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Decreased Cardiac Output — Arrhythmia Nursing Care Plans

Nurseslabs — Sat, 05 May 2012 04:30:08 +0000

NURSING DIAGNOSIS: Cardiac Output, risk for decreased Risk factors may include

Altered electrical conduction
Reduced myocardial contractility

Desired Outcomes

Maintain/achieve adequate cardiac output as evidenced by BP/pulse within normal range, adequate urinary output, palpable pulses of equal quality, usual level of mentation.
Display reduced frequency/absence of dysrhythmia(s).
Participate in activities that reduce myocardial workload.

Nursing Interventions & Rationale

Nursing Interventions	Rationale
Palpate pulses (radial, carotid, femoral, dorsalis pedis), noting rate, regularity, amplitude (full/thready), and symmetry. Document presence of pulsus alternans, bigeminal pulse, or pulse deficit.	Differences in equality, rate, and regularity of pulses are indicative of the effect of altered cardiac output on systemic/peripheral circulation.
Auscultate heart sounds, noting rate, rhythm, presence of extra heartbeats, dropped beats.	Specific dysrhythmias are more clearly detected audibly than by palpation. Hearing extra heartbeats or dropped beats helps identify dysrhythmias in the unmonitored patient.
Monitor vital signs. Assess adequacy of cardiac output/tissue perfusion, noting significant variations in BP/pulse rate equality, respirations, changes in skin color/temperature, level of consciousness/sensorium, and urine output during episodes of dysrhythmias.	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.
Determine type of dysrhythmia and document with rhythm strip (if cardiac/telemetry monitoring is available): Sinus tachycardia; Sinus bradycardia; Atrial dysrhythmias, e.g., PACs, atrial flutter, atrial fibrillation (AF), atrial supraventricular tachycardias) (i.e., PAT, MAT, SVT); Ventricular dysrhythmias, e.g., premature ventricular contractions/ventricular premature beats (PVCs/VPBs), ventricular tachycardia (VT), ventricular flutter/ fibrillation (VF); Heart blocks.	Useful in determining need for/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 patients with ischemic heart disease because of shortened diastolic filling time and increased oxygen demands. These patients may require medications. Bradycardia is common in patients 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. Patients 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 atrial fibrillation. Acute and chronic atrial flutter and/or fibrillation (the most common dysrhythmia) can occur with coronary artery or valvular disease and may or may not be pathological. Rapid atrial flutter/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, digitalis 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, e.g., VT or sudden death/cardiac arrest from ventricular flutter/fibrillation. 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 drug related, e.g., 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, coronary artery disease with reduced blood supply to sinoatrial (SA) or atrioventricular (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.
Provide calm/quiet environment. Review reasons for limitation of activities during acute phase.	Reduces stimulation and release of stress-related catecholamines, which can cause/aggravate dysrhythmias and vasoconstriction, increasing myocardial workload.
Demonstrate/encourage use of stress management behaviors, e.g., relaxation techniques, guided imagery, slow/deep breathing.	Promotes patient participation in exerting some sense of control in a stressful situation.
Investigate reports of chest pain, documenting location, duration, intensity (0–10 scale), and relieving/aggravating factors. Note nonverbal pain cues, e.g., facial grimacing, crying, changes in BP/heart rate.	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 (e.g., impending/evolving MI).
Be prepared to initiate cardiopulmonary resuscitation(CPR) as indicated.	Development of life-threatening dysrhythmias requires prompt intervention to prevent ischemic damage/death.
Monitor laboratory studies:Electrolytes; Drug levels.	Imbalance of electrolytes, such as potassium, magnesium, and calcium, adversely affects cardiac rhythm and contractility.Reveal therapeutic/toxic level of prescription medications or street drugs that may affect/contribute to presence of dysrhythmias.
