Nursing Care Plan Common Dysrhytmias

COMMON DYSRHYTHMIAS

Tachycardias
I. Sinus Tachycardia
a. Sinus node creates rate that is faster than normal (greater
than 100)
b. Associated with physiological or psychological stress;
medications, such as catecholamines, aminophylline,
atropine, stimulants, and illicit drugs; enhanced
automaticity; and autonomic dysfunction
II. Atrial Flutter
a. Occurs in the atrium and creates regular atrial rates between
250 and 400. Because AV node cannot keep up with
conduction of all these impulses, not all atrial impulses are
conducted into the ventricle, causing a therapeutic block at
the AV node.
III. Atrial Fibrillation (AF)
a. Rapid, irregular twitching of the atrial musculature with an
atrial rate of 300 to 600 and a ventricular rate of 120 to
200 if untreated
b. Associated with advanced age, valvular heart disease,
hyperthyroidism, pulmonary disorder, pulmonary disease,
alcohol ingestion (“holiday heart syndrome”), hypertension,
diabetes, CAD, or after open-heart surgery
IV. Paroxysmal Supraventricular Tachycardia (PSVT,
also called SVT)
a. Pathways in the AV node or atrium allow an altered
conduction of electricity, causing a regular and fast rate of
sometimes more than 150 to 200.
b. Ventricle, sensing the electrical activity coming through
the AV node, beats along with each stimulation.
c. Rarely a life-threatening event, but most people feel
uncomfortable when PSVT occurs.
V. Ventricular Tachycardia (VT)
a. Rapid heartbeat initiated within the ventricles, characterized
by three or more consecutive premature ventricular
beats with elevated and regular heart rate (such as 160 to
240 beats per minute)
b. Heart rate sustained at a high rate causes symptoms such
as weakness, fatigue, dizziness, fainting, or palpitations
c. Potentially lethal disruption of normal heartbeat that can
degenerate to ventricular fibrillation
VI. Ventricular Fibrillation (VF)
a. Aside from myocardial ischemia, other causes of ventricular
fibrillation may include severe weakness of the heart
muscle, electrolyte disturbances, drug overdose, and
poisoning.
b. Electrical signal is sent from the ventricles at a very fast
and erratic rate, impairing the ability of ventricles to fill
with blood and pump it out, markedly decreasing cardiac
output, and resulting in very low blood pressure and loss
of consciousness.
c. Sudden death will occur if VF not corrected.

Bradycardias
I. Sinus Bradycardia
a. Rarely symptomatic until heart rate drops below 50, then
fainting or syncope may be reported
b. Causes include hypothyroidism, athletic training, sleep,
vagal stimulation, increased intracranial pressure, MI, hypovolemia,
hypoxia, acidosis, hypokalemia and hyperkalemia,
hyperglycemia, hypothermia, toxins, tamponade, tension
pneumothorax, thrombosis (cardiac or pulmonary), and
trauma.
c. Medications, such as beta blockers, calcium channel blockers,
and amiodarone, also slow the heart rate (AHA, 2005).
II. Sick Sinus Syndrome (SSS)
a. Varity of conditions affecting SA node function, including
bradycardia, sinus arrest, sinoatrial block, episodes of
tachycardia, and carotid hypersensitivity
b. Signs and symptoms related to cerebral hypoperfusionc. May be associated with rapid rate (tachycardia) or alternate
between too fast and too slow (bradycardia-tachycardia
syndrome). A long pause (asystole) may occur between
heartbeats, especially after an episode of tachycardia.
III. Heart Blocks
a. First-degree AV block
i. Asymptomatic; usually an incidental finding on electrocardiogram
(ECG)
b. Second-degree AV (type I and type II)
i. Usually asymptomatic, although some clients can feel
irregularities (palpitations) of the heartbeat, or syncope
may occur, which usually is observed in more advanced
conduction disturbances such as Mobitz II AV block
ii. Medications affecting AV node function, such as digoxin,
beta blockers, calcium channel blockers, may contribute
c. Third-degree AV block (also called complete heart block)
i. May be associated with acute MI either causing the block
or related to reduced cardiac output from bradycardia in
the setting of advanced atherosclerotic CAD
ii. Symptomatic with fatigue, dizziness, and syncope and
possible loss of consciousness
iii. Can be life-threatening, especially if associated with heart
failure

Other Dysrhythmias
I. Premature Atrial Complex (PAC)
a. Electrical impulse starts in the atrium before the next normal
impulse of the sinus node.
b. Causes include caffeine, alcohol, and nicotine use, stretched
atrial myocardium; anxiety; hypokalemia; and hypermetabolic
states (pregnancy), or may be related to atrial ischemia, injury,
or infarction.

II. Premature Ventricular Contraction (PVC)
a. Electrical signal originates in the ventricles, causing them to
contract before receiving the electrical signal from the atria.
b. PVCs not uncommon and are often asymptomatic.
c. Increase to several per minute may cause symptoms such as
weakness, fatigue, dizziness, fainting, or palpitations.
d. Irritability of the heart demonstrated by frequent and or
multiple back-to-back PVCs can lead to VF.

Care Settings
Generally, minor dysrhythmias are monitored and treated in
the community setting; however, potential life-threatening
situations (including heart rates above 150 beats per minute)
may require a short inpatient stay.

Nursing Priorities
1. Prevent or treat life-threatening dysrhythmias.
2. Support client and significant other (SO) in dealing with
anxiety and fear of potentially life-threatening situation.
3. Assist in identification of cause or precipitating factors.
4. Review information regarding condition, prognosis, and
treatment regimen.

Discharge Goals
1. Free of life-threatening dysrhythmias and complications
of impaired cardiac output and tissue perfusion.
2. Anxiety reduced and managed.
3. Disease process, therapy needs, and prevention of complications
understood.
4. Plan in place to meet needs after discharge.

NURSING DIAGNOSIS: risk for decreased Cardiac Output

Risk factors may include
Altered electrical conduction
Reduced myocardial contractility
Possibly evidenced by
(Not applicable; presence of signs and symptoms establishes an actual diagnosis)
Desired Outcomes/Evaluation Criteria—Client Will
Cardiac Pump Effectiveness
Maintain or achieve adequate cardiac output as evidenced by BP and pulse within normal range, adequate urinary output,
palpable pulses of equal quality, and usual level of mentation.
Display reduced frequency or absence of dysrhythmia(s).
Participate in activities that reduce myocardial workload.

ACTIONS/INTERVENTIONS
Dysrhythmia Management
Independent
Palpate radial, carotid, femoral, and dorsalis pedis pulses,
noting rate, regularity, amplitude (full or thready), and symmetry.
Document presence of pulsus alternans, bigeminal
pulse, or pulse deficit.
Auscultate heart sounds, noting rate, rhythm, presence of
extra heartbeats, and dropped beats.
Monitor vital signs. Assess adequacy of cardiac output and
tissue perfusion, noting significant variations in BP, pulse
rate equality, respirations, changes in skin color and temperature,
level of consciousness and sensorium, and urine
output during episodes of dysrhythmias.
Determine type of dysrhythmia and document with rhythm
strip if cardiac or telemetry monitoring is available:
Sinus tachycardia
Sinus bradycardia
Atrial dysrhythmias, such as PACs, atrial flutter, AF, and
atrial supraventricular tachycardias (i.e., paroxysmal atrial
tachycardia [PAT], multifocal atrial tachycardia [MAT], SVT)
Ventricular dysrhythmias, such as PVCs and ventricular premature
beats (VPBs), VT, and ventricular flutter and VF
Heart blocks
Provide calm and quiet environment. Review reasons for
limitation of activities during acute phase.
Demonstrate and encourage use of stress management
behaviors such as relaxation techniques; guided imagery;
and slow, deep breathing.
Investigate reports of chest pain, documenting location,
duration, intensity (0 to 10 scale), and relieving or aggravating
factors. Note nonverbal pain cues, such as facial
grimacing, crying, changes in BP and heart rate.
Be prepared to initiate cardiopulmonary resuscitation (CPR), as
indicated.
Collaborative
Monitor laboratory studies, such as the following:
Electrolytes
Medication and drug levels
Administer supplemental oxygen, as indicated.
Prepare for and assist with diagnostic and treatment procedures
such as EP studies, radiofrequency ablation (RFA), and
cryoablation (CA).
Administer medications, as indicated, for example:
Potassium
Antidysrhythmics, such as the following:
Class I drugs:
Class Ia, such as disopyramide (Norpace), procainamide
(Procan SR), quinidine (Cardioquin), and moricizine
(Ethmozine)
Class Ib, such as lidocaine (Xylocaine), phenytoin
(Dilantin), tocainide (Tonocard), and mexiletine (Mexitil)
Class Ic, such as flecainide (Tambocor) and propafenone
(Rhythmol)
Class II drugs, such as atenolol (Tenormin), propranolol
(Inderal), nadolol (Corgard), acebutolol (Sectral), esmolol
(Brevibloc), sotalol (Betapace), and bisoprolol (Zebeta)
Class III drugs, such as bretylium tosylate (Bretylol), amiodarone
(Cordarone), sotalol (Betapace), ibutilide
(Corvert), and dofetilide (Tikosyn)
Class IV drugs, such as verapamil (Calan), nifedipine
(Procardia), and diltiazem (Cardizem)
Class V drugs, such as atropine sulfate, isoproterenol
(Isuprel), and cardiac glycosides (digoxin [Lanoxin])
Adenosine (Adenocard)
Prepare for and assist with elective cardioversion.
Assist with insertion and maintain pacemaker (external or temporary,
internal or permanent) function.
Insert and maintain intravenous (IV) access.
Prepare for surgery, such as aneurysmectomy, CABG, and
Maze, as indicated.
Prepare for placement of ICD when indicated.

