Friday, November 26, 2010

Decrease Cardiac output

Decreased Cardiac Output

NANDA Definition
Inadequate blood pumped by the heart to meet the metabolic demands of the body.

Discussion of the Problem
Though advances in diagnostic procedures that allow prompt and more precise diagnoses so that early management could be initiated before significant debilitation occur, heart disease still remains a chronic condition. Common etiologies of decreased cardiac output include the following:  angina, myocardial infarction, severe hypertension, valvular heart disease, congenital heart disease, cardiomyopathy, pulmonary disease, arrhythmias, chronic heart failure, cardiac surgery, acute and chronic renal failure, Grave’s disease, drug effects, fluid overload, decreased fluid volume, and electrolyte imbalance. Geriatric patients are at high risk of developing this problem since their ventricles have reduced compliance due to aging process. The overall goals of management are to relieve patient symptoms, to improve functional status and quality of life, and to extend survival.

Nursing Interventions Classification (NIC)
  • Cardiac Care
  • Hemodynamic Regulation
  • Teaching: Disease Process

Nursing Outcomes Classification (NOC)
  • Cardiac Pump Effectiveness
  • Circulation Status
  • Knowledge: Disease Process
  • Knowledge: Treatment Program

Goal and Objectives
  • Patient will demonstrate an enhancement in activity tolerance
  • Patient will demonstrate unwavering cardiac rhythm and rate within own normal range.
  • Patient will maintain BP within standard limits; have regular cardiac rhythms; maintain warm, dry skin; clear lung sounds, and strong bilateral, equal peripheral pulses.
  • Patient will participate in activities that decrease BP or cardiac workload

Subjective and Objective Data
  • Abnormal heart sounds
  • Angina
  • Anxiety, restlessness
  • Arrhythmias, electrocardiogram (ECG) changes
·         Chest pain
  • Confusion, change in mental status
·         Cool, ashen skin; diaphoresis
  • Decreased peripheral pulses, ejection fraction less than 40%
·         Decreased urine output
·         Extra heart sounds (S3, S4)
·         JVD, liver engorgement, edema
  • Pulsus alternans
  • Rales, tachypnea, dyspnea, orthopnea, cough, abnormal arterial blood gases (ABGs), frothy sputum
  • Syncope, dizziness
  • Variations in hemodynamic parameters (blood pressure [BP], heart rate, central venous pressure [CVP], pulmonary artery pressures, venous oxygen saturation [SVO2], cardiac output)
  • Weakness, fatigue
  • Weight gain, edema, decreased urine output
Related Factors
  • Alteration in afterload
·         Alterations in heart rate, rhythm, electrical conduction
  • Cardiac muscle disease
  • Decreased oxygenation
  • Impaired contractility/inotropic changes
  • Increased or decreased ventricular filling (preload)
·         Structural changes (e.g., valvular defects, ventricular aneurysm)

Assessment (Dx)
  • Assess color and temperature of skin and time of capillary refill. Cold, clammy skin is due to compensatory increase in sympathetic nervous system stimulation, reduced cardiac output, and desaturation.

  • Assess mentation status. In the early stages, restlessness is seen; in later stages, severe anxiety and confusion are being manifested.

  • Auscultate apical pulse; monitor heart rate, rhythm (if telemetry is available record dysrhythmia). To compensate for reduced ventricular contractility, tachycardia is usually present even at rest. Common dysrythmias associated with heart failure are as follows: Premature atrial contractions (PACs), paroxysmal atrial tachycardia (PAT), PVCs, multifocal atrial tachycardia (MAT), and atrial fibrillation (AF).

  • Monitor heart rate and blood pressure. In the early stages, sinus tachycardia and augmented arterial blood pressure are being manifested; blood pressure drops as the state deteriorates. Geriatric patients have diminished response to catecholamines, hence their response to decreased cardiac output may be blunted, with lower rise in heart rate. In heart failure patients, pulsus alternans (alternating strong-then-weak pulse) is often seen.

  • Observe changes in sensorium(anxiety, confusion, depression, disorientation, and lethargy). This may indicate insufficient cerebral perfusion secondary to reduced cardiac output.

  • Observe presence and quality of central and peripheral pulses. With reduced cardiac output, pulses are weak. In addition, bounding carotid, femoral, jugular, and radial pulses may be noted or palpated. Due to the effects of vasoconstriction and venous congestion, pulses in the legs or feet may be reduced.

