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Pulmonary edema resident survival guide

Introduction

Overview

Overview

Pulmonary edema is fluid accumulation in the lungs. This fluid accumulation leads to impaired gas exchange and hypoxia. The history of a patient with pulmonary edema varies according to the underlying cause. The most common symptom of pulmonary edema is shortness of breath (dyspnea). Depending on the cause, it may occur acutely or have a gradual onset. When pulmonary edema is due to an acute myocardial infarction chest pain is common symptom. Patients with pulmonary edema usually appear agitated. Physical examination of patients with pulmonary edema is usually remarkable for dyspnea, tachypnea. The presence of abnormal cardiac examination on physical examination is diagnostic of cardiogenic pulmonary edema. Patients with noncardiogenic pulmonary edema may have warm extremities, whereas patients with cardiogenic pulmonary edema may have cool extremities. Pulmonary artery catheterization is the gold standard test for the diagnosis of pulmonary edema. Elevated pulmonary-artery pressure indicates cardiogenic pulmonary edema or pulmonary edema due to volume overload. The main goal of a treatment are alleviate symptoms and improving hemodynamics. The initial management of patients is following the ABCs of resuscitation, that is, airway, breathing, and circulation. Medical treatment of cardiogenic pulmonary edema focuses on preload reduction, afterload reduction and inotropic support.

Causes

Causes

Life Threatening Causes

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

Common Causes

Classification

Classification

Pulmonary edema may be classified according to etiology into 2 groups:

Cardiogenic pulmonary edema, which can be secondary to:

Non-cardiogenic pulmonary edema which can be secondary to:

FIRE: Focused Initial Rapid Evaluation

FIRE: Focused Initial Rapid Evaluation

A Focused Initial Rapid Evaluation (FIRE) should be performed to identify patients of pulmonary edema in need of immediate intervention.[1]

Boxes in red signify that an urgent management is needed.

Abbreviations: BU: Blood urea nitrogen; COPD: Chronic obstructive pulmonary disease; D5W: 5% dextrose solution in water ; HF: Heart failure; IV: Intravenous; MAP: Mean arterial pressure; Na: Sodium; NSAID: Non steroidal anti-inflammatory drug; SBP: Systolic blood pressure; S3: Third heart sound;

 
 
Identify cardinal findings that increase the pretest probability of pulmonary edema

âť‘ Anxiety, restlessness
âť‘ Dyspnea
âť‘ Cool extremities/Warm extremities
âť‘ Cough, particularly coughing up blood or bloody froth
âť‘ Excessive sweating or diaphoresis
âť‘ Grunting or gurgling sounds with breathing
âť‘ Pale or blue skin
âť‘ Blue or cyanotic lips
âť‘ Orthopnea
âť‘ Wheezing
âť‘ Peripheral edema
âť‘ Decreased urine output
âť‘ Pulmonary crepitations/rales/crackles
âť‘ Third heart sound (S3) âť‘ Past medical history of heart failure
âť‘ History of opioid and aspirin overdose
âť‘ History of rapidly ascend to altitudes above 12,000 to 13,000 feet
âť‘ History of recent pulmonary embolism
âť‘ History of infections
âť‘ History of head injury, intracranial surgery, grand mal seizures, subarachnoid or intracerebral hemorrhage, and electroconvulsive therapy

âť‘ History of paroxysmal nocturnal dyspnea
 
 
 
 
 
 
 
 
 
Does the patient have any of the following findings that require hospitalization and urgent management?
âť‘ Hypotension (SBP < 90 mmHg or drop in MAP >30 mmHg) and/or cardiogenic shock
âť‘ Altered mental status
âť‘ Cold and clammy extremities
âť‘ Urine output <0.5mL/kg/hr

âť‘ Dyspnea at rest manifested by tachypnea or oxygen saturation <90%
âť‘ Atrial fibrillation with a rapid ventricular response resulting in hypotension

âť‘ Acute coronary syndrome
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Yes
 
No
 
 
 
 
 
 
 
 
 
 
 
