Chapter 24 Management of Patients w/Structural, Infectious, & Inflammatory Cardiac Disorders Flashcards
Functions of the Heart
Pumping
-Pumping oxygenated blood to the other body parts
- Pump hormones and other vital substances to different parts of the body
Receiving deoxygenated blood and carrying metabolic waste products from the body
Maintain BP
Heart Failure (HF)
A clinical syndrome resulting from structural or functional cardiac disorders that impair the ability of a ventricle to fill or eject blood
-The heart is unable to pump enough blood to meet the body’s metabolic demands or needs
Heart Failure Risk Factors
Cigarette smoking, obesity, poorly managed diabetes,
and metabolic syndrome
The onset of HF is typically a …
…morbid consequence of another disease
- CAD, HTN, cardiomyopathy, valvular disorders, and renal dysfunction
What is the primary cause of heart failure?
Atherosclerosis
Pathophysiology of HF
Significant myocardial dysfunction occurs before the patient experiences signs/symptoms of HF such as SOB, edema, or fatigue.
- Ischemic Heart Disease
- Hyperthyroidism
- MI
- Valve disease
- Alcohol, cocaine use
- HTN
-> Leads to decreased CO, decreased systemic BP, and decreased kidney perfusion
As HF develops the body compensates to cope with the HF and are responsible for the signs/symptoms.
-Baroreceptor activation
->Stimulation of vasomotor regulatory centers in medulla
-> SNS activation
-> Increased secretion of epinephrine & norepinephrine
- RAAS system activation
* Increased aldosterone secretion
-> Na+ & water reabsorption
Both lead to vasoconstriction
- Increased afterload
- Increased BP & HR
The most common type of HF is systolic HF, also HF w/reduced Ejection Fracture (EF).
LT Sided Heart Failure
Occurs when the LV, the heart’s main pumping power source is gradually weakened
- The heart is unable to pump
O2-rich blood from the lungs to heart’s LT atrium, into the LV and on through the body and the heart must work harder
Clinical Manifestations of LT-sided HF
Pulmonary Congestion
-Dyspnea & cough
-Crackles & decreased O2 sat
-S3 gallop & orthopnea
-Paraoxysmal nocturnal dyspnea (PND)
Decreased Tissue Perfusion
- Decreased CO
- Decreased EF
- Decreased SV
- Increased Catecholamines (impedes perfusion over time)
Progressive Symptoms
- Decreased GI perfusion
- Decreased brain perfusion (lightheadedness, confusion, restlessness, & anxiety)
- Pale, ashen, cool, & clammy skin
- Tachycardia, palpitations, fatigue, nocturia
S3 Sound
Early diastolic sound
Low pitched
Suggest poor systolic function and/or volume overload
Occurs when mitral valve opens & blood enters overfilled ventricle
Paraoxysmal Nocturnal Dyspnea
Shortness of breath that occurs suddenly during sleep
RT-Sided Heart Failure
Inability of the RT ventricle to fill or eject sufficient blood into pulmonary circulation
Pathophysiology of RT-sided HF
Increased venous pressure leads to JVD and ↑ capillary hydrostatic pressure throughout the venous system → systemic clinical manifestations.