RATIONALE
Differences in equality, rate, and regularity of pulses are
indicative of the effect of altered cardiac output on systemic
and peripheral circulation.
(
Specific dysrhythmias are more clearly detected audibly than
by palpation. Hearing extra heartbeats or dropped beats
helps identify dysrhythmias in the unmonitored client.
Although not all dysrhythmias are life-threatening, immediate
treatment may be required to terminate dysrhythmia in the
presence of alterations in cardiac output and tissue perfusion.
Useful in determining need and type of intervention required.
Tachycardia can occur in response to stress, pain, fever,
infection, coronary artery blockage, valvular dysfunction,
hypovolemia, hypoxia, or as a result of decreased vagal
tone or of increased sympathetic nervous system activity
associated with the release of catecholamines. Although it
generally does not require treatment, persistent tachycardia
may worsen underlying pathology in clients with ischemic
heart disease because of shortened diastolic filling time
and increased oxygen demands. These clients may require
medications.
Bradycardia is common in clients with acute MI (especially
anterior and inferior) and is the result of excessive
parasympathetic activity, blocks in conduction to the SA or
AV nodes, or loss of automaticity of the heart muscle.
Clients with severe heart disease may not be able to
compensate for a slow rate by increasing stroke volume;
therefore, decreased cardiac output, HF, and potentially
lethal ventricular dysrhythmias may occur.
PACs can occur as a response to ischemia and are normally
harmless, but can precede or precipitate AF. Acute and
chronic atrial flutter or fibrillation (the most common dysrhythmia)
can occur with coronary artery or valvular disease
and may or may not be pathological. Rapid atrial flutter
or fibrillation reduces cardiac output as a result of
incomplete ventricular filling (shortened cardiac cycle) and
increased oxygen demand.
PVCs or VPBs reflect cardiac irritability and are commonly
associated with MI, digoxin toxicity, coronary vasospasm,
and misplaced temporary pacemaker leads. Frequent, multiple,
or multifocal PVCs result in diminished cardiac output
and may lead to potentially lethal dysrhythmias, such as VT
or sudden death or cardiac arrest from ventricular flutter or
VF. Note: Intractable ventricular dysrhythmias unresponsive
to medication may reflect ventricular aneurysm.
Polymorphic VT (torsades de pointes) is recognized by
inconsistent shape of QRS complexes and is often related
to use of drugs such as procainamide (Pronestyl), quinidine
(Quinaglute), disopyramide (Norpace), and sotalol
(Betapace).
Reflect altered transmission of impulses through normal conduction
channels (slowed, altered) and may be the result of
MI, CAD with reduced blood supply to SA or AV nodes,
drug toxicity, and sometimes cardiac surgery. Progressing
heart block is associated with slowed ventricular rates,
decreased cardiac output, and potentially lethal ventricular
dysrhythmias or cardiac standstill.
Reduces stimulation and release of stress-related catecholamines,
which can cause or aggravate dysrhythmias
and vasoconstriction, increasing myocardial workload.
Promotes client participation in exerting some sense of control
in a stressful situation.
Reasons for chest pain are variable and depend on underlying
cause. However, chest pain may indicate ischemia due
to altered electrical conduction, decreased myocardial
perfusion, or increased oxygen need, such as impending or
evolving MI.
Development of life-threatening dysrhythmias requires prompt
intervention to prevent ischemic damage or death.
Imbalance of electrolytes, such as potassium, magnesium, and
calcium, adversely affects cardiac rhythm and contractility.
Reveal therapeutic and toxic level of prescription medications
or street drugs that may affect or contribute to presence of
dysrhythmias.
Increases amount of oxygen available for myocardial uptake,
reducing irritability caused by hypoxia.
Treatment for several tachycardia dysrhythmias, including
SVT, atrial flutter, Wolf-Parkinson-White ( WPW) syndrome,
AF, and VT, is often carried out as first-line treatment via
heart catheterization or angiographic procedures. After
rhythm is confirmed with EP study, the client will then often
have either an RFA or CA to terminate or disrupt the dysfunctional
pattern. Medications may be tried first or added
after ablation for increased treatment success.
Correction of hypokalemia may be sufficient to terminate
some ventricular dysrhythmias. Note: Potassium imbalance
is the number one cause of AF.
Class I drugs depress depolarization and alter repolarization,
stabilizing the cell. These drugs are divided into groups a,
b, and c, based on their unique effects.
These drugs increase action potential, duration, and effective
refractory period and decrease membrane responsiveness,
prolonging both QRS complex and QT interval. This also
results in decreasing myocardial conduction velocity and
excitability in the atria, ventricles, and accessory pathways.
They suppress ectopic focal activity. Useful for treatment of
atrial and ventricular premature beats and repetitive dysrhythmias,
such as atrial tachycardias and atrial flutter and
AF. Note: Myocardial depressant effects may be potentiated
when class Ia drugs are used in conjunction with any drugs
possessing similar properties.
These drugs shorten the duration of the refractory period
(QT interval), and their action depends on the tissue
affected and the level of extracellular potassium. These
drugs have little effect on myocardial contractility, AV and
intraventricular conduction, and cardiac output. They also
suppress automaticity in the His-Purkinje system. Drugs of
choice for ventricular dysrhythmias, they are also effective
for automatic and re-entrant dysrhythmias and digoxininduced
dysrhythmias. Note: These drugs may aggravate
myocardial depression.
These drugs slow conduction by depressing SA node
automaticity and decreasing conduction velocity through
the atria, ventricles, and Purkinje’s fibers. The result is
prolongation of the PR interval and lengthening of the QRS
complex. They suppress and prevent all types of ventricular
dysrhythmias. Note: Flecainide increases risk of druginduced
dysrhythmias post-MI. Propafenone can worsen
or cause new dysrhythmias, a tendency called the
“pro-arrhythmic effect.”
Beta-adrenergic blockers have antiadrenergic properties and
decrease automaticity. They reduce the rate and force of
cardiac contractions, which in turn decrease cardiac output,
blood pressure, and peripheral vascular resistance.
Therefore, they are useful in the treatment of dysrhythmias
caused by SA and AV node dysfunction, including SVTs,
atrial flutter and AF. Note: These drugs may exacerbate
bradycardia and cause myocardial depression, especially
when combined with drugs that have similar properties.
These drugs prolong the refractory period and action potential
duration, consequently prolonging the QT interval. They
decrease peripheral resistance and increase coronary blood
flow. They have anti-anginal and anti-adrenergic properties.
They are used to terminate VF and other life-threatening
ventricular dysrhythmias and sustained ventricular tachyarrhythmias,
especially when lidocaine and procainamide
are not effective. Note: Sotalol is a nonselective beta
blocker with characteristics of both class II and class III.
Calcium antagonists, or calcium channel blockers, slow
conduction time through the AV node, prolonging PR interval
to decrease ventricular response in SVTs, atrial flutter
and AF. Calan and Cardizem may be used for bedside
conversion of acute AF.
Miscellaneous drugs useful in treating bradycardia by increasing
SA and AV conduction and enhancing automaticity.
Cardiac glycosides may be used alone or in combination
with other antidysrhythmic drugs to reduce ventricular
rate in presence of uncontrolled or poorly tolerated atrial
tachycardias or atrial flutter and AF.
First-line treatment for PSVT. Slows conduction and interrupts
reentry pathways in AV node. Note: Contraindicated in
clients with second- or third-degree heart block or those
with SSS who do not have a functioning pacemaker.
May be used in AF after trials of first-line drugs, such as atenolol,
metoprolol, diltiazem, and verapamil, have failed to control
heart rate or in certain unstable dysrhythmias to restore
normal heart rate or relieve symptoms of heart failure.
Temporary pacing may be necessary to accelerate impulse
formation in bradydysrhythmias, synchronize electrical
impulsivity, or override tachydysrhythmias and ectopic
activity to maintain cardiovascular function until spontaneous
pacing is restored or permanent pacing is initiated.
These devices may include atrial and ventricular pacemakers
and may provide single chamber or dual chamber
pacing. The placement of implantable cardioverter defibrillators
(ICDs) is on the rise.
Patent access line may be required for administration of emergency
drugs.
Differential diagnosis of underlying cause may be required
to formulate appropriate treatment plan. Resection of
ventricular aneurysm may be required to correct intractable
ventricular dysrhythmias unresponsive to medical therapy.
Surgery such as CABG may be indicated to enhance
circulation to myocardium and conduction system. Note:
A Maze procedure is an open heart surgical procedure
sometimes used to treat refractive AF by surgically redirecting
electrical conduction pathways.
This device may be surgically implanted in those clients with
recurrent, life-threatening ventricular dysrhythmias unresponsive
to tailored drug therapy. The latest generation
of devices can provide multilevel or “tiered” therapy, that
is, antitachycardia and antibradycardia pacing, cardioversion,
or defibrillation depending on how each device is
programmed.

Nursing Care Plan Myocardial Infarction

MYOCARDIAL INFARCTION

I. Pathophysiology
a. Marked reduction or loss of blood flow through one or more
of the coronary arteries, resulting in cardiac muscle
ischemia, and over a finite period, resulting in necrosis
b. Occurs most often due to coronary artery disease (CAD)
c. Cellular ischemia and necrosis can affect the heart’s rhythm,
pumping action, and blood circulation.
d. Other problems may also ensue, such as heart failure, lifethreatening
arrhythmias, and death.
e. Delay in seeking treatment is the largest barrier to receiving
therapy quickly.

II. Classification
a. Type of myocardial infarction (MI) can be identified on the
electrocardiogram (ECG).
i. ST-segment elevation (also called STEMI)
ii. Non-ST elevation
b. Location of MI can be identified on the ECG.
i. Anterior wall of the ventricle
ii. Inferior wall of the ventricle
iii. Posterior wall of the ventricle
iv. Lateral wall of the ventricle

c. Infarcts are usually classified by size.
i. Microscopic (focal necrosis)
ii. Small (<10% of the left ventricle)
iii. Medium (10% to 30% of the left ventricle)
iv. Large (>30% of the left ventricle)
d. Point of time can be identified on the ECG by the Q wave
and the client’s history.
i. Acute or evolving infarction is characterized by the presence
of polymorphonuclear leukocytes unless the interval
between the onset of infarction and death is brief (e.g.,
6 hours), minimal, or no polymorphonuclear leukocytes
may be seen.
ii. Old or healed infarction is manifested as scar tissue
without cellular infiltration, a process usually requiring
5 to 6 weeks or more.
III. Etiology
a. CAD common cause with plaque formation narrowing
vessels and pieces of plaque breaking off, creating emboli
b. Severe spasm of a coronary artery is less common cause
c. Risk factors—age, being overweight or obese, smoking,
hyperlipidemia, family history
d. Greater risk in presence of kidney problems, peripheral
arterial disease, or prior MI
IV. Statistics (Centers for Disease Control and Prevention
[CDC],2007b; National Heart, Lung and Blood Institute
[NHLBI], 2007)
a. Morbidity: Approximately 1.1 million people in the United
States suffer from MI annually.
b. Mortality: almost 50% die, approximately 460,000 annually.
i. CAD is leading killer of both men and women in the
United States.
ii. Leading cause of death for American Indians, Alaskan
Natives, African Americans, Hispanics, and whites, and
second leading cause of death for Asians and Pacific
Islanders
c. Cost: Projected $258 billion spent for heart disease in 2006.

Care Setting
Myocardial infarctions are treated in the emergency room,
inpatient acute hospital, critical care unit (CCU), intensive
care unit (ICU), step-down unit, or medical unit.

Nursing Priorities
1. Relieve pain and anxiety.
2. Reduce myocardial workload.
3. Prevent, detect, and assist in treatment of life-threatening
dysrhythmias or complications.
4. Promote cardiac health and self-care.

Discharge Goals
1. Chest pain absent or controlled.
2. Heart rate and rhythm sufficient to sustain adequate cardiac
output and tissue perfusion.
3. Achievement of activity level sufficient for basic selfcare.
4. Anxiety reduced and managed.
5. Disease process, treatment plan, and prognosis understood.
6. Plan in place to meet needs after discharge, including
follow-up appointments.