Administer supplemental oxygen as indicated.	Increases amount of oxygen available for myocardial uptake, which decreases irritability caused by hypoxia.
Administer medications as indicated: Potassium Antidysrhythmics, such as: Class I drugs; Class Ia, e.g., disopyramide (Norpace), procainamide (Pronestyl, Procan SR), quinidine (Quinaglute, Cardioquin); Class Ib, e.g., lidocaine (Xylocaine), phenytoin (Dilantin), tocainide (Tonocard), mexiletine (Mexitil); moricizine (Ethmozine); Class Ic, e.g., flecainide (Tambocor), propafenone (Rhythmol), encainide (Enkaid); Class II drugs: e.g., atenolol (Tenormin), propranolol (Inderal), nadolol (Corgard), acebutolol (Sectral), esmolol (Brevibloc), sotalol (Betapace); bisoprolol (Zebeta); Class III drugs: e.g., bretylium tosylate (Bretylol), amiodarone (Cordarone), sotalol (Betapace), ibutilide (Corvert); Class IV drugs: e.g., verapamil (Calan), nifedipine (Procardia), diltiazem (Cardizem); Class V drugs: e.g., atropine sulfate, isoproterenol (Isuprel), cardiac glycosides: digoxin (Lanoxin); Adenosine (Adenocard).	Dysrhythmias are generally treated symptomatically. Correction of hypokalemia may be sufficient to terminate some ventricular dysrhythmias. Note: Potassium imbalance is the number one cause of atrial fibrillation. 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. Useful for treatment of atrial and ventricular premature beats, repetitive dysrhythmias (e.g., atrial tachycardias and atrial flutter/fibrillation). 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. Drugs of choice for ventricular dysrhythmias, they are also effective for automatic and re-entrant dysrhythmias and digitalis-induced 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 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 drug-induced dysrhythmias post MI. Propafenone can worsen or cause new dysrhythmias, a tendency called the “proarrhythmic effect.” Encainide is available only for patients who demonstrated a good result before the drug was removed from the market. Beta-adrenergic blockers have antiadrenergic properties and decrease automaticity. Therefore, they are useful in the treatment of dysrhythmias caused by SA and AV node dysfunction (e.g., SVTs, atrial flutter or fibrillation). 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 are used to terminate ventricular fibrillation and other life-threatening ventricular dysrhythmias/sustained ventricular tachyarrhythmias, especially when lidocaine/procainamide are not effective.Note: Sotalol is a nonselective beta-blocker with characteristics of both class II and class III. Calcium antagonists (also called calcium channel blockers) slow conduction time through the AV node (prolonging PR interval) to decrease ventricular response in SVTs, atrial flutter/fibrillation. Calan and Cardizem may be used for bedside conversion of acute atrial fibrillation. 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/poorly tolerated atrial tachycardias or flutter/fibrillation. First-line treatment for paroxysmal supraventricular tachycardia (PVST). Slows conduction and interrupts reentry pathways in AV node. Note: Contraindicated in patients with second- or third-degree heart block or those with sick sinus syndrome who do not have a functioning pacemaker.
Prepare for/assist with elective cardioversion.	May be used in atrial fibrillation or certain unstable dysrhythmias to restore normal heart rate/relieve symptoms of heart failure.
Assist with insertion/maintain pacemaker function.	Temporary pacing may be necessary to accelerate impulse formation or override tachydysrhythmias and ectopic activity, to maintain cardiovascular function until spontaneous pacing is restored or permanent pacing is initiated.
Insert/maintain IV access.	Patent access line may be required for administration of emergency drugs.
Prepare for invasive diagnostic procedures/surgery as indicated.	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, e.g., CABG, may be indicated to enhance circulation to myocardium and conduction system.
Prepare for implantation of cardioverter/defibrillator (ICD) when indicated.	This device may be surgically implanted in those patients with recurrent, life-threatening ventricular dysrhythmias unresponsive to tailored drug therapy. The latest generation of devices can provide multilevel (“tiered”) therapy, that is, antitachycardia and antibradycardia pacing, cardioversion, or defibrillation, depending on how each device is programmed.

