiograph (CXR)
  • CXR findings may lag clinical findings!
  • Progression of CXR changes
    • Vascular congestion (cephalization of vessels) →
    • Interstitial edema (Kerley B lines, haziness) →
    • Alveolar infiltrates (butterfly pattern, effusions)
  • Normal heart size? Suspect noncardiogenic pulmonary edema or acute valve failure.
  • To identify underlying causes: renal failure, anemia, MI, hyperkalemia
  • B-type natriuretic peptide (BNP)
    • Near-linear relationship between admission BNP levels and in-hospital mortality. For patients with BNP levels ≥5000 pg/mL, in-hospital mortality was 8.5% (
    • Released in response to ventricular myocyte stretch
    • Level increase with severity of CHF
    • BNP < 100 pg/dL makes heart failure unlikely.
    • BNP > 500 pg/dL makes heart failure highly probable.
    • Should be compared to patient’s baseline values
    • Can be elevated in the elderly, renal failure, PE, or cor pulmonale
    • Tends to be lower in obese patients
  • Circulating complement levels, Transaminases
  • Na
Echocardiogram Assesses systolic, diastolic, and valvular function




American College of Cardiology/American Heart Association classification of heart failure
Classification Description
Class A The absence of structural disease in a patient at high risk for the development of heart failure.
This includes patients with hypertension, atherosclerotic disease, diabetes mellitus, obesity, metabolic syndrome, or a family history of cardiomyopathy as well as those using cardiotoxins
Class B Pts have evidence of structural heart disease (e.g., a previous myocardial infarction, asymptomatic valvular disease, or evidence of left ventricular remodeling such as left ventricular hypertrophy or a low ejection fraction)
Class C Structural heart disease with prior or current symptoms of heart failure
Class D Patients have refractory heart failure requiring specialized interventions

New York Heart Association (NYHA) class
Classification Description
Class I asymptomatic
Class II experience symptoms only with moderate exertion
Class III patients experience heart failure symptoms with minimal exertion
Class IV experience symptoms at rest.



ED Management

Airway Control, Ventilation, Supplemental Oxygen for Acute Heart Failure
Stepped Measures Based on Severity Comments
1. Supplemental oxygen Initiate as initial measure or for mild to moderate illness. Use pulse oximetry to guide intensity of therapy.
2. Noninvasive ventilation Initiate for patients with moderate to marked respiratory distress. Requires patient cooperation and hemodynamic stability, avoid in patients at risk for aspiration.
3. Endotracheal intubation Initiate for patients with marked respiratory distress who cannot cooperate with noninvasive ventilation or have hemodynamic instability.

Management of Hypertensive Acute Heart Failure*
Stepwise Approach Comments
1. Administer oxygen, give sublingual nitroglycerin. --
2. If BP >150/100 mm Hg, add IV nitroglycerin or nitroprusside;
if BP falls below 100 mm Hg, stop nitrates, treat as cardiogenic shock for persistent hypotension.
Systemic and Pulmonary Hypertension; see text for discussion of these agents.
3. Start IV diuretic, furosemide, bumetanide, or torsemide in the setting of volume overload. Initiate nitrates before diuretics.
4. If severe dyspnea, begin NIV. See Table above.
5. Assess for severity of illness/high risk:  Altered mental status persistent, hypoxia despite NIV, SBP >210 mm Hg, troponin elevated, blood urea nitrogen over 43, creatinine over 2.75, tachycardia, tachypnea, inadequate urine output, ischemia, or infarction. Acute Coronary Syndromes: Acute Myocardial Infarction and Unstable Angina for ECG criteria.
6. Admit to intensive care unit if significant severity of illness or high risk. --
7. Admit to ED observation unit if good response to therapy and no high-risk features. Scoring systems may not reliably identify all patients at risk

First-Line Medications for Acute Heart Failure Syndromes
Vasodilators for Acute Heart Failure
Vasodilator Dose Titration End Point Complications
Sublingual NTG 0.4 mg every 1–5 min to Blood pressure Hypotension
IV NTG 0.2–0.4 mcg/kg/min (starting dose)