NURSING DIAGNOSIS: acute Pain

May be related to
Tissue ischemia (coronary artery occlusion)
Possibly evidenced by
Reports of chest pain with or without radiation
Facial grimacing
Restlessness, changes in level of consciousness
Changes in pulse, BP
Desired Outcomes/Evaluation Criteria—Client Will
Pain Level
Verbalize relief or control of chest pain within appropriate period for administered medications.
Display reduced tension, relaxed manner, and ease of movement.
Pain Control
Demonstrate use of relaxation techniques.

ACTIONS/INTERVENTIONS
Pain Management
Independent
Monitor and document characteristics of pain, noting verbal
reports, nonverbal cues, for example, moaning, crying,
restlessness, diaphoresis, clutching chest, rapid breathing,
and hemodynamic response (BP and heart rate changes).
Obtain full description of pain from client including location,
intensity (0 to 10), duration, characteristics (dull or
crushing), and radiation. Assist client to quantify pain by
comparing it to other experiences.
Review history of previous angina, anginal equivalent, or MI
pain. Discuss family history if pertinent.
Instruct client to report pain immediately.
Provide quiet environment, calm activities, and comfort measures,
for instance, dry or wrinkle-free linens and backrub.
Approach client calmly and confidently.
Assist or instruct in relaxation techniques, such as deep, slow
breathing and distraction.
Check vital signs before and after administration of opioid
medication.
Collaborative
Administer supplemental oxygen by means of nasal cannula
or face mask, as indicated.
Administer medications, as indicated, for example:
Aspirin (ASA)
Anti-anginals, such as nitroglycerin (Nitro-Bid, Nitrostat,
Nitro-Dur), isosorbide dinitrate (Isordil), and mononitrate
(Imdur)
Angiotensin-converting enzyme (ACE) inhibitors, such as
lisinopril (Zestril), captopril (Capoten), and benazepril
(Lotensin)
Angiotensin receptor blockers (ARBs), such as candesartan
(Atacand), olmesartan (Benicar), and valsartan (Diovan)
Aldosterone blockers, such as eplerenone (Inspra) and
spironolactone
Analgesics, such as morphine sulfate

RATIONALE
Variation of appearance and behavior of clients in pain may
present a challenge in assessment. For example, men and
women consistently present differently, or an individual may
present differently from one episode to another. However,
most clients with an acute MI appear ill, distracted, and
focused on pain. Verbal history and deeper investigation of
precipitating factors should be postponed until pain is
relieved. Respirations may be increased as a result of pain
and associated anxiety; release of stress-induced catecholamines
increases heart rate and BP.
Pain is a subjective experience and must be described
by client. Provides baseline for comparison to aid in determining
effectiveness of therapy, resolution or progression
of problem.
May differentiate current pain from preexisting patterns as
well as identify complications, such as extension of
infarction, pulmonary embolus, or pericarditis.
Delays in reporting pain hinders pain relief and may necessitate
increased dosage of medication to achieve relief. In
addition, severe pain may induce shock by stimulating the
sympathetic nervous system, thereby creating further damage
and interfering with diagnostics and relief of pain.
Decreases external stimuli, which may aggravate anxiety and
cardiac strain and limit coping abilities and adjustment to
current situation.
Helpful in decreasing perception of or response to pain.
Provides a sense of having some control over the situation,
increase in positive attitude.
Hypotension and respiratory depression can occur as a result
of opioid administration. These problems may increase
myocardial damage in presence of ventricular insufficiency.
Increases amount of oxygen available for myocardial uptake
and thereby may relieve discomfort associated with tissue
ischemia.
Giving aspirin as soon as possible (unless contraindicated)
inhibits platelet activity, interrupting platelet aggregation at
the site of plaque rupture—a key mechanism in the unfolding
acute MI. Patients who receive aspirin in the acute
phase have a 15% lower mortality rate than those who
don’t (Lackey, 2006).
Nitrates are useful for pain control by coronary vasodilating
effects, which increase coronary blood flow and myocardial
perfusion. Peripheral vasodilation effects reduce the volume
of blood returning to the heart (preload), thereby
decreasing myocardial workload and oxygen demand.
May be given to reduce hypertension and reduce risk of developing
heart failure following MI in client with diminished
ventricular EF and in those with hypertension, diabetes, or
chronic kidney disease, unless contraindicated (Smith et al,
2006).
May be used in patients who are intolerant to ACE inhibitors
and have heart failure (HF) or have had an MI with left ventricular
EF less than or equal to 40%. They block the action
of angiotensin II that causes the blood vessels to dilate and
reduce BP.
May be used in post-MI patients who have had an MI, ACS, or
left ventricular dysfunction with or without HF symptoms,
unless contraindicated. They block the effects of aldosterone
on the kidneys, allowing the kidneys to excrete
extra sodium and water, thereby reducing BP.
Although intravenous (IV) morphine is the usual drug of
choice, other injectable opioids may be used in acute-phase
or recurrent chest pain unrelieved by nitroglycerin to
reduce severe pain, provide sedation, and decrease
myocardial workload. IM injections should be avoided, if
possible, because they can alter the CPK diagnostic indicator
and are not well absorbed in underperfused tissue.

Nursing Care Plan Angina Coronary Artery Disease Acute Coronary Syndrome

ANGINA (CORONARY ARTERY DISEASE, ACUTE
CORONARY SYNDROME)

I. Pathophysiology
a. The disorder is characterized by a narrowing of coronary
arteries due to atherosclerosis, spasm or, rarely, embolism.
b. Atherosclerotic changes in coronary arteries results in damage
to the inner layers of the coronary arteries with stiffening
of vessels and diminished dilatory response.
c. Accumulation of fatty deposits and lipids, along with
development of fibrous plaques over the damaged areas in
the vessels, causes narrowing of the arteries, thus reducing
the size of the vessel’s lumen and impeding blood flow to
the myocardial tissues.
d. Decreased delivery of oxygen and nutrients to the tissues
causes transient myocardial ischemia and pain.
e. Hard plaque causes hardened arteries, whereas soft plaque
can cause formation of blood clots.
II. Types
a. Stable
i. Most common type, precipitated by physical exertion,
emotional stress, exposure to hot or cold temperatures,
heavy meals, and smoking
ii. Occurs in a regular pattern, usually lasts 5 minutes or
less, and is easily relieved by medications
b. Unstable
i. May be new onset of pain with exertion or at rest, or
recent acceleration in severity of pain
ii. Occurs in no regular pattern, usually lasts longer (30 minutes),
not generally relieved with rest or medications
iii. Sometimes grouped with myocardial infarction (MI)
under the diagnosis of acute coronary syndrome (ACS)
c. Variant (Prinzmetal’s)
i. Rare, usually occurs at rest—midnight to early morning
hours
ii. Pain possibly severe
iii. Electrocardiogram (ECG) changes due to coronary
artery spasm
III. Classification
a. New York Heart Association Classification (9th edition
update, 1994) quantifies the functional limitation imposed
by patients’ symptoms:
i. Class I—no limitation of ordinary physical activity
ii. Class II—slight limitation of ordinary physical activity
b. Prevalence: leading cause of death in Caucasians, African
Americans, Hispanics, and American Indians for both males
and females
iii. Class III—moderate limitation of activity; comfortable
at rest, but less than ordinary activities cause symptoms
iv. Class IV—unable to perform any physical activity
without discomfort, therefore severe limitation and may
be symptomatic even at rest
i. Class 1—no angina with usual physical activities such
as walking, climbing stairs; occurs with strenuous,
rapid, or prolonged exertion at work or recreation
ii. Class 2—slight limitation of ordinary activity with
angina occurring with moderate exertion such as walking
or climbing stairs rapidly, walking uphill, activity
after meals, activity in cold or wind, during emotional
stress, or during the few hours after awakening
iii. Class 3—marked limitations of ordinary physical
activity with angina occurring during mild exertion,
such as walking one to two level blocks or climbing one
flight of stairs at a normal pace
iv. Class 4—angina at any level of physical exertion; may
be present even at rest
IV. Etiology
a. Increased cardiac workload: exertion, hypertension, aortic
stenosis or regurgitation, hypertrophic cardiomyopathy
b. Decreased O2 supply: severe anemia, hypoxia
c. Risk factors: being overweight and obese, smoking, sedentary
lifestyle, diabetes, family history of early heart disease,
metabolic syndrome (fasting hyperglycemia and insulin
resistance, hypertension, central obesity, decreased highdensity
lipoprotein [HDL] and elevated low-density
lipoprotein [LDL] cholesterol, elevated triglycerides)
V. Statistics (National Heart, Lung and Blood Institute
[NHLBI], 2007; Centers for Disease Control and Prevention
[CDC], 2007b)
b. Canadian Cardiovascular Society Functional Classification
(CCSC) System of unstable angina aids in determining the
risk of adverse outcomes and level of treatment needs:
c. Mortality: There were 872,000 deaths from cardiovascular
disease in 2004; accounts for approximately
36% of total deaths.
d. Cost: An estimated $432 billion was spent in 2007.

Care Setting
Clients judged to be at intermediate or high risk for MI are
often hospitalized for further evaluation and therapeutic
intervention.

Nursing Priorities
1. Relieve or control pain.
2. Prevent or minimize development of myocardial complications.
3. Provide information about disease process, prognosis,
and treatment.
4. Support client or significant other (SO) in initiating
necessary lifestyle or behavioral changes.

Discharge Goals
1. Desired activity level achieved, with return to activity
baseline, and self-care needs met with minimal or no
pain.
2. Remains free of complications.
3. Disease process, prognosis, and therapeutic regimen
understood.
4. Participates in treatment program and behavioral
changes.
5. Plan in place to meet needs after discharge.

NURSING DIAGNOSIS: acute Pain

May be related to
Increased cardiac workload and oxygen consumption
Decreased myocardial blood flow, tissue ischemia
Possibly evidenced by
Reports of pain varying in frequency, duration, and intensity, especially as condition worsens
Narrowed focus
Distraction behaviors, such as moaning, crying, pacing, or restlessness
Autonomic responses, such as diaphoresis, BP and pulse rate changes, pupillary dilation, increased or decreased respiratory rate
Desired Outcomes/Evaluation Criteria—Client Will
Pain Level
Report anginal episodes decreased in frequency, duration, and severity.
Demonstrate relief of pain as evidenced by stable vital signs and absence of muscle tension and restlessness.