* Right-sided failure can occur as a result of left-sided failure
Clinical Manifestations of RT-sided HF
Jugular vein distension (JVD) - From increased venous pressure
Dependent edema of the lower extremities
Hepatomegaly: Results from enlargement of the liver from venous
engorgement
Ascites due to fluid in the peritoneal cavity
Loss of appetite from nausea & pain
Generalized weakness: Decreased CO & impaired circulation
Ascites
Accumulation of serous fluid in the peritoneal cavity
Acute Decompensated Heart Failure (ADHF) Early Clinical Manifestations
1) Increase in RR
2) Decrease in PaO2
Acute Decompensated Heart Failure (ADHF) Later Clinical Manifestations
1) Interstitial edema
2) Tachypnea
Acute Decompensated Heart Failure (ADHF) Further Progression Clinical Manifestations
1) Alveolar edema
2) Resp Acidemia
Nursing Process for Heart Failure
Assessment – effective of therapy, self-care strategies, explore emotional status
Health History – focus on the signs/symptoms of HF, ask about # of pillows used for sleeping (compensation for orthopnea), edema, abdominal symptoms, AMS, ADLs, and understanding of HF
Physical Examination
LOC (↓ O2 to the brain)
Respirations and lungs fields are auscultated to detect crackles and wheezes
Evaluate BP for hypotension or hypertension
Auscultated heart for S3 heart sound which is an early sign of ↑ blood volume in the ventricles
Document HR and rhythm; patient may be placed on continuous ECG if hospitalized
Assess JVD with the patient sitting at at 45-degree angle (distended > 4cm above sternal angle → Right HF
Assess pulses, skin, lower legs for edema, abdomen for hepatomegaly, monitor I/O’s, and daily weight
Planning & Goals for the Patient w/ HF
Promote activity and reduce fatigue
Relieve fluid overload symptoms
Decrease anxiety or increase the patient’s ability to manage anxiety
Encourage the patient to verbalize his or her ability to make decisions and influence outcomes
Educate the patient and family about management of the therapeutic regimen
Diagnostic Testing for Heart Failure
Echocardiogram- determines ejection fraction (EF) and confirms dx of HF. An expected EF is 55%-65% of the
ventricular volume. EF is a measure of ventricular contractility
CXR
12-lead ECG
Serum electrolytes & CBC
BUN & Creatinine
Liver function tests
BNP test (Brain natriuretic peptide)- key indicator of HF; high levels are signs of high cardiac filling pressure and
aids in diagnosis and management of HF.
Which test is the key indicator for heart failure?
BNP test
Normal BNP Level
Less than 100
What does a high BNP level indicate?
A high BNP level indicates high cardiac filling pressure & the presence of HF
-The higher the BNP, the worse the HF gets
Select Medications for the Patient w/HF
Diuretics: ↓ fluid volume overload; observe for electrolyte abnormalities ↑ K+ (spironolactone), ↓ Na, ↓ BP
ACE inhibitors: ↓ BP, ↓ afterload; observe for cough and worsening renal function, ↓ BP, ↑ K+ (critical in the Tx for
CHF
Beta Blockers: dilates blood vessels, ↓ afterload, and improves exercise capacity; observe for ↓ HR, dizziness, fatigue, and symptomatic ↓ BP
Digitalis: Improves cardiac contractility; observe for ↓ HR and digitalis toxicity
Adjunct Therapies for Heart Failure
Nutritional Therapy: Low Na+2 diet (no more than 2 g/day) to prevent fluid overload
-Omega-3 supplements are recommended to reduce fatal CV events
Supplemental Oxygen: Oxygen therapy may become necessary as HF progresses based on degree congestion and hypoxia
- Some patients require supplemental oxygen during periods of activity
Management of Sleep Disorders: Sleep apnea is common in HF patients
- Continuous positive airway pressure (CPAP) is suggested to reduce apneic episodes and improve sleep
Nursing Process for HF: Health History
Focus on the signs/symptoms of HF
Ask about # of pillows used for sleeping
-Assess for paraoxysmal nocturnal Dyspnea
Edema
Abdominal symptoms
AMS
ADLs
Understanding of HF
Nursing Process for HF: Physical Examination
LOC (↓ O2 to the brain)
Respirations and lungs fields are auscultated to detect crackles and wheezes
Evaluate BP for hypotension or HTN
Auscultated heart for S3 heart sound which is an early sign of ↑ blood volume in the ventricles
Document HR and rhythm; patient may be placed on continuous ECG if hospitalized
Assess JVD with the patient sitting at at 45-degree angle (distended > 4cm above sternal angle → Right HF
Assess pulses, skin, lower legs for edema, abdomen for hepatomegaly, monitor I/O’s, and daily weight
Nursing Interventions for the Patient w/ HF: Promote Activity Tolerance
Bed rest for acute exacerbations
Encourage regular physical activity;
build up to about 30 minutes daily
Exercise training
Pacing of activities; wait 2 hours after
eating for physical activity
Avoid activities in extreme hot, cold, or
humid weather
Modify activities to conserve energy
Positioning; elevation of the head of bed to facilitate breathing and rest, support of arms
Nursing Interventions for the Patient w/ HF: Manage Fluid Volume
Assess for symptoms of fluid overload
Daily weight
I&O
Diuretic therapy; timing of meds
Fluid intake; fluid restriction
Maintenance of sodium restriction
Treatment of Acute Decompensated HF: Reduce Volume Overload
Diuretics (Furosemide)
Treatment of Acute Decompensated HF: Improve Ventricular Function
Vasodilators (IV Nitroprusside, NTG), continuous monitoring
Treatment of Acute Decompensated HF: Increase the force of Myocardial Contraction
IV inotropes (Milrinone, Dobutamine)
Pulmonary Edema
Pathologic accumulation of fluid in the interstitial spaces & alveoli of the lungs causing severe respiratory distress
- This situation demands EMERGENT action to prevent O2 and perfusion
from becoming critical!!!
