Common Causes of Dysrhythmias

Cardiac Causes

•  Accessory Pathways
•  Cardiomyopathy
•  Conduction defects
•  Heart failure
• Myocardial cell degeneration
• Myocardial infarction
•  Valve disease

Common Causes of Dysrhythmias

Non-Cardiac Causes

•  Acid-base imbalances
•  Alcohol
•  Caffeine, tobacco
•  Connective tissue disorders
•  Drug effects (antidysrhythmia drugs, stimulants, beta-adrenergic blockers, drug toxicity
•  Electric shock
•  Electrolyte imbalances (hypo/hyperkalemia, hypo/hypercalcemia)
•  Emotional crisis
•  Herbal supplements
• Hypoxia, shock
•  Metabolic conditions (thyroid dysfunction)
•  Near-drowning
•  Poisoning

Diagnostic studies and Treatments for Dysrhythmias

• Electrophysiology Test (EPS)
• Head-upright tilt-table test
• Cardiac Stress Tests
• Holter Monitor

Normal Sinus Rhythm

•  Rate: 60-100 bpm
• Rhythm: P-P interval regular, R-R interval regular
•  P waves: Positive (upright), one precedes each QRS complex, P waves look alike.
•  PR interval: 0.12-0.20 second and consistent from beat to beat.
•  QRS duration: 0.10 second or less an intraventricular conduction delay exists.

Sinus Bradycardia

Atropine/Transcu Pacemaker

•  Rate: Less than 60 bpm
• Rhythm: P-P interval regular, R-R interval regular.
•  P waves: Positive (upright), precedes each QRS complex, P waves look alike.
•  PR interval 0.12-0.20 second consistent from beat to beat.
•  QRS duration: 0.10 second or less unless intraventricular conduction delay exists.

Sinus Tachycardia

Treat the cause

Adenosine/BBlocker

•  Rate: 101-180 bpm
•  Rhythm: P-P interval regular, R-R interval regular.
•  P waves: Positive (upright), one precedes each QRS complex, P waves look alike. At fast  rates it may be hard to tell the difference between a P wave and a T wave.
•  PR interval: 0.12-0.20 second (may shorten with faster rates) and consistent from beat to beat.

Sinus Arrhythmia

•  Rate: Usually 60-100 bpm, but may be slower or faster.
•  Rhythm: Irregular, phasic with respiration; heart rate increases gradually during inspiration (R-R intervals shorten) and decreases with expiration (R-R intervals lengthen).
•  P waves: Positive (upright), one precedes each QRS complex, P waves look alike.
•  PR interval: 0.12-0.20 second and consistent from beat to beat.
•  QRS duration: 0.10 second or less unless an intraventricular conduction delay exists.

Premature Atrial Contraction

•  Rate: usually 60-100 bpm
•  Rhythm: irregular
•  P wave: abnormal shape
•  PR interval: normal
•  QRS complex: normal (usually)

Atrial Fibrillation

Anticoags/Cardioversion

•  Rate: atrial: 350-600 bpm, ventricular:>or< 100 bpm
•  Rhythm: irregular
•  P wave: fibrillatory
•  PR interval: not measurable
•  QRS complex: normal (usually)

Atrial Flutter

•  Rate: atrial: 250-350 bpm, ventricular: >or< 100 bpm
•  Rhythm: atrial: regular, ventricular: may be regular or irregular
•  P wave: flutter(F) waves (sawtooth pattern) more flutter waves than QRS complexes;  may occur in a 2:1, 3:1, 4:1, etc. pattern
•  PR interval not measurable
•  QRS complex: normal (usually)

Paroxysmal Supraventricular Tachycardia (PSVT)

 Bare down/Ice on face

 Adenosine! Fast follow w/flush

•  Rate: 100-300 bpm
•  Rhythm: regular or slightly irregular
•  P wave: often hidden in the preceding T wave, but if seen, it may have an abnormal shape
•  PR interval: may be shortened or normal
•  QRS complex: usually normal

Junctional Dysrhthmias

•  Rate: 40-60 bpm, accelerated junctional rhythm is 61-100 bpm, junctional tachycardia 101-
• 150 bpm
•  Rhythm: regular
•  P wave: abnormal in shape and inverted or hidden in the QRS complex
•  PR interval: <0.12 when the P wave precedes the QRS complex
•  QRS complex: usually normal

Heart Blocks

First Degree Heart Block

 Rate: 60-100 bpm

 Rhythm: regular

 P wave: normal

 PR interval: >0.20 seconds

 QRS complex: normal

Second-Degree Heart Block

Type I (Mobitz I, Wenchkebach)

 Rate: atrial: 60-100 bpm, ventricular: may be slower as a result of nonconducted or blocked

 QRS complexes.