ACTIONS/INTERVENTIONS
Pain Management
Independent
Instruct client to notify nurse immediately when chest pain
occurs.
Assess and document client response and effects of
medication.
Identify precipitating event, if any; identify frequency, duration,
intensity, and location of pain.
Observe for associated symptoms, such as dyspnea, nausea,
vomiting, dizziness, palpitations, and desire to urinate.
Evaluate reports of pain in jaw, neck, shoulder, arm, or hand
(typically on left side).
Place client at complete rest during anginal episodes.
Elevate head of bed if client is short of breath.
Monitor heart rate and rhythm.
Monitor vital signs every 5 minutes during initial anginal
attack.
Stay with client who is experiencing pain or appears anxious.
Maintain quiet, comfortable environment; restrict visitors as
necessary.
Provide light meals. Have client rest for 1 hour after meals.
Collaborative
Provide supplemental oxygen, as indicated.
Administer anti-anginal medication(s) promptly, as indicated,
for example:
Nitrates: NTG sublingual (Nitrostat, NitroQuick); extended
release tablets and capsules, such as Nitrong and
Nitrogard SR; metered-dose spray (Nitrolingual); transdermal
patch (Minitran, Nitrodisc); transdermal ointment
(Nitrol, Nitro-Bid); isosorbide (Isordil, Imdur)
Beta blockers, such as atenolol (Tenormin), carteolol
(Cartrol), labetalol (Normodyne), nadolol (Corgard),
metroprolol (Tropol XL), and propranolol (Inderal)
Calcium channel blockers, such as bepridil (Vascor),
amlodipine (Norvasc), nicardipine (Cardene), nifedipine
(Procardia), felodipine (Plendil), isradipine (DynaCirc),
and diltiazem (Cardizem)
Analgesics, such as acetaminophen (Tylenol)
Morphine sulfate (MS)
Monitor serial ECG changes.

RATIONALE
Pain and decreased cardiac output may stimulate the sympathetic
nervous system to release excessive amounts of
norepinephrine, which increases platelet aggregation, and
release of thromboxane A2. This potent vasoconstrictor
causes coronary artery spasm, which can precipitate,
complicate, and prolong an anginal attack. Unbearable
pain may cause vasovagal response, thus decreasing BP
and heart rate.
Provides information about disease progression. Aids in
evaluating effectiveness of interventions and may indicate
need for change in therapeutic regimen.
Helps differentiate chest pain and aids in evaluating possible
progression to unstable angina. Stable angina usually lasts
3 to 15 minutes and is often relieved by rest and sublingual
nitroglycerin (NTG); unstable angina is more intense,
occurs unpredictably, may last longer, and is not usually
relieved by NTG or rest.
Decreased cardiac output, which may occur during ischemic
myocardial episode, stimulates sympathetic or parasympathetic
nervous system, causing a variety of vague
sensations that client may not identify as related to
anginal episode.
Cardiac pain may radiate; for example, pain is often referred
to more superficial sites served by the same spinal cord
nerve level.
Reduces myocardial oxygen demand to minimize risk of
tissue injury and necrosis.
Facilitates gas exchange to decrease hypoxia and resultant
shortness of breath.
Clients with unstable angina have an increased risk of acute
life-threatening dysrhythmias, which occur in response to
ischemic changes and stress.
BP may initially rise because of sympathetic stimulation and
then fall if cardiac output is compromised. Tachycardia also
develops in response to sympathetic stimulation and may
be sustained as a compensatory response if cardiac output
falls.
Anxiety releases catecholamines, which increase myocardial
workload and can escalate or prolong ischemic pain.
Presence of nurse can reduce feelings of fear and
helplessness.
Mental or emotional stress increases myocardial workload.
Decreases myocardial workload associated with work of
digestion, reducing risk of anginal attack.
Increases oxygen available for myocardial uptake and reversal
of ischemia.
NTG has been the standard for treating and preventing
anginal pain for more than 100 years. Today, it is available
in many forms and is still the cornerstone of anti-anginal
therapy. Rapid vasodilator effect lasts 10 to 30 minutes
and can be used prophylactically to prevent, as well as
abort, anginal attacks. Long-acting preparations are used
to prevent recurrences by reducing coronary vasospasms
and reducing cardiac workload. May cause headache,
dizziness, and light-headedness—symptoms that usually
pass quickly. If headache is intolerable, alteration of dose
or discontinuation of drug may be necessary. Note: Isordil
may be more effective for clients with variant form of
angina.
Reduce angina by reducing the heart’s workload. (Refer to
ND: risk for decreased Cardiac Output following.) Note:
Often, these drugs alone are sufficient to relieve angina in
less severe conditions.
Produce relaxation of coronary vascular smooth muscle,
dilate coronary arteries, and decrease peripheral vascular
resistance.
Usually sufficient analgesia for relief of headache caused by
dilation of cerebral vessels in response to nitrates.
Potent opioid analgesic may be used in acute onset because
of its beneficial effects. Such effects include peripheral
vasodilatation and reduced myocardial workload; sedation,
which produces relaxation; and interrupted flow of vasoconstricting
catecholamines, thereby effectively relieving
severe chest pain. MS is given intravenously (IV) for rapid
action and because decreased cardiac output compromises
peripheral tissue absorption.
Ischemia during anginal attack may cause transient
ST-segment depression or elevation and T-wave inversion.
Serial tracings verify ischemic changes, which may
disappear when client is pain free. They also provide a
baseline against which to compare later pattern changes.


a. Morbidity: There are an estimated 79.4 million Americans
with some form of cardiovascular disease.
i. Coronary artery disease (CAD) accounting for 15.8 million;
angina, approximately 9 million
ii. 400,000 new cases annually, most are over age 65

Nursing Care Plan Pulmonary Tuberculosis PTB

PULMONARY TUBERCULOSIS (TB)

I. Pathophysiology
a. Bacterial infection by Mycobacterium tuberculosis bacilli
(TB)
i. Primarily affects the lungs (70% per Centers for Disease
Control and Prevention [CDC], 2004) although it can
invade other body systems
ii. Airborne droplets are inhaled, with the droplet nuclei
deposited within the alveoli of the lung.
b. Primary infection followed by a latent or dormant phase, or
by active disease in some individuals
c. When the immune system weakens, dormant TB organisms
can reactivate and multiply (reactivation TB).
II. Classifications
a. Latent: Body’s immune system has encapsulated the bacteria
into tiny capsules called tubercles, infection not transmissible
to others.
b. Active: Infection is spreading in the body and can be transmitted
to others.
III. Etiology
a. Following exposure, the bacilli may (1) be killed by the
immune system, (2) multiply and cause primary TB,
(3) become dormant and remain asymptomatic, or
(4) proliferate after a latency period (reactivation disease)
(Herchline & Amorosa, 2007).
b. Multidrug-resistant tuberculosis (MDR-TB)
i. Primary: caused by person-to-person transmission of a
drug-resistant organism
ii. Secondary: usually the result of nonadherence to
therapy or inappropriate treatment
iii. On the rise especially in large cities, in those previously
treated with antitubercular drugs, or in those who failed
to follow or complete a drug regimen
iv. Can progress from diagnosis to death in as little as 4 to
6 weeks
c. Risk factors: individuals with weakened immune systems
due to chronic conditions, advanced age, and malnutrition;
higher among persons with HIV infection, the homeless,
drug-addicted, and impoverished populations, as well as
among immigrants from or visitors to countries in which
TB is endemic
IV. Statistics (Centers for Disease Control and Prevention
[CDC], 2005, 2007)
a. Morbidity: In 2005, 14,903 cases of TB were reported in
the United States (down from a peak of 25,287 cases in
1993), with foreign-born individuals accounting for a
steadily increasing proportion (54%) of all reported TB
cases (Herschline, 2007); globally, 9.2 million new cases
reported annually.
b. Morbidity: Globally, 1.7 million deaths from TB occurred
in 2006, of which 0.2 million deaths were in HIV-positive
individuals (World Health Organization [WHO], 2008).

Care Setting
Most clients are treated in community clinics, but may be
hospitalized for diagnostic evaluation or initiation of therapy,
adverse drug reactions, or severe illness or debilitation.
This plan of care is intended to reflect care of the person
with active (rather than latent) TB, although if latent, when
TB is diagnosed, treatment will be initiated.

Nursing Priorities
1. Achieve and maintain adequate ventilation and oxygenation.
2. Prevent spread of infection.
3. Support behaviors and tasks to maintain health.
4. Promote effective coping strategies.
5. Provide information about disease process, prognosis,
and treatment needs.

Discharge Goals
1. Respiratory function adequate to meet individual need.
2. Complications prevented.
3. Lifestyle and behavior changes adopted to prevent spread
of infection.
4. Disease process, prognosis, and therapeutic regimen understood.
5. Plan in place to meet needs after discharge.

NURSING DIAGNOSIS: risk for Infection [spread/reactivation]

Risk factors may include
Inadequate primary defenses, decreased ciliary action and stasis of secretions
Tissue destruction, extension of infection
Lowered resistance, suppressed inflammatory process
Malnutrition
Environmental exposure
Insufficient knowledge to avoid exposure to pathogens
Possibly evidenced by
(Not applicable; presence of signs and symptoms establishes an actual diagnosis)
Desired Outcomes/Evaluation Criteria—Client Will
Risk Control
Identify interventions to prevent or reduce risk of spread of infection.
Demonstrate techniques and initiate lifestyle changes to promote safe environment.

ACTIONS/INTERVENTIONS

Infection Control
Independent
Review pathology of disease—active or inactive phases, dissemination
of infection through bronchi to adjacent tissues
or via bloodstream and lymphatic system—and potential
spread of infection via airborne droplet during coughing,
sneezing, spitting, talking, laughing, and singing.
Identify others at risk, such as household members, close
associates, and friends.
Instruct client to cough, sneeze, and expectorate into tissue
and to refrain from spitting. Review proper disposal of
tissue and good hand-washing techniques. Request return
demonstration.
Review necessity of infection control measures, such as
temporary respiratory isolation.
Monitor temperature, as indicated.
Identify individual risk factors for reactivation of tuberculosis,
such as lowered resistance associated with alcoholism,
malnutrition, intestinal bypass surgery, use of immunosuppressant
drugs, presence of diabetes mellitus or cancer, or
postpartum.
Stress importance of uninterrupted drug therapy. Evaluate
client’s potential for cooperation.
Review importance of follow-up and periodic reculturing of
sputum for the duration of therapy.
Encourage selection and ingestion of well-balanced meals.
Provide frequent small “snacks” in place of large meals as
appropriate.
Collaborative
Administer anti-infective agents, as indicated, for example:
Primary drugs: isoniazid (INH, Liniazid), rifampin (RIF,
Rifadin, Rimactane), pyrazinamide (PZA, Tebrazid), and
ethambutol (Etbi, Myambutol)
Rufabutin (Mucobutin)
Second-line drugs, such as ethionamide (Trecator-SC), paraaminosalicylate
(PAS), cycloserine (Seromycin), amikacin
(Amikin), and levofloxacin (Levoquin)
Investigational agents such as diarylquinoline (R207910)
Monitor laboratory studies, such as the following:
Sputum smear results
Liver function studies, such as aspartate aminotransferase
(AST), alinine aminotransferase (ALT)
Notify local health department.