Admit to to a level of care that allows for constant ECG monitoring given the risk of arrhythmia and order a stat chest X-ray
 
 
 
 
 
 
 
 
 
 
 

Initial stabilization:
âť‘ Assess the airway
âť‘ Position the patient upright at an angle of 45 degrees, with legs dangling off the bedside (decrease preload)
âť‘ Monitor heart rate and blood pressure continuously
âť‘ Monitor oxygen saturation continuously
âť‘ If hypoxemia is present (Sa02 < 90% or Pa02 <60 mmHg), administer oxygen with/without noninvasive ventilation
âť‘ Morphine to decrease symptoms and Afterload (avoid IV morphine, may increase mortality / duration of intubation, generally not advisable, may relieve refractory symptoms)
âť‘ Secure intravenous access with 18 gauge cannula
âť‘ Monitor fluid intake and urine output carefully (guide the adjustment of the diuretics dose)

Assess congestion and perfusion:
Congestion at rest (dry vs. wet)
“Wet” suggested by orthopnea, ↑JVP, rales, S3, pedal edema
Low perfusion at rest (warm vs. cold)
“Cold” suggested by narrow pulse pressure, cool extremities, hypotension
The patient is:
âť‘ Warm and dry, OR
âť‘ Warm and wet, OR
âť‘ Cold and dry, OR
âť‘ Cold and wet

Identify precipitating factor and treat accordingly:
Click on the precipitating factor for more details on the management
âť‘ Myocardial infarction
âť‘ Myocarditis
âť‘ Renal failure
âť‘ Hypertensive crisis
âť‘ Non adherence to medications
âť‘ Worsening Aortic stenosis
âť‘ Drugs (NSAIDS, thiazides, calcium channel blocker, beta blockers)
âť‘ Toxins (alcohol, anthracyclines)
âť‘ Atrial fibrillation

Rate control of atrial fibrillation is the mainstay of arrhythmia therapy. Avoid the use of drugs with negative inotropic effects such as beta blockers and non-dihydropyridine calcium channel blockers e.g., verapamil in the treatment of acute decompensated systolic heart failure
Consider cardioversion if the patient is in cardiogenic shock or if new onset atrial fibrillation is the clear precipitant of the hemodynamic decompensation

âť‘ COPD
âť‘ Pulmonary embolism
âť‘ Anemia
âť‘ Thyroid abnormalities
âť‘ Systemic infection
âť‘ Opioid and aspirin overdose
âť‘ Recent pulmonary embolism
âť‘ Recent ascend from high altitude
âť‘ Head injury, intracranial surgery, grand mal seizures, subarachnoid or intracerebral hemorrhage, and electroconvulsive therapy

Treat congestion and optimize volume status:
Diuretics
âť‘ Administer IV loop diuretics as intermittent boluses or continuous infusion (I-B)

❑ If patient is already on loop diuretics: IV dose ≥ home PO dose (I-B); rule of thumb: IV dose =
2.5x equivalent oral daily dose
âť‘ If patient is not already on loop diuretics, administer IV starting dose:
Furosemide 20 to 40 mg, OR
Torsemide 5 to 10 mg, OR
Bumetanide 0.5 to 1 mg
âť‘ Adjust dose according to volume status (I-B)
âť‘ Perform serial assessment of fluid intake and output, vital signs, daily body weight (measured every day, with the same scale, at the same time, after first void) and symptoms
âť‘ Order daily electrolytes, BUN, creatinine (I-C)

âť‘ Low sodium diet (<2 g daily)
âť‘ In case of persistent symptoms:

âť‘ Increase dose of IV loop diuretics (I-B)- double dose at 2 hour interval up to maximal daily dose
Furosemide maximal dose: 40 to 80 mg
Torsemide maximal dose: 20 to 40 mg
Bumetanide maximal dose: 1 to 2 mg
OR
âť‘ Add a second diuretics, such as thiazide (I-B)

âť‘ Consider low dose dopamine infusion for improved diuresis and renal blood flow (IIb-B)
âť‘ Consider renal replacement therapy/ultrafiltration in obvious volume overload (IIb-B) refractory to higher dose/combination of IV diuretics

Venodilators
âť‘ Consider IV nitroglycerin, nitroprusside, or nesiritide as add-on to diuretics to relieve dyspnes (IIb-A)

Do not administer vesodilators among patients with hypotension.