 Rhythm: atrial: regular, ventricular: irregular

 PR interval: progressive lengthening

 QRS complex: normal QRS, with pattern of one nonconducted or blocked QRS complex.

Second-Degree Heart Block

Type II (Mobitz II)

 Rate: atrial: usually normal, ventricular: slower

 Rhythm: atrial: regular, ventricular: regular or irregular

 P wave: more P waves than QRS complexes (2:1, 3:1)

 PR interval: normal or prolonged

 QRS complex: widened QRS width, with pattern of one nonconducted (blocked) QRS

 complex

Third-Degree Heart Block

 Rate: atrial: 60-100 bpm, ventricular: 20-40 bpm

 Rhythm: atrial: regular but may appear irregular due to P waves hidden in the QRS

 complexes

 P wave: normal, but no connection with the QRS complex

 PR interval: variable

QRS complex: normal or widened, no relationship with P waves

Ventricular Tachycardia

 Rate: 150-250 bpm

 Rhythm: regular or irregular

 P waves: occurring independently of the QRS complex, and usually buried in the QRS

 complex

 PR interval: not measurable

 QRS complex: distorted

What drug is used for Ventricular Dysrythmias

Lidocaine

Ventricular Fibrillation

Course ventricular fibrillation

Fine ventricular fibrillation

For V-Fib we D-Fib

Asystole

CPR/

Asystole

P-wave asystole (also known as ventricular standstill)

Pulseless Electrical Activity (PEA)

• Pulseless electrical activity (PEA) describes a situation in which electrical activity can be observed on the ECG but there is no mechanical activity of the ventricles and the patient has no pulse.
• Prognosis is poor unless the underlying cause can be identified and quickly corrected.

Causes of PEA

5 T’s

Toxins

Tamponade (cardiac)

Tension pneumothorax

Thrombosis (coronary or pulmonary)

Trauma

6 H's

Hypovolemia

Hypoxia

Hydrogen ion (acidosis)

Hypo/hyperkalemia

Hypoglycemia

Hypothermia

Antidysrhythmia Drugs

• Amiodarone-
• Adenosine-PSVT
•  Atropine- symptomatic bradycardia
• Diltiazem
• Digoxin
• Lidocaine-Ventricular Dsyrth.

Digoxin

Check for digoxin or digitalis toxicity. Pulse rate (heart rate) should be above 60 bpm. Monitor serum level of digoxin (therapeutic range: 0.5 to 2 ng/ml).

[image]

Therapeutic Effects/Uses To treat HF, atrial tachycardia, flutter, or fibrillation

Contraindications Ventricular dysrhythmias, second- or third-degree heart block

Caution:AMI, renal disease, hypothyroidism, hypokalemia

HEART FAILURE

Heart failure (HF) is an abnormal clinical condition involving impaired cardiac pumping. It results in the characteristic pathophysiologic changes of vasoconstriction and fluid retention.

HF is characterized by ventricular

dysfunction, reduced exercise tolerance, diminished quality of life, and shortened life

expectancy.

Primary causes of HF

CAD

Hypertension

Diabetes

Has low systemic arterial blood pressure (BP), low CO, and poor renal perfusion. Poor exercise tolerance and ventricular dysrhythmias are also common.

Fatigue

Dyspnea

Tachycardia

Edema

Nocturia

Skin changes

Behavioral changes

Chest pain

Weight changes

Pleural Effusion

Dysrhythmias

Left Ventricular Thrombus

Hepatomegaly

Renal Failure

History and Physical exam

Chest x-ray

Electrocardiogram

Laboratory data

Cardiac enzymes

BNP

Serum chemistries

LFT’s, TFT’s, CBC

Echocardiogram

Stress testing

Cardiac catheterization

Decreasing Intravascular Volume

Decreasing Venous Return

Decreasing Afterload

Improving Gas Exchange and Oxygenation

Improving Cardiac Function

Reducing Anxiety

Diuretics

Vasodilators

ACE –inhibitors

Nitrates

Human b-Type Natriuretic Peptide

Beta-blockers

Positive Inotropes

Digitalis Glycosides, B-adrenergic anonists, Calcium sensitizers

Angiogensin II Receptor Blockers

BiDil

The edema of chronic HF is often treated by dietary restriction of sodium.Fluid restrictions are not commonly  prescribed for the client with mild to moderate HF. Instructing clients to weigh themselves daily is important for monitoring fluid retention, as well as weight reduction.