RATIONALE
Helps client realize and accept necessity of adhering to medication
regimen to prevent reactivation and complications.
Understanding of how the disease is passed and awareness
of transmission possibilities help client and significant
other (SO) take steps to prevent infection of others.
Those exposed may require a course of drug therapy to
prevent development of infection.
Behaviors necessary to prevent spread of infection.
May help client understand need for protecting others while
acknowledging client’s sense of isolation and social stigma
associated with communicable diseases. Note: AFB can
pass through standard masks; therefore, particulate
respirators are required.
Febrile reactions are indicators of continuing presence of
infection.
Knowledge about these factors helps client alter lifestyle and
avoid or reduce incidence of exacerbation.
Contagious period may last only 2 to 3 days after initiation of
drug regimen, but in the presence of cavitation or moderately
advanced disease, risk of spread of infection may
continue up to 3 months. Compliance with multidrug
regimens for prolonged periods is difficult; therefore, DOT
should be considered.
Aids in monitoring the effects of medications and client’s
response to therapy.
Presence of anorexia or preexisting malnutrition lowers
resistance to infectious process and impairs healing. Small
snacks may enhance overall intake.
The goals for treatment of TB are to cure the individual and to
minimize transmission to other persons. It is essential that
treatment be tailored and supervision be based on each
client’s clinical and social circumstances. DOT may be the
most effective way to maximize the completion of therapy.
These four drugs should not be given in divided doses; all four
drugs should be given together. Evidence shows this
promotes the therapy’s effectiveness (CDC, 2005). INH is
usually drug of choice for those exposed and who are
at risk for developing TB. Extended therapy for up to
24 months is indicated for reactivation cases, extrapulmonary
reactivated TB, or in the presence of other medical
problems, such as diabetes mellitus or silicosis.
Prophylaxis with INH for 12 months should be considered
in HIV-positive clients with positive PPD test.
Therapeutic agent for atypical mycobacterium. May be used in
client with advanced HIV disease with TB.
These second-line drugs may be required when infection is
resistant to or intolerant of primary drugs or may be used
concurrently with primary antitubercular drugs. Note:
MDR-TB requires minimum of 18 to 24 months’ therapy
with at least three drugs in the regimen known to be
effective against the specific infective organism and that
client has not previously taken. Treatment is often extended
to 24 months in clients with severe symptoms or HIV
infection.
Innovative compounds are being developed based on new
drug targets and structure to provide shorter and more
effective treatment options. This agent, currently starting
human trials, cuts off the energy supply of the mycobacterium
and may be effective against drug-resistant forms
of TB.
Client who has three consecutive negative sputum smears
over a 3- to 5-month period is adhering to drug regimen
and who is asymptomatic will be classified as a nontransmitter.
The most common serious adverse effect of drug
therapy—particularly RIF, but possibly others as well—is
drug-induced hepatitis.
Required by law, and should be reported within 1 week of
diagnosis. Helpful in identifying contacts to reduce spread
of infection. Treatment course is long and usually handled
in the community, with public health nurse monitoring.

Nursing Care Plan Ventilatory Assistance

VENTILATORY ASSISTANCE (MECHANICAL)

I. Pathophysiology—impairment of respiratory function
affecting O2 uptake and CO2 elimination, requiring mechanical
assist to support or replace spontaneous breathing
a. Inability to maintain adequate oxygenation (hypoxemia)
b. Inability to maintain adequate ventilation due to apnea or
alveolar hypoventilation causing a rise in PaCO2 and a fall
in serum pH (respiratory acidosis)
c. Inability to continue the work of breathing (respiratory muscle
weakness or failure)
II. Mechanical Ventilators
a. Classified by method of cycling from the inspiratory phase to
the expiratory phase with signal to terminate the inspiratory
activity of the machine:
i. Preset volume (volume-cycled ventilator)
ii. Preset pressure limit (pressure-cycled ventilator)
iii. Preset time factor (time-cycled ventilator)
b. Mode of ventilation
i. Assist control: provides a breath with either a preset volume
for ventilator-initiated breaths or peak pressure
every time client takes a breath
ii. Pressure support ventilation: delivers preset level of positive
airway pressure, rather than volume, to decrease
work of breathing between ventilator-initiated breaths
iii. Continuous positive airway pressure (CPAP): continuous
level of elevated pressure during client-initiated breaths
to maintain adequate oxygenation and decrease the work
of breathing and the work of the heart
iv. Positive end-expiratory pressure (PEEP): adjunct to
mechanical ventilation using elevated pressure during the
expiratory phase of the ventilatory cycle to increase functional
residual capacity and surface area for gas exchange
c. Complications
i. Associated with endotracheal (ET) tube: tissue damage
to lips, tongue, throat; mucous plugs impairing ventilation
and obstruction caused by client biting tube; auto
PEEP; sinusitis or otitis; cuff herniation (rare)
ii. Associated with the ventilator: infection, hemodynamic
instability from positive-pressure ventilation, barotrauma,
gastrointestinal (GI) bleeding due to stress ulcer
III. Etiology
a. Acute respiratory hypoxemia: pulmonary edema, severe
pneumonia, sepsis, shock, acute respiratory distress syndrome
(ARDS), embolism, drug reaction of overdose, lung
trauma, high altitude
b. Acute respiratory acidosis: acute exacerbation of chronic
emphysema or asthma
c. Respiratory muscle weakness or failure: paralysis of the
diaphragm due to Guillain-Barré syndrome, myasthenia
gravis, spinal cord injury, or the affects of anesthetic and
muscle relaxant drugs; central nervous system (CNS) conditions,
such as stroke, brain tumor, infections, sleep apnea;
chest trauma, including fractures, pneumothorax
IV. Statistics
a. Morbidity: Acute respiratory failure requiring mechanical
ventilation accounts for approximately 30% of admissions
to intensive care units (ICUs) (Esteban et al, 2002).
b. Mortality: Hospital rate is 36%; 6-month mortality rate is
approximately 67% for ages 65 and older (Seneff et al, 2000).
c. Cost: Mean ICU cost in United States is $31,574 to $42,570
per year (Dasta et al, 2005); average total hospital stay,
$78,474; daily costs, $2,655; estimated cost for long-term
acute-care facility admissions, $56,825 (Seneff, 2000).

Care Setting
The focus of this plan of care is the client with invasive
mechanical ventilation who remains on a ventilator, whether in
an acute or postacute care setting. The expectation is that the
majority of clients will be weaned before discharge. However,
some clients are either unsuccessful at weaning or are not candidates
for weaning. For these clients, portions of this plan of
care would need to be modified for the discharge care setting,
whether it be an extended care facility or home.

Client Assessment
Database
Gathered data depend on the underlying pathophysiology
and reason for ventilatory support. Refer to the appropriate
plan of care.
Discharge Plan
Considerations
If ventilator-dependent, the plan may require changes in
physical layout of home, acquisition of equipment and
supplies, provision of a back-up power source, instruction
of significant other (SO) and caregivers, provision
for continuation of plan of care, assistance with transportation,
and coordination of resources and support
systems.

NURSING DIAGNOSIS: ineffective Breathing Pattern/impaired Spontaneous
Ventilation

May be related to
Respiratory center depression
Respiratory muscle weakness or paralysis
Noncompliant lung tissue (decreased lung expansion)
Alteration of client’s usual O2/CO2 ratio
Possibly evidenced by
Changes in rate and depth of respirations
Dyspnea and increased work of breathing, use of accessory muscles
Reduced VC and total lung volume
Tachypnea and bradypnea or cessation of respirations when off the ventilator
Cyanosis
Decreased PO2 and SaO2, increased PCO2
Increased restlessness, apprehension, and metabolic rate
Desired Outcomes/Evaluation Criteria—Client Will
Respiratory Status: Ventilation
Reestablish and maintain effective respiratory pattern via ventilator with absence of retractions and use of accessory muscles,
cyanosis, or other signs of hypoxia; ABGs and oxygen saturation within acceptable range.
Participate in efforts to wean (as appropriate) within individual ability.
Caregiver Will
Demonstrate behaviors necessary to maintain client’s respiratory function.