Pathophysiology of Pulmonary Edema
It’s triggered when the LV fail and blood backs up quickly into the pulmonary circulation causing edema; PE can also develop slowly when caused by noncardiac disorders such as kidney injury
The LV can’t handle the fluid overload → ↑ pulmonary pressure which forces fluid into the capillaries, interstitial spaces, and alveoli
Pulmonary Edema Clinical Manifestations
Anxious, pale, cyanotic
Cool and clammy skin
Dyspnea
Orthopnea
Tachypnea
Use of accessory muscles
Incessant coughing w/ frothy, blood-tinged sputum
Crackles and wheezes
Tachycardia
Hypotension or HTN
Abnormal S3 or S4
Medical Management of Pulmonary Edema
Easier to prevent than to treat
Early recognition: monitor lung sounds and for signs of decreased activity tolerance and increased fluid retention
Minimize exertion and stress
Oxygen; nonrebreather
Medications
-Diuretics (furosemide)
-Vasodilators(nitroglycerin)
Nursing Management of Pulmonary Edema
Positioning the patient to promote circulation
-Positioned upright w/ legs dangling
Providing psychological support
Reassure patient and provide anticipatory care
Monitoring medications
-I&O
Which classification of meds play a pivotal role in the management of HF caused by systolic dysfunction?
A) ACE inhibitors
B) Beta-Blockers
C) Diuretics
D) Digitalis
A) ACE inhibitors
Which of the following is NOT an appropriate recommendation for an exercise program for the
patient with HF?
A) Follow the exercise period with a cool-down
activity
B) High-intensity training will provide the most
benefit
C) Wait 2 hours after eating a meal before
performing the physical activity
D) Begin with low-impact activities such as walking
B) High-intensity training
Cardiomyopathy
The heart can’t efficiently pump blood to the rest of the body due to a series of progressive events that culminates in impaired cardiac output
What is major electrolyte involved with
cardiomyopathy?
Sodium
Pathophysiology of Cardiomyopathy
Decreased SV stimulates the SNS & the RAAS-> Increased systemic vascular resistance & increased Na+ & fluid retention
-> Places an increased workload on the heart
The decrease in CO can be seen on the echocardiogram as a decrease in ejection fraction -> can lead to HF
Hypertrophic Cardiomyopathy
An autosomal genetic disorder that leads to ↑ heart muscle size and mass
-The heart muscle becomes abnormally
thick
The thickened muscle impairs the
pumping action of the heart
Thickness of the heart reduces the size
of the ventricles
Leads to ventricular hypertrophy &
diastolic failure
Dilated Cardiomyopathy
The heart muscle begins to dilate,
stretch, and become thin → enlarged
LV
- Most common form of cardiomyopathy
- Impaired contractility causes the
heart to weaken → HF
- Poor blood flow through the ventricle
may → ventricular or atrial thrombi,
which may embolize to other parts
of the body
Which type of cardiomyopathy is the most common?
Dilated cardiomyopathy
Ischemic Cardiomyopathy
Term frequently used to describe an enlarged heart caused by CAD
-Usually accompanied by HF
Clinical Manifestations of Cardiomyopathy
Patients may remain stable and w/out symptoms for many years.