Treat low perfusion:
âť‘ Inotropes (click here for details)

If the total body and intravascular volumes are overloaded and the patient is normotensive, then diuresis alone should be undertaken. If the patient is volume overloaded but hypotensive, then inotropes must be administered in addition to diuretics.

Invasive hemodynamic monitoring:
âť‘ Consider pulmonary artery catheterization in case of failure to respond to medical therapy, respiratory distress, shock, uncertainty regarding volume status, or increase in creatinine; assess the following parameters:

âť‘ PCWP
âť‘ Cardiac output
âť‘ Systemic vascular resistance

Pulmonary embolism:
âť‘ Anticoagulation in the absence of contraindications (I-B)

Aspirin toxicity:
âť‘ Sodium bicarbonate is the treatment for aspirin toxicity, usually common in elderly

Opioid overdose treatment
âť‘ Naloxone is used to reverse for opioid overdose

Infections treatment
âť‘ Start antibiotics depending upon the type of infections

Chronic medical therapy:
âť‘ Chronic ACE inhibitor: Hold if patient is hemodynamically unstable
âť‘ Chronic beta blocker:

âť‘ Hold if patient is hemodynamically unstable and/or in need or inotropes
❑ Decrease dose by ≥ half if patient is in moderate heart failure

âť‘ DO NOT INITIATE ACE INHIBITORS during an acute decompensation
âť‘ DO NOT INITIATE BETA BLOCKER during an acute decompensation; initiate beat blockers at a low dose in stable patients following optimization of volume status and D/C IV diuretics and inotropes (I-B)

Monitor laboratory tests:
❑CBC with differentials
❑ESR
❑Lactate
❑Urine toxins
❑Albumin
âť‘ BUN
âť‘ Creatinine
âť‘ Sodium (to detect hyponatremia which carries a poor prognosis), chloride, bicarbonate (to detect contraction alkalosis), serum potassium (to detect hypokalemia as a result of diuresis and which can precipitate arrhythmias), and magnesium

Management of hyponatremia:
âť‘ Water restriction

âť‘ <2 L/day if the Na is < 130 meq/L
âť‘ < 1 L/day or more if the Na is < 125 meq/L
Keep in mind that juices are essentially free water with sugar.
In the hyponatremia patient, drips should not be in D5W.

âť‘ Optimization of chronic home medications

âť‘ Persistent hyponatremia and risk of cognitive impairment: vasopressin antagonist for short term (hypervolemic)
 
 
 
 
 
Complete Diagnostic Approach

Complete Diagnostic Approach

A complete diagnostic approach should be carried out after a focused initial rapid evaluation is conducted and following initiation of any urgent intervention.

Abbreviations: ANA: Antinuclear antibody; ARDS: Acute respiratory distress syndrome; BNP: B-type natriuretic peptide; BUN: Blood urea nitrogen; CAD: Coronary artery disease; CBC: Complete blood count; CCB: Calcium channel blocker; CHF: Congestive heart failure; CT: Computed tomography; CXR: Chest X-ray; DM: Diabetes mellitus; ECG: Electrocardiogram; JVP: Jugular venous pressure; HF: Heart failure; HTN: Hypertension; LVEF: Left ventricular ejection fraction; LVH: Left ventricular hypertrophy; MI: Myocardial infarction; MRI: Magnetic resonance imaging; NT-pro BNP: N-terminal pro-brain natriuretic peptide; OCPs: Oral contraceptive pills; PAWP: Pulmonary artery wedge pressure; SBP: Systolic blood pressure; S1: First heart sound; S3: Third heart sound; TSH: Thyroid stimulating hormone

 
 
 
 
 
 
 
Characterize the symptoms:

Symptoms of Cardiogenic pulmonary edema
âť‘ Anxiety, restlessness
âť‘ Dyspnea

âť‘ At rest
âť‘ Exertional

âť‘ Paroxysmal nocturnal dyspnea
âť‘ Orthopnea
âť‘ Cough
âť‘ Excessive sweating or diaphoresis
âť‘ Grunting or gurgling sounds with breathing
âť‘ Pale or blue skin
âť‘ Blue or cyanotic lips

Symptoms of Noncardiogenic pulmonary edema
âť‘ Symptoms of noncardiogenic pulmonary edema are similar to cardiogenic pulmonary edema, the only difference is the acute onset of symptoms after inciting event

Symptoms suggestive of precipitating events
âť‘ Chest pain (suggestive of myocardial ischemia)
âť‘ Palpitations (suggestive of arrhythmias)
âť‘ Fever (suggestive of infection)
âť‘ Seizures (suggestive of CNS insult)


Nonspecific symptoms
âť‘ Nausea
âť‘ Weight gain


Obtain a detailed history:
âť‘ Past medical history

âť‘ Atrial fibrillation
âť‘ Cardiomyopathy
âť‘ Diabetes mellitus
âť‘ Hypertension
âť‘ Myocarditis
âť‘ Previous myocardial infarction
âť‘ Prior heart failure
âť‘ COPD
âť‘ Valvular heart disease
âť‘ Central nervous system injury

âť‘ Medication history

âť‘ Noncompliance with previously prescribed medications for heart failure
âť‘ Intake of the following drugs:
âť‘ Anticoagulants
âť‘ Aspirin
âť‘ Narcotics
âť‘ Heroin
âť‘ NSAID
âť‘ Morphine
âť‘ Methadone
âť‘ Dextropropoxyphene

âť‘ Family history

âť‘ History of dilated cardiomyopathy
âť‘ Radiation to the chest

âť‘ Surgical history

❑Recent surgery
❑Valve replacement surgeries

❑Recent history

âť‘ Opioid and aspirin overdose
âť‘ High altitudeascend
âť‘ Pulmonary embolism
âť‘ Head injury
âť‘ Seizures
âť‘ Electroconvulsive therapy

 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Examine the patient:

General appearance:
âť‘ Ill-looking
âť‘ In respiratory distress
âť‘ Inability to speak in full sentences

Vitals:
âť‘ Temperature

âť‘ Fever (suggestive of underlying infection)

âť‘ Pulse

âť‘ Tachycardia
âť‘ Narrow pulse pressure (<25% of SBP)

âť‘ Blood pressure

âť‘ Hypotension (suggestive of circulatory collapse)
âť‘ Hypertension

âť‘ Respiration

âť‘ Tachypnea (most common symptom)

❑ Pulse oximetry (maintain oxygen sat ≥ 94% unless COPD)

Weight:
âť‘ Measure weight daily at the same time after the first void
âť‘ Subtract ‘dry weight’ from current weight to estimate extent of volume overload and edema

Skin
âť‘ Cool and clammy (suggestive of hypoperfusion)
âť‘ Cyanosis (suggestive of severe hypoxemia)
âť‘ Anasarca
âť‘ Jaundice (suggestive of liver dysfunction secondary to right-sided fluid overload)

Neck examination:
âť‘ Jugular vein distention (suggestive of right-sided fluid overload)
âť‘ Positive hepatojugular reflux (suggestive of right-sided fluid overload)

Respiratory examination
âť‘ Tachypnea
âť‘ Wheeze
âť‘ Dullness at lung bases (suggestive of pleural effusion, may be present in chronic HF secondary to lymphatic compensation)
âť‘ Crackles/crepitations/rales (suggestive of pleural effusion)
âť‘ Cheyne-stokes respiration

Cardiovascular examination
âť‘ Displaced apex beat (suggestive of enlarged left ventricle)
âť‘ Parasternal heave (suggestive of elevated right ventricular pressure)
âť‘ S3 (typical) or S4 or both
âť‘ Soft S1
âť‘ Pulsus alternans
âť‘ S4 (suggestive of diastolic dysfunction)
âť‘ New or changed murmur (suggestive of an underlying valvular heart diseases)