ACTIONS/INTERVENTIONS
Mechanical Ventilation Management: Invasive
Independent
Investigate etiology of respiratory failure.
Observe overall breathing pattern. Note respiratory rate,
distinguishing between spontaneous respirations and
ventilator breaths.
Auscultate chest periodically, noting presence or absence and
equality of breath sounds, adventitious breath sounds, and
symmetry of chest movement.
Count client’s respirations for 1 full minute and compare with
desired respirations and ventilator set rate.
Verify that client’s respirations are in phase with the ventilator.
Position client by elevating head of bed or chair if possible;
place in prone position, as indicated.
Inflate tracheal or ET tube cuff properly, using minimal leak
and occlusive technique. Check cuff inflation every 4 to 8
hours and whenever cuff is deflated and reinflated.
Check tubing for obstruction, such as kinking or accumulation
of water. Drain tubing as indicated, avoiding draining
toward client or back into the reservoir.
Check ventilator alarms for proper functioning. Do not turn off
alarms, even for suctioning. Remove from ventilator and
ventilate manually if source of ventilator alarm cannot be
quickly identified and rectified. Ascertain that alarms can be
heard in the nurses’ station.
Keep resuscitation bag at bedside and ventilate manually
whenever indicated.
Assist client in “taking control” of breathing if weaning is
attempted or ventilatory support is interrupted during procedure
or activity.
Collaborative
Assess ventilator settings routinely and readjust, as indicated:
Note operating mode of ventilation, that is, AC, pressure
support (PS), and so on.
Observe oxygen concentration percentage (FiO2); verify that
oxygen line is in proper outlet or tank; and monitor in-line
oxygen analyzer or perform periodic oxygen analysis.
Observe end-tidal CO2 (ETCO2) values.
Assess set respiratory frequency (f).
Assess VT. Verify proper function of spirometer, bellows, or
computer readout of delivered volume; note alterations
from desired volume delivery.
Flow rate
Pressure limit
Monitor I:E ratio
Set sigh rate, when used
Note inspired humidity and temperature; use heat moisture
exchanger (HME), as indicated.
Monitor serial ABGs and pulse oximetry
RATIONALE
Understanding the underlying cause of client’s particular
ventilatory problem is essential to the care of client, for
example, decisions about future capabilities and ventilation
needs and most appropriate type of ventilatory support.
Client on a ventilator can experience hyperventilation,
hypoventilation, or dyspnea and “air hunger” and attempt
to correct deficiency by overbreathing.
Provides information regarding airflow through the tracheobronchial
tree and the presence or absence of fluid,
mucous obstruction. Note: Frequent crackles or rhonchi
that do not clear with coughing or suctioning may indicate
developing complications, such as atelectasis, pneumonia,
acute bronchospasm, and pulmonary edema. Changes in
chest symmetry may indicate improper placement of the ET
tube or development of barotrauma.
Respirations vary depending on problem requiring ventilatory
assistance; for example, client may be totally ventilator dependent
or be able to take breath(s) on own between ventilatordelivered
breaths. Rapid client respirations can produce respiratory
alkalosis and prevent desired volume from being delivered
by ventilator. Slow client respirations and hypoventilation
increases PaCO2 levels and may cause acidosis.
Adjustments may be required in flow, tidal volume, respiratory
rate, and dead space of the ventilator, or client may need
sedation to synchronize respirations and reduce work of
breathing and energy expenditure.
Elevating the client’s head and helping client get out of bed while
still on the ventilator is both physically—helps decrease risk of
aspiration—and psychologically beneficial. Note: Use of prone
position is thought to improve oxygenation in client with
severe hypoxic respiratory failure. However, it is not widely
used due to the difficulties associated with placing and providing
care to the intubated client in prone position as well as
lack of studies showing its benefit in reducing mortality or
duration of ventilation (Sud et al, 2008).
The cuff must be properly inflated to ensure adequate ventilation
and delivery of desired tidal volume and to decrease
risk of aspiration. Note: In long-term clients, the cuff may
be deflated most of the time or a noncuffed tracheostomy
tube used if the client’s airway is protected.
Kinks in tubing prevent adequate volume delivery and increase
airway pressure. Condensation in tubing prevents proper
gas distribution and predisposes to bacterial growth.
Ventilators have a series of visual and audible alarms, such
as oxygen, low volume or apnea, high pressure, and inspiratory/
expiratory (I:E) ratio. Turning off or failure to reset
alarms places client at risk for unobserved ventilator failure
or respiratory distress or arrest.
Provides or restores adequate ventilation when client or
equipment problems require client to be temporarily
removed from the ventilator.
Coaching client to take slower, deeper breaths; practice
abdominal or pursed-lip breathing; assume position of
comfort; and use relaxation techniques can be helpful in
maximizing respiratory function.
Controls or settings are adjusted according to client’s primary
disease and results of diagnostic testing to maintain
parameters within appropriate limits.
Client’s respiratory requirements, presence or absence of an
underlying disease process, and the extent to which client
can participate in ventilatory effort determine parameters of
each setting. PS has advantages for client on long-term
ventilation because it allows client to strengthen pulmonary
musculature without compromising oxygenation and
ventilation during the weaning process.
FiO2 is adjusted (21% to 100%) to maintain an acceptable
oxygen percentage and saturation, for example, 90%, for
client’s condition.
Measures the amount of exhaled CO2 with each breath and is
displayed graphically to spot CO2 exchange problems early
before they show up on ABGs. In some cases, a slightly
higher level of CO2 can be beneficial, such as for the client
with long-standing emphysema. In this instance, elevated
PCO2 is accepted without correction, leading to the term
“permissive hypercapnia” (Byrd et al, 2006).
Respiratory rate of 10 to 15 per minute may be appropriate
except for client with COPD and CO2 retention. In these individuals,
rate and volume should be adjusted to achieve personal
baseline PaCO2, not necessarily a “normal” PaCO2.
Monitors amount of air inspired and expired. Changes may
indicate alteration in lung compliance or leakage through
machine or around tube cuff. Note: For the client without
preexisting lung disease, the VT and rate are traditionally
selected by using VT of 12 mL/kg delivered 12 times per
minute in the AC mode. For clients with COPD, the VT and
rate are slightly reduced to 10 mL/kg at 10 breaths per minute
to prevent overinflation and hyperventilation (Girard &
Bernard, 2007). Many clinicians now use a smaller VT (6 to
8 mL/kg), especially in clients with ARDS and sometimes in
obstructive and restrictive lung disease, in order to reduce
air-trapping and mechanical stress on the lung.
Speed with which the VT is delivered is usually about 50 L/min,
but is variable in order to maintain I:E ratio appropriate for
specific situation.
Regulates the amount of pressure the volume-cycled ventilator
can generate to deliver the preset VT with usual setting at
10 to 20 cm H2O above the client’s peak inspiratory pressure.
Airway pressure should remain relatively constant.
Increased pressure alarm reading reflects (1) increased
airway resistance as may occur with bronchospasm;
(2) retained secretions; and (3) decreased lung compliance
as may occur with obstruction of the ET tube, development
of atelectasis, ARDS, pulmonary edema, worsening COPD,
or pneumothorax. Low airway-pressure alarms may be
triggered by pathophysiological conditions causing
hypoventilation, such as disconnection from ventilator, low
ET cuff pressure, ET tube displaced above the vocal cords,
client “overbreathing,” or out of phase with the ventilator.
Expiratory phase is usually twice the length of the inspiratory
rate, but may be longer to compensate for air-trapping to
improve gas exchange in the client with COPD.
Clinicians once recommended that periodic machine breaths
that were 1.5 to 2 times the preset VT be given 6 to 8 times
per hour. At present, accounting for sighs is not recommended
if the client is receiving VT of 10 to 12 mL/kg or if
PEEP is required. When a low VT is used, sighs are preset at
1.5 to 2 times the VT and delivered 6 to 8 times per hour if
the peak and plateau pressures are within acceptable limits
(Byrd et al, 2006).
Usual warming and humidifying function of nasopharynx is
bypassed with intubation. Dehydration can dry up normal
pulmonary fluids, cause secretions to thicken, and increase
risk of infection. Temperature should be maintained at
about body temperature to reduce risk of damage to cilia
and hyperthermia reactions. The introduction of a heated
wire circuit to the traditional system significantly reduces
the problem of “rainout” or condensation in the tubing.
Adjustments to ventilator settings may be required, depending
on client’s response and trends in gas exchange
parameters.

Nursing Care Plan Heart Failure Chronic

HEART FAILURE: CHRONIC

I. Pathophysiology
a. Remodeling of the myocardium (as a structural response to
injury) changes the heart from an efficient football shape
to an inefficient basketball shape, making coordinated
contractility difficult.
i. Ventricular dilation (systolic dysfunction) results in poor
contractility and inadequate emptying of chamber.
ii. Ventricular stiffening (diastolic dysfunction) impairs
ability of chamber to relax and receive and eject blood.
b. Failure of the left and/or right chambers of the heart results
in insufficient output to meet metabolic needs of organ and
tissues.
c. Cardiac-related elevation of pulmonary or systemic venous
pressures leads to organ congestion.
d. Backward heart failure (HF): passive engorgement of the
veins caused by elevated systemic venous pressure or a
“backward” rise in pressure proximal to the failing cardiac
chambers (right ventricular failure)
e. Forward HF: decreased cardiac output with reduced forward
flow into the aorta, systemic circulation (inadequate renal
blood flow leads to sodium and water retention), and increasing
pulmonary venous pressure results in fluid accumulation
in alveoli (left ventricular failure)
f. Myocardial muscle dysfunction associated with left ventricular
hypertrophy (LVH) causes decreased cardiac output, activating
neurohormones.
g. Elevated circulating or tissue levels of neurohormones,
norepinephrine, angiotensin II, aldosterone, endothelin,
vasopressin, and cytokines, causes sodium retention and
peripheral vasoconstriction, increasing hemodynamic
stresses on the ventricle.
II. Classification
a. New York Heart Association Functional Classification
System for HF (9th ed, 1994)
i. Class I—normal physical activity is not limited by
symptoms.
ii. Class II—ordinary physical activity results in fatigue,
dyspnea, or other symptoms.
iii. Class III—marked limitation in normal physical
activity
iv. Class IV—symptoms at rest or with any physical
activity
b. American College of Cardiology/American Heart
Association (ACC/AHA) 2005 Guidelines include specific
recommendations for each stage (Hunt et al, 2005).
i. Stage A—high risk for HF associated with such conditions
as hypertension, diabetes, and obesity. Treatment is
focused on comorbidity.
ii. Stage B—presence of structural heart disease, such as
left ventricular remodeling, LVH, or previous myocardial
infarction (MI), but is asymptomatic. Treatment is
focused on retarding the progression of ventricular
remodeling and delaying the onset of HF symptoms.
iii. Stage C—clients with past or current HF symptoms
associated with structural heart disease, such as
advanced ventricular remodeling. Treatment is focused
on modifying fluid and dietary intake and drug therapies
as well as nonpharmacological measures, such as
biventricular pacing and valvular or revascularization
surgery.
iv. Stage D—refractory advanced HF symptoms at rest or
with minimal exertion and frequently requiring intervention
in the acute setting. Treatment is focused on promoting
clinical stability including supportive therapy to sustain
life, such as left ventricular assist device, continuous
intravenous (IV) inotropic therapy, experimental surgery
or drugs, a heart transplant, or end-of-life or hospice care.
III. Etiology
a. Multifactoral
i. Complex clinical syndrome resulting from any structural
or functional cardiac disorder that impairs the ability of
the ventricle to fill with or eject blood (ACC/AHA 2005
Guidelines; see Hunt et al, 2005).
ii. Risk factors and comorbidities—hypertension; obesity;
diabetes; coronary artery disease (CAD); peripheral and
cerebrovascular disease; valvular heart disease with onset
of atrial fibrillation (AF); sleep disorders such as sleep
apnea; history of exposure to cardiotoxins, for example,
chemotherapy, alcohol, and cocaine; family history of
cardiomyopathy
IV. Statistics
a. High morbidity and mortality, particularly in clients with
New York Heart Association Class IV symptoms (Hunt et
al, 2005)
b. Morbidity: 5.2 million Americans have HF. (National
Heart, Lung and Blood Institute [NHLBI], 2007)
i. Approximately 550,000 new cases reported annually
(Centers for Disease Control and Prevention [CDC],
2006b).
ii. 1.1 million hospitalizations reported annually (CDC,
2006b).
c. Mortality: 287,000 deaths reported annually (CDC, 2006b).
d. Cost: $29.6 billion spent in 2006, making HF the most
common reason for hospitalization of Medicare clients
(CDC, 2006b).

Care Setting
Although generally managed at the community level, an
in-client stay may be required for periodic exacerbation of
failure or development of complications.

Nursing Priorities
1. Improve myocardial contractility and systemic perfusion.
2. Reduce fluid volume overload.
3. Prevent complications.
4. Provide information about disease and prognosis, therapy
needs, and prevention of recurrences.

Discharge Goals
1. Cardiac output adequate for individual needs.
2. Complications prevented or resolved.
3. Optimum level of activity and functioning attained.
4. Disease process, prognosis, and therapeutic regimen
understood.
5. Plan in place to meet needs after discharge.