Flash Pulm Edema:
Loading Dose: 400 mcg/min over 2 min.
5-200 mcg/min IV
(Start Low if pt Hypo/Normo-tensive)

to Symptoms Headache, hypotension
Nitroprusside Starting Dose: 0.3 mcg/kg/min
Max: 10 mcg/kg/min
Blood pressure Hypotension, cyanide/thiocyanate toxicity, ?coronary steal
Diuretics for Heart Failure
Diuretic Dose (IV) Effect Complications
Furosemide No prior use: 40 mg IVP

Loading dose: 40-100 mg IV bolus over 1-2 min. then 10-40 mg/hr drip.
Repeat loading dose before increasing infusion rate
Diuresis starts within 15-20 min

Duration of action: 4-6 h

K+, Mg2+, hyperuricemia, hypovolemia
If prior use: give usual PO dose as IV bolus
Ototoxicity, prerenal azotemia, sulfa allergy
If no effect by 20-30 min, increase subsequent dose
Bumetanide 1-3 mg IV

Loading dose: 1 mg IV, then 0.5-2 mg/hr
Repeat loading dose before increasing infusion rate.
Diuresis starts within 10 min

Peak action at: 60 min

Same as above
Torsemide 10-20 mg IV Diuresis starts within 10 min

Peak action in: 1-2 h

Same as above


The treatment of pt in acute pulmonary edema include O2, preload reducers, diuretics, afterload reducers, & inotropic agents
  1. O2 up to 100% delivered by non-rebreather mask should be administered to achieve an O2 sat of at least 95% by pulse oximetry.
  2. If hypoxia persists despite Oxygen Tx, or if pt is showing signs of respiratory distress ( eg, tripod stature, accessory muscle use, inability to speak), continuous positive airway pressure (CPAP) or  biphasic positive airway pressure (BiPAP) should be applied.
  3. Immediate intubation is indicated for unconscious or visibly tiring pts
  4. NTG 0.4 mg should be administered SL (may be repeated q 1-5 min). If pt does not respond, or if the ECG shows ischemia, NTG 0.4 mcg/kg/min should be initiated as an IV drip & titrated rapidly to BP & symptom reduction.
  5. After nitrates, an IV diuretic can be administered, such as furosemide 40-80 mg IV, bumetanide 0.5-1 mg IV, or torsemide 10 mg IV. Electrolytes (especially serum potassium) should be monitored.
  6. Transient hypotension may develop after nitroglycerine is started. This may be due to marked clinical improvement, & should improve with decreasing the dose or cessation of nitrogylcerin. If hypotension persist, initiate a fluid bolus (250 - 1000 cc) and be suspicious of a right ventricular infarction, valvular pathology (severe aortic stenosis), hypovolemia, or recent use of medications for erectile dysfunction.
  7. For pt with resistant hypertension or those who are not responding well to NTG, nitroprusside (0.3 mcg/kg/min & titrate) may be used.
  8. For hypotensive pt or pt in need of additional inotropic support, see ICU or ER hypotensive section.
  9. Coexisting dysrhythmia or electrolyte disturbances should be treated, and those therapies that impair the inotropic state of the heart should be avoided.

Acute mitral valve or aortic valve regurgitation should be considered, especially if the heart is of normal size, because the pt may need emergency surgery. Until excluded, acute MI should be considered as the cause of pulmonary edema exacerbation. Because the initial EKG may fail to demonstrate ischemic changes, repeat EKGs are indicated for those pts with initially normal tracings, who fail to improve.

Morphine (2-5mg IV) can be used and repeated as needed for pain control. For anuric (dialysis) pts, sorbitol & phlebotomy may have some benefit; however, dialysis is the treatment of choice in these pts who prove resistent to nitrates.