Decreased Cardiac Output — Arrhythmia Nursing Care Plans Original source at: Nurseslabs

3 Placenta Previa Nursing Care Plans

Nurseslabs — Wed, 29 Feb 2012 16:48:54 +0000

Placenta praevia (placenta previa AE) is an obstetric complication in which the placenta is attached to the uterine wall close to or covering the cervix. It can sometimes occur in the later part of the first trimester, but usually during the second or third. It is a leading cause of antepartum hemorrhage (vaginal bleeding). It affects approximately 0.5% of all labors.

Read our Placenta Previa Nursing Care Plans below

1. Deficient Fluid Volume

Fluid volume deficit is a state in which an individual is experiencing decreased intravascular, interstitial and/or intracellular fluid. Active Blood Loss or Hemorrhage due to disrupted placental implantation during pregnancy may manifest signs and symptoms of fluid vol. deficient that may later lead to hypovolemic shock and cause maternal and fetal death.

NDx: Deficient Fluid Volume r/t Active Blood Loss Secondary to Disrupted Placental Implantation

Assessment

Planning

Nursing
Interventions

Rationale

Expected Outcome

S-

O-> Bleeding Episodes (amount, duration)

> Facial Grimace due of Pain

> Complaint of pain

Abdomen soft/hard when palpated

> Manifest Body Weakness

> Low BP

Increased HR

Decreased RR

Fetal HR >120-160 bpm

> Decreased Urine Out

> Increased Urine Concentration

> Pale, Cool Skin

>Increased Capillary Refill

Short Term:After 4 hours of NI, the pt will verbalize understanding of causative factors.Long Term:After 4 days of NI, the pt will maintain fluid volume at a functional level AEB individually adequate urinary output and stable vital signs.

1. Establish Rapport2. Monitor Vital Signs3. Assess color, odor, consistency and amount of vaginal bleeding; weigh pads4. Assess hourly intake and output.

5. Assess baseline data and note changes. Monitor FHR.

6. Assess abdomen for tenderness or rigidity- if present, measure abdomen at umbilicus (specify time interval)

7. Assess SaO2, skin color, temp, moisture, turgor, capillary refill (specify frequency)

8. Assess for changes in LOC: note for complaints of thirst or apprehension

9. Provide supplemental O2 as ordered via facemask or nasal cannula @ 10-12 L/min.

10. Initiate IV fluids as ordered (specify fluid type and rate).

11. Position Pt. in supine with hips elevated if ordered or left lateral position.

12. Monitor lab. Work as obtained: Hgb & Hct, Rh and type, cross match for 2 units RBCs, urinalysis, etc. Scheduled for ultrasound as ordered.

1. To gain patient’s trust2. To obtain baseline data3. Provides information about active bleeding versus old blood, tissue loss and degree of blood loss4. Provides information about maternal and fetal physiologic compensation to blood loss

5. Assessment provides information about possible infection, placenta previa or abruption. Warm, moist, bloody environment is ideal for growth of microorganisms.

6. Detecting increased in measurement of abdominal girth suggests active abruption

7. Assessment provides information about blood vol., O2 saturation and peripheral perfusion

8. To detect signs of cerebral perfusion

9. Intervention increases available O2 to saturate decreased hemoglobin

10. For replacement of fluid vol. loss

11. Position decreases pressure on placenta and cervical os. Left lateral position improves placental perfusion

12. Lab. Work provides information about degree of blood loss; prepares for possible transfusion. Ultra sound provides info about the cause of bleeding

Short Term:The pt shall have verbalized understanding of causative factors.Long Term:The pt shall have maintained fluid volume at a functional level AEB individually adequate urinary output and stable vital signs.

3 Placenta Previa Nursing Care Plans Original source at: Nurseslabs

5 Congestive Heart Failure Nursing Care Plans

Nurseslabs — Mon, 27 Feb 2012 14:35:50 +0000

Congestive heart failure (CHF), or heart failure, is a condition in which the heart can’t pump enough blood to the body’s other organs. To fully understand CHF, see the pathophysiology here.

1 Fluid Volume Excess

Goals:

Body weight will remain within normal limits
Electrolyte levels will be within normal limits
Will demonstrate adequate knowledge concerning medical condition.
Will maintain optimal fluid balance
Will verbalize less dyspnea and be more comfortable.

Interventions:

Administer Oxygen as ordered
Asess for symptoms such as dizziness, weaknes/fatigue, nausea/vomiting, confusion, sweatiness, cyanosis. Notify physician as appropriate.
Assess for presence of edema
Check breath sounds and assess for labored breathing.
Check Vital Signs
Keep head of bed elevated
Monitor fluid intake, restrict sodium intake as ordered.
Monitor Lab work; K+, NA, BUN, Creatinine
Observe for signs and symptoms of malnutrition, Do not force resident to eat. Offer small frequent feedings. Assess food preferences.
Weigh patient daily

5 Congestive Heart Failure Nursing Care Plans Original source at: Nurseslabs

5 Coronary Artery Disease Nursing Care Plans

Nurseslabs — Fri, 03 Feb 2012 18:19:49 +0000

Coronary artery disease (CAD) is a condition in which plaque builds up inside the coronary arteries. These arteries supply your heart muscle with oxygen-rich blood. Plaque is made up of fat, cholesterol, calcium, and other substances found in the blood. Plaque narrows the arteries and reduces blood flow to your heart muscle. It also makes it more likely that blood clots will form in your arteries. Blood clots can partially or completely block blood flow. When your coronary arteries are narrowed or blocked, oxygen-rich blood can’t reach your heart muscle. This can cause angina or a heart attack. Without quick treatment, a heart attack can lead to serious problems and even death.