Infective endocarditis

Acute pericarditis

Myocarditis

Rheumatic fever and heart disease

Cardiomyopathy

Valvular heart disease

Mitral valve stenosis/regurgitation/prolapse

Aortic valve stenosis/regurgitation

Tricuspid and pulmonic valve disease

Treatment with PCN therapy

Propholatic antibiotics prior to dental work or surgeries!

The subacute form typically affects those with preexisting valve disease and has a clinical course that may extend over months. In contrast, the acute form typically affects those with healthy valves and presents as a rapidly progressive illness.

Prior endocarditis

Prosthetic valves

Acquired valve disease (e.g., mitral valve prolapse with murmur, calcified aortic stenosis)

Cardiac lesions (e.g., ventricular septal defect)

Rheumatic heart disease (e.g., mitral valve regurgitation)

Congenital heart disease

Pacemakers

Marfan syndrome

Asymmetric septal hypertrophy

Cardiomyopathy

Noncardiac Conditions

Intravenous drug abuse

Nosocomial bacteremia

Procedure-Associated Risks

Intravascular devices (e.g., pulmonary artery catheters)

Procedures

Fever

Chills

Weakness

Malaise

Fatigue

Anorexia

Arthralgia

Myalgias

Back pain

Abdominal pain

Weight loss

Headache

Clubbing of fingers

Vascular manifestations

Splinter hemorrhages

Petichiae

Microembolization of vegatative lesions

Rheumatic heart disease was, at one time, the most common cause of IE; it now accounts for <20% of cases. Currently, the main contributing factors include (1) aging (>50% of older people have calcified aortic stenosis); (2) IVDA; (3) use of prosthetic valves; (4) proliferation of intravascular device placement, resulting in nosocomial infections; and (5) renal dialysis. Left-sided endocarditis is more common in patients with bacterial infections and underlying heart disease. The primary cause of right-sided endocarditis is IVDA. However, there has been an increase in left-sided valves being affected, especially with

cocaine abuse. S. aureus is the most common etiologic organism in IVDA IE.

Health history and physical assessment including any recent procedures or surgeries

Previous history of IVDA, heart disease, recent cardiac catheterization, cardiac surgery,intravascular device placement, renal dialysis, or infections

Lab data

Blood cultures, CBC

New or changed cardiac murmur

Intracardiac mass or vegetation noted on echocardiography

TEE

Chest x-ray

Acute pericarditis most often is idiopathic, with a variety of suspected viral causes. The coxsackievirus B group is the most commonly identified virus. In addition to idiopathic or viral pericarditis, other causes of this condition include uremia, bacterial infection, acute

myocardial infarction (MI), tuberculosis, neoplasm, and trauma. Pericarditis in the acute MI patient may be described as two distinct syndromes. The first is acute pericarditis, which may occur within the initial 48 to 72 hours after an MI. The second is Dressler syndrome

(late pericarditis), which appears 4 to 6 weeks after an MI.

Hallmark finding is pericardial friction rub

Severe chest pain

Dyspnea

Rapid, shallow respirations

Fever

Anxiety

Pericardial effusion- accumulation of excess fluid around the pericardium.

Cardiac tamponade- develops as the pericardial effusion progresses, increasing the pressure

surrounding the heart to increase

Chest pain

Confusion, anxiety and restlessness

Muffled heart sounds

Narrowed pulse pressure

Tachypnea

Tachycardia

JVD

Pulsus paradoxus

Corticosteroids (if not responding to NSAIDs) 

Pericardiocentesis

History and physical

ECG

Chest x-ray

CT/MRI

Laboratory tests

CRP, ESR, WBCs

Patient teaching: report any fever/early sign, stay away from people with colds/flu. Good oral hygeine. Monitor temp.

The management of the patient's pain and anxiety during acute pericarditis is a primary nursing consideration. Assessment of the amount, quality, and location of the pain is important, particularly in distinguishing the pain of myocardial ischemia (angina) from the

pain of pericarditis. Pericarditic pain is usually located in the precordium or left trapezius ridge and has a sharp, pleuritic quality that increases with inspiration. Pain is often relieved by sitting or leaning forward, and worsened when lying supine. ECG monitoring can aid in

distinguishing these types of pain because ischemia usually involves localized ST segment changes, as compared to the diffuse ST segment changes present in acute pericarditis.