âť‘ Mitral regurgitation – Holosystolic murmur
âť‘ Aortic regurgitation – Decrescendo diastolic murmur
âť‘ Aortic stenosis – Crescendo-decrescendo systolic ejection murmur with ejection click

Abdominal examination
The following findings suggest volume overload and / or poor forward cardiac output:
âť‘ Hepatojugular reflux
âť‘ Hepatomegaly
âť‘ Ascites

Extremity examination
âť‘ Pedal edema

Neurological examination
âť‘ Altered mental status
âť‘ Syncope (suggestive of aortic stenosis or pulmonary embolism)


Determine status of congestion and perfusion based on physical exam:
Congestion at rest (dry vs. wet)

“Wet” suggested by orthopnea, ↑JVP, positive hepatojugular reflux, abnormal valsalva response, rales, dullness upon percussion in bases, S3, peripheral edema, hepatomegaly, ascites, jaundice

Low perfusion at rest (warm vs. cold)

“Cold” suggested by narrow pulse pressure, cool extremities, hypotension, soft S1, pulsus alternans, decreased urinary output

The patient is:
âť‘ Warm and dry, OR
âť‘ Warm and wet, OR
âť‘ Cold and dry, OR
âť‘ Cold and wet

 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Order tests:

Routine (Class I, level of evidence C)

âť‘ CBC with differentials(rule out anemia and infections)
âť‘ ESR
âť‘ Lactate
âť‘ Urine toxicology
âť‘ Troponin
âť‘ Elevated in myocardial ischemia and acute cardiogenic pulmonary edema, particularly if creatinine clearance (CrCl) is reduced
❑ Troponin T ≥ 0.1 ng/mL (associated with poor survival)[2]
âť‘ Electrolytes
âť‘ Sodium: hyponatermia may occur due to fluid overlaod
âť‘ Serum calcium
âť‘ Serum magnesium can be lowered by diuresis
âť‘ Serum bicarbonate: to monitor contraction alkalosis with diuresis
âť‘ BUN, creatinine: may be elevated due to poor renal perfusion
âť‘ Urinalysis
âť‘ Fasting blood sugar
âť‘ Fasting lipid profile
âť‘ Liver function tests: can be elevated secondary to peripheral hypoperfusion
âť‘ TSH

âť‘ BNP or NT-pro BNP
Heart failure is unlikely if:[3][4]

❑ BNP ≤ 100 pg/mL, or
❑ NT-pro BNP ≤ 300 pg/mL

âť‘ Chest X-ray of Cardiogenic pulmonary edema (Class I, level of evidence C)

âť‘ Cardiomegaly (cardiothoracic ratio >50%)
âť‘ Cardiogenic pulmonary edema
âť‘ Kerley B lines
âť‘ Peribronchial cuffing
âť‘ Cephalization

âť‘ Chest X-ray findings of non-cardiogenic edema
❑Patchy alveolar infiltrates
âť‘ Air bronchograms

Chest X-ray findings in a patient with acute heart failure

âť‘ ECG (to help identify the cause of heart failure)

âť‘ Low QRS voltage (suggestive of infiltrative or dilated cardiomyoapthy)
âť‘ Arrhythmia (atrial fibrillation carries a poor prognosis and requires slowing of the heart rate to improve filling & cardiac output)
âť‘ Poor R wave progression (suggestive of a prior MI)
âť‘ Left ventricular hypertrophy (consistent with a history of hypertension)
âť‘ Left bundle branch block (LBBB) due to prior MI, may result in dysynchrony)
âť‘ Left atrial enlargement (due to valvular disease or hypertension)
âť‘ Non-specific ST segment and T wave changes may suggest ischemia

âť‘ 2-D echocardiography with Doppler
(Class I, level of evidence C)

âť‘ Assess chambers size, wall thickness, wall motion, and valve function
âť‘ Assess ejection fraction

âť‘ Radionuclide ventriculography or MRI

âť‘ To assess LVEF and volume when echocardiography is inadequate
âť‘ To assess myocardial infiltrative processes or scar burden (MRI)