CAD is the most common type of heart disease. Lifestyle changes, medicines, and/or medical procedures can effectively prevent or treat CAD in most people. Other names for Coronary Artery Disease are Atherosclerosis, Coronary heart disease, Hardening of the arteries, Heart disease, Ischemic heart disease, and Narrowing of the arteries.

Here are 5 Coronary Artery Disease Nursing Care Plans

1. Decreased Cardiac Output - Coronary Artery Disease Nursing Care Plans

NDx: Decreased cardiac output r/t increased vascular resistance

Cad causes narrowing of blood vessels. This condition leads to intense pressure exerted on the walls of the blood vessels. The body’s compensatory mechanism is to increase the work load of the heart and thus the patient has decreased cardiac output.

Assessment

Planning

Nursing interventions

Rationale

Expected outcome

S= ∅

O=The patient may manifest:

restlessness
increased bp
cold clammy skin
decreased peripheral pulses

Short term:

After 2-3 hours of nursing interventions, the patient will verbalize understanding of disease process.

Long term:

After two days of nursing interventions the patient will participate in activities to decrease in the heart’s workload

assess patient’s condition
monitor and record vital signs
encourage patient to verbalize concerns
encourage patient to change position every two hours
encourage patient to do relaxation techniques
encourage patient to engage in divertional activities such as chatting with family and friends.
reinforced low salt and low fat diet

to determine possible prolems
for baseline data
to make client express his feelings
to improve venous return
to reduce stress
to divert attention and help patient lessen experienced pain and anxiety
to prevent further complications of the disease

Short term:

The patient shall have verbalizedUnderstanding of disease process.

Long term:

The patient shall have participated in activities to decrease in the heart’s workload

5 Coronary Artery Disease Nursing Care Plans Original source at: Nurseslabs

10 Congestive Heart Failure Nursing Care Plans

Nurseslabs — Tue, 24 Jan 2012 17:32:53 +0000

Heart failure (HF) or Congestive Heart Failure (CHF) is a physiologic state in which he heart cannot pump enough blood to meet the metabolic needs of the body. Heart failure results from changes in systolic or diastolic function of the left ventricle. The heart fails when, because of intrinsic disease or structural it cannot handle a normal blood volume or, in absence of disease, cannot tolerate a sudden expansion in blood volume. Heart failure is not a disease itself; instead, the term refers to a clinical syndrome characterized by manifestations of volume overload, inadequate tissue perfusion, and poor exercise tolerance. Whatever the cause, pump failure results in hypoperfusion of tissues, followed by pulmonary and systemic venous congestion.

Because heart failure causes vascular congestion, it is often called congestive heart failure, although most cardiac specialist no longer use this term. Other terms used to denote heart failure include chronic heart failure, cardiac decompensation, cardiac insufficiency and ventricular failure (Joyce M. Black, 2008).

Here are 10 Congestive Heart Failure Nursing Care Plans

1. Decreased Cardiac Output - Congestive Heart Failure Nursing Care Plans

The heart fails to pump enough blood to meet the metabolic needs of the body. The blood flow that supplies the heart is also decreased thus decrease in cardiac output occurs, blood then is insufficient and making it difficult to circulate the blood to all parts of the body thus may cause altered heart rate and rhythm, weakness and paleness

NDx: Decreased cardiac output r/t altered heart rate and rhythm AEB bradycardia

Assessment

Planning

Nursing Interventions

Rationale

Evaluation

Subjective:(none)

Objectives:

The patient manifested the following:

with pale conjunctiva, nail beds and buccal mucosa
irregular rhythm of pulse
bradycardic
pulse rate of 34 beats/min
generalized weakness

Short Term:After 3-4 hours of nursing interventions, the patient will participate in activities that reduce the workload of the heart.

Long Term:

After 2-3 days of nursing interventions, the patient will be able to display hemodynamic stability.

Assess for abnormal heart and lung sounds.
Monitor blood pressure and pulse
Assess mental status and level of consciousness.
Assess patient’s skin temperature and peripheral pulses.
Monitor results of laboratory and diagnostic tests.
Monitor oxygen saturation and ABGs.
Give oxygen as indicated by patient symptoms, oxygen saturation and ABGs.
Implement strategies to treat fluid and electrolyte imbalances.
Administer cardiac glycoside agents, as ordered, for signs of left sided failure, and monitor for toxicity.
Encourage periods of rest and assist with all activities.
Assist the patient in assuming a high Fowler’s position.
Teach patient the pathophysiology of disease, medications
Reposition patient every 2 hours
Instruct patient to get adequate bed rest and sleep
Instruct the SO not to leave the client unattended
Allows detection of left-sided heart failure that may occur with chronic renal failure patients due to fluid volume excess as the diseased kidneys are unable to excrete water.