Myocarditis is a focal or diffuse inflammation of the myocardium. Possible causes include viruses, bacteria, fungi, radiation therapy, and pharmacologic and chemical factors. Viruses, particularly coxsackievirus types A and B, are the most common etiologic agents in the United States and Canada. Autoimmune disorders (e.g., polymyositis) also have been associated with the development of myocarditis. Myocarditis may also occur when no causative agent or factor can be identified (i.e., idiopathic). Myocarditis is frequently associated with acute pericarditis, particularly when it is caused by coxsackievirus B strains.

Fever

Fatigue

Malaise

Myalgias

Pharyngitis

Dyspnea

Lymphadenopathy

Nausea/vomiting

Sudden Cardiac Death

Digoxin

Diuretics

Nitropress

Inocor

Primacor

Prednisone

Imuran

Cyclosporine

IVIG

Antiviral agents

Oxygen

Bedrest/restricted activity

ECG

Laboratory studies

Endomyocardial biopsy (EMB)

MRI

Echocardiogram

Decreased CO is an ongoing nursing diagnosis in the care of the patient with myocarditis. Interventions focus on assessment for the signs and symptoms of HF. Important nursing measures to decrease cardiac workload include the use of the semi-Fowler's position, spacing of activity and rest periods, and provisions for a quiet environment. Prescribed medications that increase the heart's contractility and decrease preload, afterload, or both require careful monitoring. Ongoing evaluation of the effectiveness of these interventions is necessary.

Rheumatic Fever and Heart Disease

Rheumatic fever is an inflammatory disease of the heart potentially involving all layers (endocardium, myocardium, and pericardium) of the heart. Rheumatic heart disease is a chronic condition resulting from rheumatic fever that is characterized by scarring and deformity of the heart valves.

Rheumatic fever is an inflammatory disease of the heart potentially involving all layers (endocardium, myocardium, and pericardium) of the heart. Rheumatic heart disease is a chronic condition resulting from rheumatic fever that is characterized by scarring and deformity of the heart valves.

Major Criteria

Carditis

Mono/polyarthritis-most common/swelling,red, tender large joints/knees

Chorea

Erythema marginatum

Subcutaneous nodules

Minor Criteria

Evidence of Infection

Myocardial involvement is characterized by Aschoff bodies

A complication that can result from ARF is chronic rheumatic carditis. It results from changes in valvular structure that may occur months to years after an episode of ARF. Rheumatic endocarditis can result in fibrous tissue growth in valve leaflets and chordae tendineae with scarring and contractures. The mitral valve is most frequently involved. Other valves that may be affected are the aortic and tricuspid valves.

History and physical examination

Laboratory findings

Chest x-ray

Echocardiogram

ECG

Bed rest

Antibiotics

Corticosteroids

Salicylates

NSAIDs

Cardiomyopathy (CMP) constitutes a group of diseases that directly affect the structural or functional ability of the myocardium. A diagnosis of CMP is made based on the patient's clinical manifestations and noninvasive and invasive diagnostic procedures.

Dilated Cardiomyopathy

Hypertrophic Cardiomyopathy

Restrictive Cardiomyopathy

Fatigue

Dyspnea at rest

Paroxysmal nocturnal dyspnea

Orthopnea

Dry cough

Palpitations

Abdominal bloating

Nausea/vomiting

Anorexia

Dysrhythmias

Abnormal S3 or S4

Crackles

Peripheral edema

Weak peripheral pulses

Pallor

Hepatomegaly

JVD

History and physical

ECG

Laboratory tests

Chest x-ray

Echocardiogram

Nuclear imaging studies

Cardiac catheterization

Endocardial biopsy

Treatment of underlying cause

Drug therapy

Nitrates

Beta blockers

Antidysrhythmics

ACE inhibitors

Diuretics

Digitalis

Anticoagulants

Ventricular assist device

Cardiac resynchronization therapy

ICD

Surgical correction

Cardiac transplant

Chronic constrictive pericarditis results from scarring with consequent loss of elasticity of the pericardial sac. It usually begins with an initial episode of acute pericarditis (often secondary to idiopathic causes, cardiac surgery, or radiation) and is characterized by fibrin

deposition with a clinically undetected pericardial effusion. Reabsorption of the effusion slowly follows, with progression toward the chronic stage of fibrous scarring, thickening of the pericardium from calcium deposition, and eventual obliteration of the pericardial space.