As the disease progress, patients present
with:
Dyspnea on exertion (DOE)
Syncope and Fatigue
Paroxysmal nocturnal dyspnea (PND)
Cough, Orthopnea, Peripheral edema
Early satiety, chest pain, palpitations
Assessments & Diagnostic Findings Associated w/ Cardiomyopathy
History (predisposing factors, family history)
Chest pain
Review of systems: presence of orthopnea,
syncope
Review of diet (Na reduction, vitamin supplements)
Psychosocial history: impact on family, stressors,
depression
Physical assessment: VS, pulse pressure; pulsus
paradoxus; weight gain or loss; PMI; murmurs; S3
or S4; pulmonary auscultation for crackles, JVD,
and edema
Nursing Interventions for the Patient with Cardiomyopathy
Improve cardiac output and peripheral blood flow
-Rest, positioning (legs down), supplemental O2, medications, low Na diet, avoid dehydration
Increase activity tolerance and improve gas exchange
-Cycle rest and activity, ensure patient recognizes symptoms that indicate the need for rest
Reduce anxiety
-Eradicate or alleviate perceived stressors, educate family about diagnosis, assist with anticipatory grieving
Decrease the sense of powerlessness
-Assist patients in identifying things that have been lost (i.e., ability to play sports), assist patients in identifying amount of control they still have left
Promote home and community-based care
-Educate patients about ways to balance lifestyle and work while accomplishing therapeutic activities
-Assess patient and family and their adjustment to lifestyle changes, educate family about CPR and AEDs, establish trust
The nurse is providing education to a client newly diagnosed with cardiomyopathy. Which statement should the nurse use to best describe cardiomyopathy to the client?
A) Cardiomyopathy is another term for high blood pressure.
B) Cardiomyopathy is an abnormal heart rate.
C) Cardiomyopathy causes ineffective pumping of the heart.
D) Cardiomyopathy develops when the kidneys cannot regulate blood
pressure.
C) Cardiomyopathy causes ineffective pumping of the heart
Rationale: Cardiomyopathy is a disease process in which the heart is weakened, which interferes with its ability to pump blood through the body. The other statements do not accurately describe cardiomyopathy.
Valvular Regurgitation
The valve does not close properly, and blood backflows through the valve
Valvular Stenosis
The valve does not open completely, and blood flow through the valve is reduced
Valvular Prolapse
The stretching of the valve leaflet into the atrium
during systole
Mitral Valve Regurgitation
Blood flows from the LV back into the left atrium due to valve not closing properly
Clinical Manifestations of Mitral Valve Regurgitation
SOB with exertion/SOB lying flat
Fatigue
Reduced ability to exercise
Palpitations
Swelling in legs, abdomen, and neck veins
Chest pain (less common)
A blowing systolic murmur heard at the apex
- Confirmed w/ Echocardiography
Treatment for Mitral Valve Regurgitation w/ HF
ACE Inhibitors, Beta Blockers and Valve Replacement
Aortic Regurgitation
This is a back flow of blood into the LV from the aorta due to the aortic valve not closing tightly
Clinical Manifestations of Aortic Regurgitation
SOB with exertion/SOB lying flat
Fatigue
Palpitations
Swelling in legs, abdomen, and neck veins
Chest pain or tightness with exertion
High pitched, blowing diastolic murmur at the 3rd or 4th ICS at the left sternal border
Treatment for Aortic Regurgitation
ACE Inhibitors & Ca Channel blockers for HTN management, and Aortic Valve replacement or Valvuloplasty
How is mitral valve and aortic regurgitation confirmed?
ECHOcardiography
Nursing Management: Valvular Heart Disorders
Educate the patient about the diagnosis and treatment
Teach to report new symptoms or changes to the
provider
Explain that bacterium can easily adhere to a diseased heart valve more readily→ Endocarditis and further damage to the valve
Measure VS and compare results with previous data
Assess heart/lung sounds and peripheral pulses
Assess signs/symptoms of HF, arrhythmias, symptoms of syncope, and chest pain
Educate patient to relieve chest pain (angina) with rest
before taking nitroglycerin
Nursing Management of Patients with Valvular Heart Disorders
Patient education
Monitor VS trends, heart and lung sounds, peripheral pulses
Monitor for complications
-Heart failure
-Arrhythmias
-Other symptoms: dizziness, syncope,
angina pectoris
Medication schedule: plan and education
Daily weights: monitor for weight gain
Plan activities with rest periods
Valvuloplasty
Cardiac valve repair
Annuloplasty
Repair of annulus of heart valve
Annulus
Junction at which valve leaflets connect to the heart wall
Leaflet Repair
Repair of cardiac valves movable “flaps” leaflets”
Candidates for Valve Replacement
Patients w/:
-Valves w/extensive calcification
-Severely fibrotic or fused leaflets, chordae tendineae, or papillary muscles
Bioprostheses
Valves made from animal tissues (heterograft)
-Used for aortic, mitral, & tricuspid valve replacement
Less risk of thromboembolism
Shorter life than mechanical valves
Long-term anticoagulation is not required
-However, patients with biologic valves and atrial fibrillation must be on long-term anticoagulation
Homografts
AKA “Allografts”
Obtained from cadaver tissue donations used for aortic & pulmonic valve replacement
Not always available-> highly expensive
Lasts for 10-15 yrs
Autografts
AKA “Autologous Valves”
Obtained by excising the patient’s own pulmonic valve & a portion of the pulmonary artery for use as the aortic valve
Mechanical Valves
Last longer than biologic
Higher risk of thromboembolism
Require long-term anticoagulation
INR values of 2.5-3.5 considered therapeutic
The nurse is caring for a client with mitral valve regurgitation. Which of the following is an expected assessment finding for this disorder?