âť‘ Coronary angiography looking for CAD
âť‘ Comprehensive metabolic panel if no evidence of CAD on coronary angiography
âť‘ Consider pulmonary artery catheterization in case of failure to respond to medical therapy, respiratory distress, shock, uncertainty regarding volume status, or increase in creatinine; assess the following parameters:

âť‘ PCWP
âť‘ Cardiac output
âť‘ Systemic vascular resistance

Order additional tests to rule out other etiologies:
âť‘ ANA and rheumatoid factor (for rheumatologic diseases)
âť‘ Diagnostic tests for hemochromatosis and pheochromocytoma
âť‘ Endomyocardial biopsy (when myocarditis is suspected)

 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Consider alternative diagnoses:

Alternative diagnosesFeatures
Acute asthmaâť‘ Wheeze
âť‘ Reversal of symptoms following
administration of bronchodilators
COPDâť‘ Increased cough
âť‘ Increased dyspnea
âť‘ Increased sputum production
ARDSâť‘ Severe hypoxia
âť‘ Bilateral opacities on chest X-ray
âť‘ PCWP < 15 mmHg
Pneumoniaâť‘ Fever, cough, sputum
âť‘ Consolidation on chest X-ray
Pulmonary embolismâť‘ Pleuritic chest pain, cough, S4
âť‘ Risk factors: trauma, immobilization, smoking, OCPs
âť‘ Clot in pulmonary artery on CT pulmonary angiography
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Assess the stage of heart failure using the ACCF/AHA staging system to guide chronic therapy
 
 
Prevention of pulmonary edema

Prevention of pulmonary edema

 
 
Prevention of pulmonary edema
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Non-cardiogenic pulmonary edema
 
Cardiogenic pulmonary edema
 
 
 
 
 
 
 
 
 
 
 
 
 
 

âť‘ Encourage healthy lifestyle and exercise
âť‘ Prevention for pulmonary edema associated with high altitude

âť‘ Gradual ascent
âť‘ Preacclimization
âť‘ Avoiding alcohol and drugs like ibuprofen, acetazolamide, sumatriptan, spironolactone, and steroids
âť‘ Adequate hydration
 

âť‘ Treat hypertension
âť‘ Treat dyslipidemia
âť‘ Control obesity
âť‘ Treat DM
âť‘ Avoid tobacco
âť‘ Avoid cardiotoxic agents

âť‘ Encourage healthy lifestyle and exercise
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

Consider additional measures in selected patients: âť‘ Administer ACE-I if history of MI or ACS and reduced EF to prevent symptoms and reduce mortality (I-A), in all decreased EF to prevent symptoms (I-A)
âť‘ Administer beta-blockers if history of MI or ACS and reduced EF to reduce mortality (I-B), in all reduced EF to prevent symptoms (I-C)
âť‘ Administer statins if history of MI or ACS to prevent symptoms (I-A)

❑ Consider ICD placement to prevent sudden death if asymptomatic ischemic cardiomyopathy, > 40 days post-MI, LVEF ≤30%, on adequate medical therapy, and good 1 year survival
 
 
 
Treatment of pulmonary edema

Treatment of pulmonary edema

 
 
 
 
Pulmonary edema treatment based on classification
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Cardiogenic pulmonary edema
 
 
 
 
Noncardiogenic pulmonary edema
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
âť‘ First step is to stabilize the patient
by following the ABCs of resuscitation,
that is, airway, breathing, and circulation
âť‘ Any associated arrhythmia
or myocardial infarction should be treated appropriately
❑Following drugs are used:
âť‘ ACE-I or ARB
❑Beta blockers
âť‘ Bisoprolol
âť‘ Carvedilol
âť‘ Sustained release metoprolol succinate

PLUS
❑Loop diuretics

âť‘ Starting dose
âť‘ Furosemide 20 to 40 mg, OR
âť‘ Torsemide 10 to 20 mg, OR
âť‘ Bumetanide 0.5 to 1 mg