The fibrotic, thickened, and adherent pericardium encases the heart, thereby impairing the ability of the atria and ventricles to stretch adequately during diastole.

ECG

Echo

Chest X-Ray

MI

Chronic Rheumatic Heart Disease

Mitral Valve Prolaspe

Ischemic papillary muscle dysfunction

IE

Rapid assessment (e.g., cardiac catheterization) and intervention (e.g., valve repair or replacement) are critical for a positive outcome.

Acute—generally poorly tolerated, with fulminating pulmonary edema and shock developing rapidly; new systolic murmur. Thready pulses and cool clammy extremities.

Chronic—weakness, fatigue, exertional dyspnea, palpitations; an S₃ gallop, holosystolic or pansystolic murmur. Orthopnea, PND, periphal edema

In this valvular abnormality, the mitral leaflets have prolapsed back into the left atrium.

MVP is the most common form of valvular heart disease in the United States, occurring 2 times more frequently in women than men.

Palpitations, dyspnea, chest pain, activity intolerance, syncope; midsystolic click, late or holosystolic murmur

1. Teach patient the importance of antibiotic prophylaxis for endocarditis before undergoing certain dental or surgical procedures if the patient has MVP with regurgitation (see Table 37-3)

2. Instruct patient to take medications as prescribed (e.g., β-adrenergic blockers to control palpitations, chest pain).

3. Advise patient to adopt healthy eating patterns and to avoid caffeine because it is a stimulant and may exacerbate symptoms.

4. Counsel patient who uses diet pills or other over-the-counter drugs to check for common ingredients that are stimulants (e.g., caffeine, ephedrine) as these will exacerbate symptoms.

5. Help patient to develop and implement an exercise program to maintain optimal health.

6. Instruct patient to contact Emergency Medical Services or health care provider if symptoms develop or worsen (e.g., palpitations, fatigue, shortness of breath, anxiety).

Rheumatic Heart Disease

Dyspnea on exertion, hemoptysis; fatigue; palpitations; loud, accentuated S₁; low-pitched, rumbling diastolic murmur; atrial fibrillation on ECG

Congenitally abnormal stenotic aortic valves are generally discovered in childhood, adolescence, or young adulthood. In older patients, aortic stenosis is a result of rheumatic fever or senile fibrocalcific degeneration that may have an etiology similar to coronary artery disease

Angina, syncope, dyspnea on exertion, heart failure; normal or soft S₁, diminished or absent S₂, systolic crescendo-decrescendo murmur, prominent S4

Aortic valve regurgitation may be the result of primary disease of the aortic valve leaflets, the aortic root, or both. Acute aortic regurgitation (AR) is caused by IE, trauma, or aortic dissection and constitutes a life-threatening emergency. Chronic AR is generally the result of rheumatic heart disease, a congenital bicuspid aortic valve, syphilis, or chronic rheumatic conditions such as ankylosing spondylitis or Reiter's syndrome.

Acute—abrupt onset of profound dyspnea, chest pain, left ventricular failure and shock

Chronic—fatigue, exertional dyspnea, orthopnea, PND; water-hammer pulse; heaving precordial impulse; diminished or absent S₁, S₃, or S₄; soft decrescendo high-pitched diastolic murmur, Austin-Flint murmur, systolic ejection click

Instruct patient to take all medications as prescribed and to follow up with health care provider.

 Encourage patient to use a low-sodium diet (if ordered) and to read all product labels (food and over-the-counter drugs) for sodium content.

 Unless fluids are restricted, patient should be encouraged to drink 6 to 8 glasses of water a day.

 Encourage patient to achieve and maintain a reasonable weight and avoid large meals.

Advise patient to avoid alcohol, caffeine, diet pills, and over-the-counter cold medicines that may contain stimulants.

 Teach patient to balance activity and rest periods.

 Instruct patient to avoid heavy lifting or vigorous isometric exercises and to check with health care provider for exercise guidelines.

 Encourage the use of stress reduction activities: relaxation to relieve tension, guided imagery, diversional activities (see Chapter 9).

 Instruct patient to report any signs of heart failure to health care provider, including weight gain, edema, shortness of breath, and increased fatigue.

Suggest that family members learn CPR because of the potential of sudden cardiac arrest (see Appendix A).

Instruct patient to notify health care provider or dentist before any invasive medical/dental procedures as patients with cardiomyopathy are at risk for endocarditis (see Table 37-3).