NURSING DIAGNOSIS: decreased Cardiac Output

May be related to
Altered myocardial contractility, inotropic changes
Alterations in rate, rhythm, electrical conduction
Structural changes, such as valvular defects and ventricular aneurysm
Possibly evidenced by
Increased heart rate (tachycardia), dysrhythmias, ECG changes
Changes in BP (hypotension, hypertension)
Extra heart sounds (S3, S4)
Decreased urine output
Diminished peripheral pulses
Cool, ashen skin and diaphoresis
Orthopnea, crackles, JVD, liver engorgement, edema
Chest pain
Desired Outcomes/Evaluation Criteria—Client Will
Cardiac Pump Effectiveness
Display vital signs within acceptable limits, dysrhythmias absent or controlled, and no symptoms of failure, for example,
hemodynamic parameters within acceptable limits and urinary output adequate.
Report decreased episodes of dyspnea and angina.
Cardiac Disease Self-Management
Participate in activities that reduce cardiac workload.

ACTIONS/INTERVENTIONS
Hemodynamic Regulation
Independent
Auscultate apical pulse; assess heart rate, rhythm, and document
dysrhythmia if telemetry available.
Note heart sounds.
Palpate peripheral pulses.
Monitor BP.
Inspect skin for pallor and cyanosis.
Monitor urine output, noting decreasing output and dark or
concentrated urine.
Note changes in sensorium, for example, lethargy, confusion,
disorientation, anxiety, and depression.
Encourage rest, semirecumbent in bed or chair. Assist with
physical care, as indicated.
Provide quiet environment, explain medical and nursing management,
help client avoid stressful situations, listen and
respond to expressions of feelings or fears.
Provide bedside commode. Have client avoid activities eliciting
a vasovagal response, for instance, straining during defecation
and holding breath during position changes.
Elevate legs, avoiding pressure under knee. Encourage active
and passive exercises. Increase ambulation and activity as
tolerated.
Check for calf tenderness; diminished pedal pulse; and
swelling, local redness, or pallor of extremity.
Withhold digoxin, as indicated, and notify physician if marked
changes occur in cardiac rate or rhythm or signs of digoxin
toxicity occur.
Collaborative
Administer supplemental oxygen, as indicated.
Administer medications, as indicated, for example:
Loop diuretics, such as furosemide (Lasix), ethacrynic acid
(Edecrin), and bumetanide (Bumex); thiazide and thiazidelike
diuretics, such as hydrocholorothiazide (HydroDiuril)
and metolazone (Zaroxolyn)
ACE inhibitors, such as benazepril (Lotensin), captopril
(Capoten), lisinopril (Prinivil), enalapril (Vasotec),
quinapril (Accupril), ramipril (Altace), and moexipril
(Univasc)
ARBs (also known as angiotensin II receptor antagonists),
such as candesartan (Atacand), losartan (Cozaar),
eprosartan (Teveten), ibesartan (Avapro), and valsartan
(Diovan)
Vasodilators, such as nitrates (Nitro-Dur, Isordil); arteriodilators
such as hydralazine (Apresoline); combination
drugs, such as prazosin (Minipress) and nesiritide
(Natrecor)
-adrenergic receptor antagonists (also called beta blockers),
such as carvedilol (Coreg), bisoprolol (Zebeta), and metoprolol
(Lopressor)
Digoxin (Lanoxin)
Inotropic agents, such as amrinone (Inocor), milrinone
(Primacor), and vesnarinone (Arkin-Z)
Aldosterone antagonist, such as eplerenone (Inspra)
Morphine sulfate
Anti-anxiety agents and sedatives
Anticoagulants, such as low-dose heparin and warfarin
(Coumadin)
Administer IV solutions, restricting total amount, as indicated.
Avoid saline solutions.
Monitor and replace electrolytes, as indicated.
Monitor serial ECG and chest x-ray changes.
Measure cardiac output and other functional parameters, as
indicated.
Prepare for insertion and maintain pacemaker or
pacemaker/defibrillator, if indicated.
Prepare for surgery, such as valve replacement, angioplasty,
coronary artery bypass grafting (CABG), as indicated:
Cardiomyoplasty
Transmyocardial revascularization
Assist with and maintain mechanical circulatory support
system, such as intra-aortic balloon pump (IABP) or leftventricular
assist device (LVAD), when indicated.

RATIONALE

Tachycardia is usually present, even at rest, to compensate for
decreased ventricular contractility. Premature atrial contractions
(PACs), paroxysmal atrial tachycardia (PAT), PVCs,
multifocal atrial tachycardia (MAT), and AF are common
dysrhythmias associated with HF, although others may also
occur. Note: Intractable ventricular dysrhythmias unresponsive
to medication suggest ventricular aneurysm.
S1 and S2 may be weak because of diminished pumping
action. Gallop rhythms are common (S3 and S4), produced
as blood flows into noncompliant, distended chambers.
Murmurs may reflect valvular incompetence and stenosis.
Decreased cardiac output may be reflected in diminished radial,
popliteal, dorsalis pedis, and post-tibial pulses. Pulses may
be fleeting or irregular to palpation, and pulsus alternans
may be present.
In early, moderate, or chronic HF, BP may be elevated because
of increased SVR. In advanced HF, the body may no longer
be able to compensate, and profound or irreversible
hypotension may occur. Note: Many clients with HF have
consistently low systolic BP (80 to 100 mm Hg) due to their
disease process and the medications they take, and most
tolerate these BPs without incident (Wingate, 2007).
Pallor is indicative of diminished peripheral perfusion secondary
to inadequate cardiac output, vasoconstriction, and
anemia. Cyanosis may develop in refractory HF. Dependent
areas are often blue or mottled as venous congestion
increases.
Kidneys respond to reduced cardiac output by retaining water
and sodium. Urine output is usually decreased during the
day because of fluid shifts into tissues, but may be
increased at night because fluid returns to circulation when
client is recumbent.
May indicate inadequate cerebral perfusion secondary to
decreased cardiac output.
Physical rest should be maintained during acute or refractory
HF to improve efficiency of cardiac contraction and to
decrease myocardial oxygen consumption and workload.
Physical and psychological rest helps reduce stress, which can
produce vasoconstriction, elevating BP and increasing heart
rate and work.
Commode use decreases work of getting to bathroom or
struggling to use bedpan. Vasovagal maneuver causes
vagal stimulation followed by rebound tachycardia, which
further compromises cardiac function and output.
Decreases venous stasis and may reduce incidence of thrombus
and embolus formation.
Reduced cardiac output, venous pooling and stasis, and
enforced bedrest increases risk of thrombophlebitis.
Incidence of toxicity is high (20%) because of narrow margin
between therapeutic and toxic ranges. Digoxin may have to
be discontinued in the presence of toxic drug levels, a slow
heart rate, or low potassium level. (Refer to CP:
Dysrhythmias; ND: risk for Poisoning: digoxin toxicity.)
Increases available oxygen for myocardial uptake to combat
effects of hypoxia and ischemia.
A variety of medications (usually a combination of a
diuretic, an ACEI, or ARB and beta blocker) may be used
to increase stroke volume, improve contractility, and
reduce congestion.
Diuretics, in conjunction with restriction of dietary sodium and
fluids, often lead to clinical improvement in clients with
stages I and II HF. In general, type and dosage of diuretic
depend on cause and degree of HF and state of renal function.
Preload reduction is most useful in treating clients with
a relatively normal cardiac output accompanied by congestive
symptoms. Loop diuretics block chloride reabsorption,
thus interfering with the reabsorption of sodium and water.
ACE inhibitors represent first-line therapy to control HF by
decreasing ventricular filling pressures and SVR, while
increasing cardiac output with little or no change in BP and
heart rate.
Antihypertensive and cardioprotective effects are attributable
to selective blockade of AT1 (angiotensin II) receptors and
angiotensin II synthesis. Note: ARBs used in combination
with ACE inhibitors and beta blockers are thought to have
decreased hospitalizations for HF clients.
Vasodilators are used to increase cardiac and renal output,
reducing circulating volume (preload and afterload), and
decreasing SVR, thereby reducing ventricular workload.
Note: Nesiritide is used in acutely decompensated congestive
HF and has been used with digoxin, diuretics, and ACE
inhibitors. Parenteral vasodilators are reserved for clients
with severe HF or those unable to take oral medications.
Useful in the treatment of HF by blocking the cardiac effects of
chronic adrenergic stimulation. Many clients experience
improved activity tolerance and EF.
Increases force of myocardial contraction when diminished
contractility is the cause of HF and slows heart rate by
decreasing conduction velocity and prolonging refractory
period of the atrioventricular (AV) junction to increase cardiac
efficiency and output.
These medications are useful for short-term treatment of HF
unresponsive to cardiac glycosides, vasodilators, and diuretics
in order to increase myocardial contractility and produce
vasodilation. Positive inotropic properties have reduced
mortality rates (by 50%) and improved quality of life.
Approved by the Food and Drug Administration (FDA) in 2003,
eplerenone has been shown to improve survival in HF,
especially following MI.
Decreases vascular resistance and venous return, reducing
myocardial workload, especially when pulmonary congestion
is present.
Allays anxiety and breaks the feedback cycle of anxiety to
catecholamine release to anxiety. Promotes rest and relaxation,
reducing oxygen demand and myocardial workload.
May be used prophylactically to prevent thrombus and embolus
formation in the presence of risk factors, such as venous
stasis, enforced bedrest, cardiac dysrhythmias, and history
of previous thrombolic episodes.
Because of existing elevated left ventricular pressure, client
may not tolerate increased fluid volume (preload). Clients
with HF also excrete less sodium, which causes fluid retention
and increases myocardial workload.
Fluid shifts and use of diuretics can alter electrolytes (especially
potassium and chloride), which affect cardiac rhythm and
contractility.
ST-segment depression and T-wave flattening can develop
because of increased myocardial oxygen demand, even if
no CAD is present. Chest x-ray may show enlarged heart
and changes of pulmonary congestion.
Cardiac index, preload and afterload, contractility, and cardiac
work can be measured noninvasively by using thoracic
electrical bioimpedance (TEB) technique. TEB is useful in
determining effectiveness of therapeutic interventions and
response to activity.
May be necessary to correct bradydysrhythmias unresponsive
to drug intervention, which can aggravate congestive
failure and produce pulmonary edema. Note: Biventricular
pacemaker and cardiac defibrillators are designed to provide
resynchronization for the heart by simultaneous electrical
activation of both the right and left sides of the heart,
thereby creating a more effective and efficient pump.
HF due to ventricular aneurysm or valvular dysfunction may
require aneurysmectomy or valve replacement to improve
myocardial contractility and function. Revascularization of
cardiac muscle by CABG may be done to improve cardiac
function.
Cardiomyoplasty, an experimental procedure in which the
latissimus dorsi muscle is wrapped around the heart and
electrically stimulated to contract with each heartbeat, may
be done to augment ventricular function while the client is
awaiting cardiac transplantation or when transplantation is
not an option.
Other new surgical techniques include transmyocardial revascularization,
such as percutaneous transmyocardial revascularization
(PTMR), using CO2 laser technology, in which a
laser is used to create multiple 1-mm-diameter channels in
viable but underperfused cardiac muscle.
An IABP may be inserted as a temporary support to the failing
heart in the critically ill client with potentially reversible HF.
A battery-powered LVAD may also be used positioned
between the cardiac apex and the descending thoracic or
abdominal aorta. This device receives blood from the left
ventricle and ejects it into the systemic circulation, often
allowing client to resume a nearly normal lifestyle while
awaiting heart transplantation, or in some instances,
allowing the heart to recover and regain its function. With
end-stage HF, cardiac transplantation may be indicated.