âť‘ Monitor volume status and adjust dose
âť‘ No response: double oral diuretics dose rather than administer BID
❑No or minimal response despite maximal diuretic dose
then administer another diuretics BID or TID PLUS

❑Aldosterone antagonist
❑Vasopressin antagonists
âť‘ Conivaptan
❑Tolvaptan
âť‘ Type III phosphodiesterease inhibitors
❑Milrinone and enoximone
 
 
 
 
❑Treatment of the underlying cause is very important
âť‘ If the cause of pulmonary edema is overdose of

opioid overdose:

âť‘ Naloxone is used for the reversal of symptoms

âť‘ Salicylate toxicity

âť‘ Sodium bicarbonate is used for the treatment

âť‘ High altitude pulmonary edema treatment:

âť‘ Oxygen therapy is the first line therapy
âť‘ Nifedipine
❑Tadalafil and Sildenafil

❑Anticoagulants are used for the treatment of pulmonary edema due to pulmonary embolism

❑Antibiotics are used to treat underlying infections
 
 

Medications

Drug Class Drug Daily dose Maximum daily dose
Loop diuretics Furosemide
(duration of action: 6 to 8 h)
PO dose for chronic heart failure: 20 to 40 mg once or twice

IV dose for acute heart failure:

Initial dose given slowly (1 to 2 minutes)
❑ If patient is already on loop diuretics: IV dose ≥ home PO dose (rule of thumb: IV dose = 2.5x equivalent oral daily dose)
âť‘ If patient is not already on loop diuretics, administer IV starting dose of 20 to 40 mg
Continuous IV infusion:

Initial IV bolus administered slowly over 1 to 2 minutes, then continuous IV infusion rate of 10-40 mg/h

600 mg
Bumetanide
(duration of action: 4 to 6 h)
PO dose for chronic heart failure: 0.5 to 1.0 mg once or twice 10 mg
Torsemide
(duration of action: 12 to 16 h)
PO dose for chronic heart failure: 10 to 20 mg once 200 mg
Thiazide diuretics Chlorothiazide
(duration of action: 6 to 12 h)
PO: 250 to 500 mg once or twice 1000 mg
Hydrochlorothiazide
(duration of action: 6 to 12 h)
PO: 25 mg once or twice 200 mg
Metolazone
(duration of action: 12 to 24 h)
PO: 2.5 mg once 20 mg
K+– sparing diuretic Amiloride
(duration of action: 24 h)
PO: 5 mg once 20 mg
Spironolactone
(duration of action: 1 to 3 h)
PO: 12.5 to 25.0 mg once 50 mg
Triamterene
(duration of action: 7 to 9 h)
PO: 50 to 75 mg twice 200 mg
ACE inhibitors Enalapril 2.5 mg twice 10 to 20 mg twice
Lisinopril 2.5 to 5 mg once 20 to 40 mg once
Ramipril 1.25 to 2.5 mg once 10 mg once
ARBs Candesartan 4 to 8 mg once 32 mg once
Losartan 25 to 50 mg once 50 to 150 mg once
Valsartan 20 to 40 mg twice 160 mg twice
Beta blockers Bisoprolol 1.25 mg once 10 mg once
Carvedilol 3.125 mg twice 50 mg twice
Carvedilol CR 10 mg once 80 mg once
Metoprolol succinate extended release 12.5 to 25.0 mg once 200 mg once
Aldosterone antagonists Spironolactone 12.5 to 25.0 mg once 25 mg once or twice
Eplerenone 25 mg once 50 mg once
Inotropes Dopamine 5 to 10 mcg/kg/min, OR
10 to 15 mcg/kg/min
Dobutamine 2.5 to 5 mcg/kg/min, OR
5 to 20 mcg/kg/min
Milrinone 0.125 to 0.75 mcg/kg/min
Vasodilators Nitroglycerin 5 to 10 mcg/min, increase dose by 5-10mcg/min
every 3-5 mins as tolerated
Max is 400mcg/min
Nitroprusside 5 to 10 mcg/min, increase dose by 5-10mcg/min
every 5 mins as tolerated
Max is 400mcg/min
Nesiritide 2 mcg/kg bolus; then 0.01 mcg/kg/minute continuous infusion Max of 0.03 mcg/kg/minute
Morphine sulfate  2.5 – 5 mg bolus Max is 5mg
Hydralazine and isosorbide dinitrate Fixed-dose combination 37.5 mg hydralazine/20 mg isosorbide dinitrate 3 times daily 75 mg hydralazine/40 mg isosorbide dinitrate 3 times daily
Individual doses Hydralazine: 25 to 50 mg 3 or 4 times daily
Isosorbide dinitrate: 20 to 30 mg 3 or 4 times daily
Hydralazine: 300 mg daily in divided doses
Isosorbide dinitrate: 120 mg daily in divided doses
Digoxin