Long Term Management

Long term Management
ACEI (Preferred)
improve mortality in heart failure
ACEI superior to ARBs
β-blockers improve mortality in heart failure
** ß-blockers should be started when the patient is stable and euvolemic
– Use in pt with CHF + HTN

– ONLY 3 have sufficient data to support their use:
• Metoprolol succinate (XL)
• Carvedilol
• Bisoprolol

Contraindications to ß-blocker use include:
– Hemodynamic instability
– Heart block
– Bradycardia
– Severe asthma

ß-blockers may be initiated in patients with mild asthma or COPD, as long as they are monitored for potential complications.
Aldosterone antagonists
(Spironolactone & eplerenone)
– Reduce all-cause mortality
Improve ejection fractions in systolic HF

AVOID aldosterone antagonists if serum potassium level >5.0 mEq/L and a serum creatinine level >2.5 mg/dL for men or >2.0 mg/dL for women
–  NSAIDs and COX-2 inhibitors should be avoided
–  Potassium supplements should be discontinued or reduced.
MONITORING: Close monitoring of serum potassium is recommended; serum potassium levels should be checked 3 days and 7 days after starting an aldosterone antagonist, followed by monthly measurement for the first 3 months
Furosemide improve symptoms and reduce hospitalizations in systolic HF.
– Furosemide may decrease mortality.
Digoxin Improve symptoms and reduce hospitalizations in systolic HF.
– Aim for a serum level of < 1.0 ng/mL
Hydralazine plus isosorbide dinitrate Reduces mortality rates and improves quality-of-life measures
• When standard treatment with diuretics, β-blockers, and an ACEI (or ARB) is insufficient to control symptoms or cannot be tolerated
• Particularly effective in African-Americans with NYHA class III or IV heart failure
Verapamil CONTRAINDICATED due to its negative inotropic effect, is associated with worsening heart failure and an increased risk of adverse cardiovascular events.
Dihydropyridine calcium channel blockers (amlodipine,felodipine, etc.) No direct role in the treatment of heart failure
• May be used for blood pressure lowering if standard HF therapy does not provide adequate control
- Mono Therapy can worsen CHF

Rx for Decompensated Failure and Pulm Edema:

Medications for Decompensated Heart Failure and Pulmonary Edema
NTG Preload
Afterload (high dose)
Coronary vasodilation
Severe hypotension with:
Viagra use
Aortic stenosis
Hypertrophic cardiomypoathy
RV infarct
Morphine Catecholamines
Preload (mild)
Anxiety, pain
CNS & respiratory depression
Furosemide Preload
Immediate venodilator effect ( preload)
Delayed diuresis
Hypotension from hypovolemia
ACEI, ARB Afterload  
Spironolactone, eplerenone Aldosterone-antagonist therapy  
Afterload & Preload
Coronary vasodilation
Coronary steal
Nesiritide Diuresis
Renal failure
? increase mortality

Heart Failure uncontrolled w/ Optimal Medical Mgnt

  • Biventricular pacing with implantable defibrillator
  • Heart transplant if survival > 1 yr & no other major medical problems
  • DO NOT use intermittent IV dobutamine -- it increases risk of death.

Valve Replacement

Aortic Valve Stenosis

  • Aortic valve replacement remains the best therapy for correction of aortic stenosis.
  • However, the natural history of aortic stenosis is generally one of slow, steady progression, and sometimes little change occurs for many years.
  • Even in severe stenosis, the rates of surgical and delayed complications outweigh the benefits in the majority of asymptomatic patients.
  • Patients with more severe aortic narrowing should be followed very closely for the onset of symptoms, with prompt intervention once symptoms occur.
  • Some selected patients may benefit from surgery prior to the onset of symptoms, but there is not yet general consensus or clear evidence to support this recommendation.
  • General Criteria for Aortic Valve replacement:
    • Symptomatic patient
    • Aortic valve area < 1 cm2
    • Aortic valve gradient > 50 mm Hg

A 75-year-old Hispanic male presents with dyspnea on exertion which has worsened over the last several months. He denies chest pain and syncope, and was fairly active until the shortness of breath slowed him down recently. You hear a grade 3/6 systolic ejection murmur at the right upper sternal border which radiates into the neck. Echocardiography reveals aortic stenosis, with a mean transvalvular gradient of 55 mm Hg and a calculated valve area of 0.6 cm2. Left ventricular function is normal. Which one of the following is appropriate management for this patient?