Patients with renal failure are most often hypertensive, which is attributable to excess fluid and the initiation of the rennin-angiotensin mechanism.
The accumulation of waste products in the bloodstream impairs oxygen transport and intake by cerebral tissues, which may manifest itself as confusion, lethargy, and altered consciousness.
Decreased perfusion and oxygenation of tissues secondary to anemia and pump ineffectiveness may lead to decreased in temperature and peripheral pulses that are diminished and difficult to palpate.
Results of the test provide clues to the status of the disease and response to treatments.
Provides information regarding the heart’s ability to perfuse distal tissues with oxygenated blood
Makes more oxygen available for gas exchange, assisting to alleviate signs of hypoxia and subsequent activity intolerance.
Decreases the risk for development of cardiac output due to imbalances.
Digitalis has a positive isotropic effect on the myocardium that strengthens contractility, thus improving cardiac output.
Reduces cardiac workload and minimizes myocardial oxygen consumption.
Allows for better chest expansion, thereby improving pulmonary capacity.
Provides the patient with needed information for management of disease and for compliance.
To prevent occurrence of bed sores
To promote relaxation to the body
To ensure safety and reduce risk for falls that may lead to injury

Short Term:After nursing interventions, the patient shall have participated in activities that reduce the workload of the heart.

Long Term:

After 2-3 days of nursing interventions, the patient shall have been able to display hemodynamic stability.

10 Congestive Heart Failure Nursing Care Plans Original source at: Nurseslabs

Hypertensive Emergency Nursing Care Plan

Nurseslabs — Fri, 06 Jan 2012 23:00:25 +0000

Hypertensive Emergency is severe hypertension (high blood pressure) with acute impairment of an organ system (especially the central nervous system, cardiovascular system and/or the renal system) and the possibility of irreversible organ-damage. In case of a hypertensive emergency, the blood pressure should be lowered aggressively over minutes to hours with an antihypertensive agent.

Several classes of antihypertensive agents are recommended and the choice for the antihypertensive agent depends on the cause for the hypertensive crisis, the severity of elevated blood pressure and the patient’s usual blood pressure before the hypertensive crisis. In most cases, the administration of an intravenous sodium nitroprusside injection which has an almost immediate antihypertensive effect is suitable but in many cases not readily available. In less urgent cases, oral agents like captopril, clonidine, labetalol, prazosin, which all have a delayed onset of action by several minutes compared to sodium nitroprusside, can also be used.

Decreased Cardiac Output - Hypertensive Emergency Nursing Care Plan

NDx: Decreased cardiac output r/t altered stroke volume secondary to hypertensive emergency

Hypertension is defined as a condition wherein there is an increase in BP beyond the normal range. Hypertensive emergency is used for BPs above 160/100mmHg. With hypertension, the blood vessels constrict. When blood vessels are constricted, there is a decrease in blood volume, decrease in cardiac output and increase in BP as blood passes through the narrowed lumen of the vessels.

Assessment

Objectives

Nursing Interventions

Rationale

Expected Outcome

dysrrhythmias
prolonged capillary refill
cold clammy skin
dyspnea
variations in BP
restlessness
BP of 190/150

Short Term:

After 6 hours of NI, the pt will manifest hemodynamic stability (BP, CO, UO, PR) pt shall also verbalize understanding of the disease process & risk factors

Long Term:

After 4 days of NI, the pt will participate in activities that decrease blood pressure

Establish Rapport
Monitor Vital Signs
History Taking
Assess patient’s condition
Review lab data
Review ECG strip
Monitor BP, PR frequently
Provide information on test procedures
Explain dietary restrictions
Encourage rest & reposition client q2
Encourage relaxation techniques
Provide PM care
Encourage to increase activity level as tolerated
Teach home BP reading & monitoring
Administer anti hypertensives

To gain pt’s trust
To obtain baseline data
To determine contributing factors
To determine present condition
For comparison with normal values
To determine alterations in electrical activity of the heart
To note response to activity
To gain pt’s participation & decrease anxiety level
To inform patient of contributing factors
To decrease stress and promote venous return
To alleviate anxiety & stress
To promote hygiene & comfort
To maintain functional ability
To detect change in VS & seek timely intervention
To decrease BP within normal ranges

The pt shall have manifested hemodynamic stability (BP, CO, UO, PR) pt shall have also verbalized understanding of the disease process & risk factors.

The pt shall have participated in activities that decrease blood pressure

Hypertensive Emergency Nursing Care Plan Original source at: Nurseslabs