Loading dose: PO- 10 to 15 mcg/kg (half the total loading dose initially, then 1/4th the loading dose every 6 to 8 hours two times), OR
IV- 8 to 12 mcg/kg (half the total loading dose initially, then 1/4th the loading dose every 6 to 8 hours two times)
Maintenance dose: PO- 3.4 to 5.1 mcg/kg/day once daily, OR
IV- 2.4 to 3.6 mcg/kg/day once daily


Drugs that increase the concentration of digoxin include amiodarone, quinidine and verapamil

Type III phosphodiesterease inhibitors (PDEIs) Milrinone Loading dose: IV infusion 50mcg/kg admnistered over 10 min

Maintenance dose: IV infusion: 0.375 to 0.75 mcg/kg/minute

Inhibit degradation of cyclic AMP

 Enoximone  IV dose ranging from two doses of 25 mg to two doses of 100 mg.
Vasopressin Antagonists Conivaptan  For euvolemic or hypervolemic hyponatremia, following regimen is used:

Loading dose: IV: 20 mg infused over 30 minutes followed by a continuous infusion of 20 mg over 24 hours (0.83 mg/hour) for 2 to 4 days

Maximum dose of 40 mg over 24 hours
Tolvaptan
For Acute respiratory distress syndrome Corticosteroids

low-molecular-weight heparin 

Moderate-dose IV methylprednisolone, to 120 mg per kg per day for up to 25 days

40 mg of enoxaparin [Lovenox] or 5,000 units of dalteparin [Fragmin] subcutaneously per day) or low-dose, unfractionated heparin(5,000 units subcutaneously twice daily)

For high-altitude pulmonary edema Acetazolamide

Dexamethasone

250 mg PO q12h

4 mg PO q6h

References

References

  1. ↑ Yancy CW, Jessup M, Bozkurt B, Butler J, Casey DE, Drazner MH; et al. (2013). “2013 ACCF/AHA guideline for the management of heart failure: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines”. Circulation. 128 (16): 1810–52. doi:10.1161/CIR.0b013e31829e8807. PMID 23741057.
  2. ↑ Perna, ER.; MacĂ­n, SM.; Parras, JI.; Pantich, R.; FarĂ­as, EF.; Badaracco, JR.; Jantus, E.; Medina, F.; Brizuela, M. (2002). “Cardiac troponin T levels are associated with poor short- and long-term prognosis in patients with acute cardiogenic pulmonary edema”. Am Heart J. 143 (5): 814–20. PMID 12040342. Unknown parameter |month= ignored (help)
  3. ↑ McMurray JJ, Adamopoulos S, Anker SD, Auricchio A, Böhm M, Dickstein K; et al. (2012). “ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2012: The Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association (HFA) of the ESC”. Eur Heart J. 33 (14): 1787–847. doi:10.1093/eurheartj/ehs104. PMID 22611136.
  4. ↑ Fuat A, Murphy JJ, Hungin AP, Curry J, Mehrzad AA, Hetherington A; et al. (2006). “The diagnostic accuracy and utility of a B-type natriuretic peptide test in a community population of patients with suspected heart failure”. Br J Gen Pract. 56 (526): 327–33. PMC 1837840. PMID 16638247.

Editor-In-Chief:
C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2], Farnaz Khalighinejad, MD [3]