A. Aortic valve replacement
B. Aortic balloon valvotomy
C. Medical management with beta-blockers and nitrates
D. Watchful waiting until the gradient is severe enough for treatment
E. Deferring the decision pending results of an exercise stress test

Correct Answer: A
Since this patient’s mean aortic-valve gradient exceeds 50 mm Hg and the aortic-valve area is not larger than 1 cm2, it is likely that his symptoms are due to aortic stenosis. As patients with symptomatic aortic stenosis have a dismal prognosis without treatment, prompt correction of his mechanical obstruction with aortic valve replacement is indicated. Medical management is not effective, and balloon valvotomy only temporarily relieves the symptoms and does not prolong survival. Patients who present with dyspnea have only a 50% chance of being alive in 2 years unless the valve is promptly replaced. Exercise testing is unwarranted and dangerous in patients with symptomatic aortic stenosis.

Ref: Carabello BA: Aortic stenosis. N Engl J Med 2002;346(9):677-682.

Heart Transplant

  • Heart transplantation is generally not performed in patients > age of 65–70.
  • The procedure typically results in 1-year mortality rates of 10%–15%.
  • Indications for heart transplantation include severe heart failure resulting from:
    • Myocarditis
    • Ischemic heart disease, or
    • Severe valvular disease, as well as
    • High-risk malignant dysrhythmias.
  • There is no shortage of recipients in this country, and the primary limiting factor is lack of donors.
  • Heart transplant recipients need lifelong immunosuppressant therapy


  • Patients benefit from frequent formal evaluation in a specialized center or monitoring in a management program.
  • Assessment should be made at each visit of the ability of a patient to perform routine and desired activities of daily living.
  • Assessment should be also made of the fluid status and weight of the patient.
  • Careful history of current use of alcohol, tobacco, illicit drugs, alternative therapies, and chemotherapy drugs, as well as diet and sodium intake, should be obtained at each visit.
  • Repeat measurement of ejection fraction and assessment of the severity of structural remodeling can provide useful information in patients with heart failure who have had a change in clinical status, or who have experienced or recovered from a clinical event, or received treatment that might have had a significant effect on cardiac function.
  • The value of serial measurements of B-type natriuretic peptide (BNP) to guide therapy for patients is still not well established.
    • Data suggest that natriuretic-guided therapy reduces hospitalization due to heart failure and that in patients younger than 75 years of age, it also provides a survival benefit. 
  • The use of telemonitoring to monitor patients remotely is an emerging strategy, but requires further evaluation


  • On discharge from the hospital patients should be instructed on:
    • Daily home weight monitoring
    • Sodium restriction (2 g to 3 g daily) and fluid restriction when necessary
    • Quit tobacco use
    • Moderate alcohol consumption ( Men = 2 drinks/day, women - 1 drink/day)
    • Regular, symptom-limited exercise (3-5 days/week)
      • BUT weight loss does not improve survival in CHF
    • Aggressive control of hypertension and diabetes
    • Lipid management
    • Routine health-care maintenance
    • OSA = cPAP can improve heart failure symptoms


Admit Orders: CHF

1. Admit to:
2. Diagnosis:
 Congestive Heart Failure

3. Condition:

4. Vital Signs:
 q1h. Call physician if P >120; BP >150/100 <80/60; T >38.5°C; R >25, <10.
5. Activity:
 Bed rest with bedside commode.
6. Nursing:
 Daily weights, measure inputs and outputs. Head-of-bed at 45 degrees.
7. Diet:
 1-2 gm salt, cardiac diet.
8. IV Fluids:
 Heparin lock with flush q shift.