A. A High pitched, blowing diastolic murmur
B. A blowing systolic murmur heard at the apex
C. A loud, harsh systolic murmur is heard over
the aortic area
D. A low-pitched, rumbling diastolic murmur
B) A blowing systolic murmur heard at the apex
Infective Endocarditis
Infection of endocardial layer of heart
Endocardial layer continuous with heart valves
Heart valves continuous with endocardium
Valves commonly affected
Vegetations form on valves or endocardial surface
-May become emboli
Most Common Cause for Infective Endocarditis
Streptococcus viridans and Staph aureus
Risk Factors for Endocarditis
IV Drug Use
Prosthetic heart valves
Prior endocarditis
Certain heart disorders:
Cardiomyopathies
Congenital heart disease
Acquired valve disease
Existing cardiac lesions
Implanted Cardiac Devices
Pacemaker/Cardioverter Defib
Hemodialysis
Clinical Manifestations of Infective Endocarditis
Onset is usually insidious
Often non-specific
Fever, malaise, weakness, anorexia
Arthralgia, myalgia
Abdominal discomfort
Cutaneous signs
Splinter hemorrhages: Reddish-brown lines & streaks that may be seen under half of fingernails & toenails
Osler’s nodes: Small painful nodules
Roth’s spots: Hemorrhages w/ pale centers caused by emboli (may be observed in fundi of eyes)
Janeway lesions: Irregular, red or purple, painless flat macules that may be present on palms, fingers, hands, soles, and toes
Pathophysiology of Infective Endocarditis
1) Clot Formation: Deformity/injury of the endocardium leads to accumulation of fibrin & platelets on the endocardium
2) Infectious organisms invade the clot & endocardial lesion
3) Infection results in platelets, fibrin, blood cells, & microorganisms that clusters as vegetations on the endocardium
-Vegetations may embolize to other vessels throughout the body
4) As the clot on the endocardium continues to expand, the infecting organism is covered by the new clot & concealed from the body’s normal defenses
5) Infection may erode through the endocardium into underlying structures (valve structures) -> causes tears or other deformities of valve leaflets, dehisence of prosthetic valves, deformity of chordae tendineae, or mural abscesses
Diagnostic Findings Associated w/ Infective Endocarditis
Blood Cultures x2 (aerobic/anaerobic)
Echocardiogram (show vegetation)
Labs: CBC (elevated WBC), Rheumatoid Factor (positive), ESR (elevated), CRP (elevated)
Transesophageal Echo (TEE)-superior in assessing vegetations
Prevention of Infective Endocarditis
Antibiotic prophylaxis: For those w/previous infective endocarditis, prosthetic heart valves, patients w/ heart transplant & valve regurgitation
- Done before dental procedures
Good Oral hygiene
Regular dental visits, brushing, flossing, and using plaque removal devices
Increased vigilance required in patients with IV catheters and during invasive procedures
Nurses must perform meticulous hand hygiene
All catheters, drains, tubes should be removed when no longer needed
Medical Management of Infective Endocarditis
Objective of Treatment: Eradicate invading organisms through adequate doses of an appropriate antibiotic
Antibiotic therapy IV for 2 to 6 weeks
Serum levels of antibiotics and blood
cultures are monitored to gauge
effectiveness of therapy
Patients may require psychosocial support
Confined to home or hospital with
restrictive IV therapy
Nursing Management of Infective Endocarditis
The nurse monitors the patient’s temperature and administers
antibiotics as prescribed
Ensure planned rest periods and space
activities due to fever→ fatigue
Practice good infection control by nurse, patient, and family members
NSAIDS prescribed for fever and discomfort
Assess heart sounds for new or worsening murmur
Assess all invasive lines and wounds
daily redness, warmth, swelling,
drainage, and tenderness
Educate the patient and family members on activity restrictions,
medications, and signs/symptoms of
infection
Pericarditis