Drug Alert - Adenosine (Adenocard)       

Monitor patient's ECG continuously. Brief period of asystole may be observed.Observe patient for flushing dizziness chest pain or palpitations.

1. Follow up with primary care provider for inspection of ICD insertion site and routine interrogation of the ICD.

2. Report any signs of infection at incision site (e.g., redness, swelling, drainage) or fever to your primary care provider immediately.

3. Keep incision dry for 4 days after insertion.

4. Avoid lifting arm on ICD side above shoulder until approved by your primary care provider.

5. Discuss resuming sexual activity with your primary care provider. It is usually safe to resume sexual activity once your incision is healed.

6. Avoid driving until cleared by your primary care provider. This decision is usually based on the ongoing presence of dysrhythmias, the frequency of ICD firings, your overall health, and state laws regarding drivers with ICDs.

7. Avoid direct blows to ICD site.

8. Avoid large magnets and strong electromagnetic fields because these may interfere with the device.

9. You should never have a magnetic resonance imaging (MRI) scan.

10. When traveling, airport security should be informed of presence of ICD because it may set off the metal detector. If handheld screening wand is used, it should not be placed directly over the ICD.

11. If your ICD fires, you should call your health care provider immediately.

12. If your ICD fires and you do not feel well, you should contact the emergency medical services (EMS) system

13. If your ICD fires more than once, you should contact EMS.

14. A Medic Alert ID or bracelet should be worn at all times.

15. Always carry the ICD identification card and a current list of your medications.

16. Family memebers should learn CPR

1. Maintain follow-up care with your primary care provider to check the pacemaker site and begin regular pacemaker function checks.

2. Report any signs of infection at incision site (e.g., redness, swelling, drainage) or fever to your primary care provider immediately.

3. Keep incision dry for 4 days after implantation.

4. Avoid lifting arm on pacemaker side above shoulder until approved by your primary care provider.

5. Avoid direct blows to pacemaker site.

6. Avoid close proximity to high-output electric generators or large magnets such as an MRI scanner. These devices can interfere with the function of the pacemaker.

7. Microwave ovens are safe to use and do not interfere with pacemaker function.

8. Travel without restrictions is allowed. The small metal case of an implanted pacemaker rarely sets off an airport security alarm.

9. Monitor pulse and inform primary care provider if it drops below predetermined rate.

10. Carry pacemaker information card at all times.

11. A Medic Alert ID or bracelet should be worn at all times.

Drug Alert - Nitroprusside (Nipride)

Too rapid rate of IV administration can reduce BP too quickly.

Headache, nausea, dizziness, dyspnea, blurred vision, sweating, and restlessness can occur.

Assess BP prior to administration and continuously during administration.

Drug Alert - Dopamine (Intropin)

Extravasation with tissue sloughing may occur with IV administration.

Monitor IV site for extravasation to prevent necrosis.

High dosages may produce ventricular dysrhythmias.

Drug Alert - Spironolactone (Aldactone)

Assess for hyperkalemia during treatment.

Use with caution in patients taking digoxin as hyperkalemia may reduce the effects of digoxin.

Instruct patient to avoid foods high in potassium (e.g., bananas, oranges, dried apricots).

Drug Alert - Captopril (Capoten)

Excessive hypotension may occur.

Monitor patient for first-dose hypotension (first-dose syncope).

Skipping doses or discontinuing the drug can result in rebound hypertension.

Drug Alert - Carvedilol (Coreg)

Overdosage can produce profound bradycardia, hypotension, bronchospasm, and cardiogenic shock.

Assess BP and pulse at beginning of treatment and q4hr.

Abrupt withdrawal may result in sweating, palpitations, and headaches.

 Written discharge instructions or educational material must be given to the patient or caregiver and include all of the following: activity level, diet, discharge medications, follow-up appointment, weight monitoring, and symptom management.

Left ventricular function must be documented in the hospital record to indicate that it was assessed before or during hospitalization or will be assessed after discharge.

 Patients with known systolic dysfunction of moderate to severe impairment (ejection fraction less than 40%) and without contraindication to angiotensin-converting enzyme inhibitor will be prescribed an angiotensin-converting enzyme inhibitor at hospital discharge. An angiotensin receptor blocker is an acceptable alternative for patients with contraindication to angiotensin-converting enzyme inhibitors.

Patients who are current smokers or former smokers who quit in the past 12 months will be given smoking cessation advice or counseling during the hospital stay.