Nursing Care Plan Hypertension: Severe

HYPERTENSION: SEVERE

I.Pathophysiology—malignant or cancerous tumor, starting
from the cells of the breast tissue and occurring primarily in
women, although men may also be affected.
b. Types (NCCN, 2007)
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cout3.This is cout3.
A. Pathophysiology—malignant or cancerous tumor, starting
from the cells of the breast tissue and occurring primarily in
women, although men may also be affected.
b. Types (NCCN, 2007)
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iv. Adaptive: e.g., regulation of intracellular Na+ and Ca++
by cell membrane ion pumps
v. Neural: variety of complex nerve mechanisms
vi. Endocrine: pheochromocytoma, primary aldosteronism
vii. Humoral: varied agents that constrict and dilate blood
vessels
viii. Hemodynamic: blood volume or viscosity, intrarenal
hemodynamics
II. Classification—2003 Guidelines National Heart, Lung, and
Blood Institute (NHLBI)
a. Normal blood pressure (BP)—less than 120/80 mm Hg
b. Prehypertension—120/80 to 139/89 mm Hg
c. Hypertension—greater than 140/90 mm Hg

III. Degree of Severity
a. Stage I (mild) - 140/90 to 159/99 mm Hg
b. Stage II (moderate) - 160/100 mm Hg or greater
c. Stage II (severe) - systolc pressure greater than 180 and diastolic pressure greater than 110
d. Stage IV (very severe) - systolic pressure greater than 210 or greater with diastolic pressure greater than 120

IV. Etiology
a. Primary (essential), which accounts for approximately 85% to 95% of all cases, has no identifiable cause
b. Secondary, which occurs as a result of an identifiable,
sometimes correctable,pathological condition, such as
kidney disorders, adrenal gland tumors, or primary
aldosteronism, medications, drugs, or other chemicals
V. Statistics (NHLBI, 2006; Centers for Disease Control and
Prevention [CDC], CDC, 2006b; 2007a)
a. Morbidity: 72 million Americans are hypertensive (nearly
1 in 3).
i. 23% of adults aged 20 to 75 are hypertensive.
ii. 70% of adults over age 75 are hypertensive.
iii. Approximately 20% are undiagnosed.
iv. Prevalence: African Americans 32%, whites 23%,
Hispanics 23%
b. Mortality: There are more than 19,000 deaths per year.
c. Cost: $47.2 billion is spent per year.

Care Setting
Although hypertension is usually treated in a community setting,
management of stages III and IV with symptoms of complications
or compromise may require inpatient care, especially
when target organ disease (TOD) is present. The majority
of interventions included here can be used in either setting.

Nursing Priorities
1. Maintain or enhance cardiovascular functioning.
2. Prevent complications.
3. Provide information about disease process, prognosis,
and treatment regimen.
4. Support active client control of condition.

Discharge Goals
1. BP within acceptable limits for individual.
2. Cardiovascular and systemic complications prevented or
minimized.
3. Disease process, prognosis, and therapeutic regimen
understood.
4. Necessary lifestyle or behavioral changes initiated.
5. Plan in place to meet needs after discharge.

NURSING DIAGNOSIS: risk for decreased Cardiac Output

Risk factors may include
Increased vascular resistance, vasoconstriction
Myocardial ischemia
Ventricular hypertrophy or rigidity
Possibly evidenced by
(Not applicable; presence of signs and symptoms establishes an actual diagnosis)
Desired Outcomes/Evaluation Criteria—Client Will
Circulation Status
Participate in activities that reduce BP and cardiac workload.
Maintain BP within individually acceptable range.
Demonstrate stable cardiac rhythm and rate within normal range.

ACTIONS/INTERVENTIONS

Hemodynamic Regulation
Independent
Measure BP in both arms or thighs. Take three readings, 3 to
5 minutes apart while client is at rest, then sitting, and then
standing for initial evaluation. Use correct cuff size and
accurate technique. Take note of elevations in systolic as
well as diastolic readings.

Auscultate heart tones and breath sounds.
Observe skin color, moisture, temperature, and capillary refill
time.
Note dependent and generalized edema.
Provide calm, restful surroundings, minimize environmental
activity and noise. Consider limiting the number of visitors
or length of visitation.
Maintain activity restrictions during crisis situation such as
bedrest or chair rest and schedule periods of uninterrupted
rest; assist client with self-care activities as needed.
Provide comfort measures, such as back and neck massage or
elevation of head.
Instruct in relaxation techniques, guided imagery, and
distractions.
Monitor response to medications that control BP.
Collaborative
Administer medications, as indicated:
Diuretics, for example, thiazide, such as chlorothiazide
(Diuril), hydrochlorothiazide (Esidrix, HydroDIURIL),
hydrochlorothiazide with triamterene (Diazide, Maxide) or
amiloride (Modiuretic), bendroflumethiazide (Naturetin),
indapamide (Lozol), metolazone (Mykrox, Zaroxolyn); and
loop diuretics, such as furosemide (Lasix), bumetanide
(Bumex), and torsemide (Demadex)
Potassium-sparing diuretics, such as spironolactone
(Aldactone), triamterene (Dyrenium), and amiloride
(Midamor)
Beta blockers, such as doxazosin (Cardura), acebutolol
(Sectral), metoprolol (Lopressor), labetalol (Normodyne),
atenolol (Tenormin), nadolol (Corgard), carvedilol
(Coreg), propranolol (Inderal), methyldopa (Aldomet),
clonidine (Catapres), prazosin (Minipress), terazosin
(Hytrin), pindolol (Visken), and timolol (Blocarden)
Calcium channel blockers, such as nifedipine (Adalat,
Procardia), verapamil (Calan, Isoptin, Verelan), diltiazem
(Cardizem), amlodipine (Norvasc), isradipine (DynaCirc),
nicardipine (Cardene), and felodipine (Plendil)
Direct-acting oral vasodilators, such as hydralazine
(Apresoline) and minoxidil (Loniten)
Direct-acting parenteral vasodilators, such as diazoxide
(Hyperstat), nitroprusside (Nitropress), and labetalol
(Normodyne)
Angiotensin-converting enzyme (ACE) inhibitors, such as
captopril (Capoten), enalapril (Vasotec), benazepril
(Lotensin), lisinopril (Zestril), fosinopril (Monopril),
ramipril (Altace), moexipril (Univasc), and trandolapril
(Mavik)
Angiotensin II receptor blockers (ARBs), such as candesartan
(Atacand), olmesartan (Benicar), valsartan (Diovan),
losartan (Cozaar), and irbesartan (Avapro)
Aldosterone blockers, such as eplerenone (Inspra) and
spironolactone
Implement dietary restrictions, as indicated, such as reducing
calories and avoiding refined carbohydrates, sodium, fat,
and cholesterol. (Refer to ND, imbalanced Nutrition.)
Prepare for surgery when indicated.

RATIONALE

Serial measurements using correct equipment provide a more
complete picture of vascular involvement and scope of
problem. Progressive diastolic readings above 120 mm Hg
are considered first accelerated, then malignant (very
severe). Systolic hypertension also is an established risk
factor for cerebrovascular disease and ischemic heart
disease even when diastolic pressure is not elevated. In
younger client with normal systolic readings, elevated
diastolic numbers may indicate prehypertension.
Bounding carotid, jugular, radial, and femoral pulses may be
observed and palpated. Pulses in the legs and feet may be
diminished, reflecting effects of vasoconstriction and
venous congestion.
S4 is commonly heard in severely hypertensive clients because
of the presence of atrial hypertrophy. Development of S3
indicates ventricular hypertrophy and impaired cardiac
functioning. Presence of crackles or wheezes may indicate
pulmonary congestion secondary to developing or chronic
heart failure.
Presence of pallor; cool, moist skin; and delayed capillary refill
time may be due to peripheral vasoconstriction or reflect
cardiac decompensation and decreased output.
Indicates heart or kidney failure or vascular impairment.
Helps reduce sympathetic stimulation and promotes
relaxation.
Reduces physical stress and tension that affect BP and the
course of hypertension.
Decreases discomfort and may reduce sympathetic
stimulation.
Can reduce stressful stimuli and produce calming effect,
thereby reducing BP.
Response to drug therapy is dependent on both the individual
drugs and their synergistic effects. Because of potential side
effects and drug interactions, it is important to use the smallest
number and lowest dosage of medications possible.
Diuretics are considered first-line medications for uncomplicated
hypertension and may be used alone or in association with
other drugs, such as beta blockers, to reduce BP in clients
with relatively normal renal function. These diuretics also
potentiate the effects of other antihypertensive agents by limiting
fluid retention and may reduce the incidence of stroke
and heart failure.
These drugs produce marked diuresis by inhibiting resorption
of sodium and chloride and are effective antihypertensives,
especially in clients who are resistant to thiazides or have
renal impairment. May be given in combination with a thiazide
diuretic to minimize potassium loss.
Beta blockers are recommended for BP control in clients with
heart failure and cardiovascular disease. Cardioselective
beta blockers, such as acebutolol, atenolol, and metroprolol,
primarily affect -1 receptors in the heart, slowing heart
rate and decreasing the heart’s workload. Nonselective
beta blockers, such as propranolol and timolol, also
decrease the heart’s workload and promote vasodilation,
but they exert effects on the -2 receptors on the bronchioles
as well, potentially increasing symptoms of reactive
airway disease and chronic obstructive pulmonary disease.
Cardioselective beta blockers are safer choices for patients
with pulmonary disorders (Woods & Moshang, 2006).
Calcium channel blockers are categorized into two types.
One group, such as amlodipine, diltiazem, and isradipine,
primarily affects blood vessels and can be used to treat
severe hypertension when a combination of a diuretic and
a sympathetic inhibitor does not sufficiently control BP.
Action is to relax vascular smooth muscle, thereby reducing
vascular resistance.
These are given intravenously (IV) for management of hypertensive
emergencies.
ACE inhibitors are generally considered first-line drugs for
clients with documented congestive heart failure (CHF),
diabetes, and those at risk for renal failure.
ARBs block the action of angiotensin II. As a result, blood
vessels dilate and BP is reduced.
Aldosterone antagonists block the effects of aldosterone on
the kidneys, allowing the kidneys to excrete extra sodium
and water, thereby reducing BP.
Limiting sodium and sodium-rich processed foods can help
manage fluid retention and, with associated hypertensive
response, decrease myocardial workload. A diet rich in
calcium, potassium, and magnesium may help lower BP.
When hypertension is due to pheochromocytoma, removing
the tumor corrects the condition.