Inflammation of pericardium, which is the sac enveloping the heart
Clinical Manifestations of Pericarditis
May be asymptomatic
Chest pain- most characteristic symptom; constant and worsens
with inspiration/relieved by sitting forward
Pericardial friction rub- most characteristic clinical manifestation
Diffuse ST segment elevation
Mild fever, elevated WBC, ESR, CRP, anemia
Non-productive cough or hiccup/SOB
Diagnostic Findings Associated w/ Pericarditis
Echocardiogram- detect inflammation
TEE
CT imaging: determine size, shape, and location of effusions
MRI: detect inflammation and adhesions
12-lead ECG: may show ST elevations
Medical Management of Pericarditis
If CO is impaired-> Pt is placed on bed rest until, fever, chest pain, and friction rub have subsided
Analgesics & NSAIDS: Aspirin, indomethacin, or ibuprofen may be prescribed for pain relief during the acute phase
-Corticosteroids (prednisone) can be used as an alternative when NSAIDS are contraindicated
Objective of Medical Management of Pericarditis
Objective: Determine the cause, administer therapy for treatment & symptom relief & detect signs & symptoms of cardiac tamponade
Key Point of Nursing Management of Pericarditis
BE ALERT for signs/symptoms
of cardiac tamponade
The nurse identifies that a patient has a characteristic symptom of pericarditis. Which symptom does the
nurse recognize as significant for this diagnosis?
a) Dyspnea
b) Constant chest pain
c) Fatigue lasting more than 1 month
d) Uncontrolled restlessness
b) Constant chest pain
Myocarditis
An inflammatory process involving the middle layer of the heart, the myocardium
Can Cause:
- Heart dilation
- Thrombi on the heart wall (mural thrombi)
- Infiltration of circulating blood cells around the coronary vessels & between muscle fibers
- Degeneration of muscle fibers
Pathophysiology of Myocarditis
Usually from an infectious source (viral: HIV, influenza A)
- Can also be autoimmune-related (rheumatic fever or autoimmune disease)
May begin in 1 small area then spread to the rest of the myocardium
- Degree of myocardial inflammation & necrosis determines the degree of interstitial collagen & elastin destruction
Clinical Manifestations of Myocarditis
May be asymptomatic as infection resolves
May develop mild-moderate symptoms & seek medical attention (most are flu-like)
- Fatigue
- Dyspnea
- Syncope
- Palpitations
- Occasional discomfort in the upper abdomen & chest
Assessment & Diagnostic Findings Associated w/ Myocarditis
May reveal no detectable abnormalities (may go undiagnosed)
Tachycardic & complain of chest pain
Endomyocardial biopsy is the most definitive diagnosis
- Cardiac MRI is used more often since it’s non-invasive
Patients w/out initial heart structure abnormalities may suddenly develop arrhythmias/ ST–T wave changes
If the patient has structural abnormalities (systolic dysfunction):
- Cardiac enlargement
- Faint heart sounds (especially S1)
- Pericardial friction rub
- Gallop rhythm or systolic murmur
Labs:
WBC- elevated
C-reactive protein- elevated
Leukocyte count - elevated
ESR - elevated
Medical Management of Myocarditis
Given specific treatment if underlying cause is known (ex: antibiotics)
Bed rest to decrease cardiac workload
Activities should be limited for a 6 month period or until heart size & function have returned to normal
- Should be increased slowly
- Notify the clinician immediately of any symptoms w/increasing activity (rapidly beating heart)
DO NOT USE NSAIDS FOR PAIN CONTROL!!!
- Implication of increased cardiac injury & viral replication
Nursing Management for Myocarditis
Assess for resolution of tachycardia, fever, & other clinical manifestations
Focus on signs & symptoms of HF & arrhythmias
Patients w/arrhythmias are to be put on continuous cardiac monitoring w/ emergent equipment ready
Sensitive to digitalis
Watch for signs of toxicity! Notify provider immediately if these symptoms are observed:
- New onset of arrhythmia
- Headache
- Anorexia
- N/V
- Malaise