9. Special Medications:
  • Oxygen 2-4 L/min by NC.


  • Furosemide (Lasix) 10-160 mg IV qd-bid or 20-80 mg PO qAM-bid or 10-40 mg/hr IV infusion OR
  • Torsemide (Demadex) 10-40 mg IV or PO qd; max 200 mg/day [5, 10, 20, 100 mg] OR
  • Bumetanide (Bumex) 0.5-1 mg IV q2-3h until response; then 0.5-1.0 mg IV q8-24h (max 10 mg/d); or 0.5-2.0 mg PO qAM.
  • Metolazone (Zaroxolyn) 2.5-10 mg PO qd, max 20 mg/d; 30 min before loop diuretic [2.5, 5, 10 mg].
ACE Inhibitors (for EF < 40%):
  • Lisinopril (Zestril, Prinivil) 5-40 mg PO qd [5, 10, 20, 40 mg] OR
  • Quinapril (Accupril) 5-10 mg PO qd x 1 dose, then 20-80 mg PO qd in 1 to 2 divided doses [5, 10, 20, 40 mg] OR
  • Benazepril (Lotensin) 10-20 mg PO qd-bid, max 80 mg/d [5, 10, 20, 40 mg] OR
  • Fosinopril (Monopril) 10-40 mg PO qd, max 80 mg/d [10, 20 mg] OR
  • Ramipril (Altace) 2.5-10 mg PO qd, max 20 mg/d [1.25, 2.5, 5, 10 mg].
  • Captopril (Capoten) 6.25-50 mg PO q8h [12.5, 25, 50, 100 mg] OR
  • Enalapril (Vasotec) 1.25-5 mg slow IV push q6h or 2.5-20 mg PO bid [5, 10, 20 mg] OR
  • Moexipril (Univasc) 7.5 mg PO qd x 1 dose, then 7.5-15 mg PO qd-bid [7.5, 15 mg tabs] OR
  • Trandolapril (Mavik) 1 mg qd x 1 dose, then 2-4 mg qd [1, 2, 4 mg tabs].
Angiotensin-II Receptor Blockers:
  • Irbesartan (Avapro) 150 mg qd, max 300 mg qd [75, 150, 300 mg]. OR
  • Losartan (Cozaar) 25-50 mg bid [25, 50 mg]. OR
  • Valsartan (Diovan) 80 mg qd; max 320 mg qd [80, 160 mg]. OR
  • Candesartan (Atacand) 8-16 mg qd-bid [4, 8, 16, 32 mg]. OR
  • Telmisartan (Micardis) 40-80 mg qd [40, 80 mg].
Adosterone Receptor Blockers:
  • Spironolactose (Aldactone) 25 mg PO qd OR
  • Eplerenone (Inspra) 25 mg PO qd.
  • Carvedilol (Coreg) 3.125 mg PO bid, then slowly increase the dose every 2 weeks to target dose of 25-50 mg bid [tab 3.125, 6.25, 12.5, 25 mg] OR
  • Metoprolol XL (Toprol XL) 12.5-100 mg PO qd OR
  • Metoprolol (Lopressor) start at 6.25 mg bid, then slowly increase to target dose of 100 mg bid [50, 100 mg] OR
  • Bisoprolol (Zebeta) start at 1.25 mg qd, then slowly increase to target of 5-10 mg qd [5, 10 mg]
  • Digoxin (Lanoxin) 0.125-0.25 mg PO or IV qd [0.125, 0.25, 0.5 mg].
  • KCL (Micro-K) 20-40 mEq PO qd if the patient is taking a loop diuretic.
  • Nitroglycerine 5 to 10 mcg/min IV, increased in increments of 5 to 10 mcg/min every 3 to 5 minutes as required (dose range 10 to 200 mcg/min).
Inotropic Agents:
  • Dobutamine (Dobutrex) 2.5-10 mcg/kg/min IV, max of 15 mcg/kg/min (500 mg in 250 mL D5W, 2 mcg/mL) OR
  • Milrinone (Primacor) loading dose of 50 mcg/kg over 10 minutes, followed by a maintenance dose of 0.375 to a maximum of 0.750 mcg/kg per min (40 mg in 200 mL NS, 0.2 mg/mL).
  • Synchronized biventricular pacing if ejection fraction <40% and QRS duration >135 msec.
10. Symptomatic Medications:
  • Heparin 5000 U SQ q12h or enoxaparin (Lovenox) 1 mg/kg SC q12h.
  • Nitroglycerin 0.4 milligrams sublingual every 5 minutes as needed for chest pain times 3 doses.
  • Docusate (Colace) 100-200 mg PO qhs.
  • Famotidine (Pepcid) 20 mg IV/PO q12h  OR
  • Lansoprazole (Prevacid) 30 mg qd.
11. Extras: CXR PA and LAT, ECG now and repeat if chest pain or palpitations, echocardiogram.
12. Labs:
 CMP, CBC; proBNP, FLP, A1c,  troponin STAT and q6h for 24h. Repeat CMP in AM. high sesitivity CRP, UA.