Check for Symmetry

ü  Compare Right to Left
ü  Compare Upper Extremity to Lower Extremity
Palpable Pulses

ü  Temporal
ü  Carotid
ü  Brachial BP, CPR in infant
ü  Radial pulse
ü  Ulnar
ü  Femoral arterial studies
ü  Popliteal
ü  Dorsalis Pedis
ü  Posterior Tibial

ü  blood clots
ü  edema of feet or legs
ü  intermittent claudication
ü  leg cramps
ü  leg ulcers
pain on walking
disappears with rest
ü  pallor of fingertips
ü  varicose veins
(Upper Extremities )
Compare Side to Side
  • Size
  • Symmetry
  • Skin/color
  • Nail Beds / Capillary Refill
  • Hair Growth
  • Venous Pattern
(Lower Extremities)
Compare Side to Side
·         Size
·         Symmetry
·         Skin -color, lesions
·         Nail Beds / Capillary Refill
·         Nails
·         Venous Pattern
Hair Growth
(Upper Extremities)

Compare Side to Side
  • Temperature
  • Capillary refill
  • Pulses
    • Radial
    • Brachial
    • Ulnar

palpate along LENGTH of artery with finger pads
  • Rate
  • Rhythm
  • Contour/elasticity
  • Strength (Amplitude)
    • +4 = bounding
    • +3 = full, increased
    • +2 = normal
    • +1 = diminished, weak
    • 0 = absent
·         irregular (dysrhythmia)
·         if irregular - take apical
( Lower Extremities)

Compare Side to Side
·         Pulses
·         Femoral
  • Popliteal Pulses
    • Dorsalis Pedis
    • Posterior Tibial
    • Femoral
    • Popliteal
  • Temperature
  • Edema
+1- +4 pitting
  • Sensation

Arterial Insufficiency of Lower Extremities
Pale on elevation
      Dusky Rubor on dependency
Shiny, thick nails, no hair
     Ulcers on Toes
Pain, more with exercise

Venous Insufficiency of Lower Extremities
Pink to cyanotic Brown pigment at ankles
Discolored, scaly
      ulcers on ankles
Pain, More with standing or sitting. Relieved with elevation/support hose

  • Auscultate lung sounds. Note any episode of paroxysmal nocturnal dyspnea (PND) or orthopnea. Orthopnea is difficulty breathing when the patient is in supine Position. PND is difficulty breathing that occurs during the night. Crackles echoes accumulation of fluid secondary to damaged left ventricular emptying. They are more apparent in the dependent areas of the lungs.

  • Monitor heart sounds, noting gallops, S3, S4. S3 indicates lowered left ventricular ejection and is a classic sign of left ventricular failure. S4 take place with lowered compliance of the left ventricle, which impairs diastolic filling.

  • Review weight gain and fluid balance. Body weight is a more accurate indicator of fluid or sodium retention than intake and output. Fluid and sodium retention may be caused by compromised regulatory mechanisms.

  • If hemodynamic monitoring is in place:
1)     Check central venous, pulmonary artery pressure, pulmonary capillary wedge pressure, and right arterial pressure. Hemodynamic parameters give information aiding in differentiation of reduced cardiac output due to fluid overload versus deficit in fluid.
2)     Watch SVO 2 continuously. One of the initial indicators of decreased cardiac output is change in oxygen saturation of mixed venous blood.
3)     Do cardiac output determination. Gives objective number to guide therapy.

  • Check ECG for rate; rhythm; ectopy; and change in PR, QRS, and QT intervals. Tachycardia, bradycardia, and ectopic beats can compromise cardiac output. Geriatric patients are particularly sensitive to the loss of atrial kick in atrial fibrillation.

            The standard 12-lead electrocardiogram (ECG/EKG) represents the heart's electrical activity recorded from electrodes on the body surface.

ECG Waves and Intervals

P wave
the sequential activation (depolarization) of the right and left atria
QRS complex
right and left ventricular depolarization (normally the ventricles are activated simultaneously)
ST-T wave
ventricular repolarization
U wave
origin for this wave is not clear - but probably represents "afterdepolarizations" in the ventricles
PR interval
time interval from onset of atrial depolarization (P wave) to onset of ventricular depolarization (QRS complex)
QRS duration
duration of ventricular muscle depolarization
QT interval
duration of ventricular depolarization and repolarization
RR interval
duration of ventricular cardiac cycle (an indicator of ventricular rate)
PP interval
duration of atrial cycle (an indicator of atrial rate)

Orientation of the 12 Lead ECG

            It is significant to consider that the 12-lead ECG provides spatial information about the heart's electrical activity of the heart in 3 approximately orthogonal directions namely: Right Left, Superior Inferior, and Anterior Posterior. Further, each of the 12 leads represents a particular orientation in space. (RA = right arm; LA = left arm, LF = left foot)

Bipolar limb leads (frontal plane):
 Lead I: RA (-) to LA (+) (Right Left, or lateral)
 Lead II: RA (-) to LF (+) (Superior Inferior)
Lead III: LA (-) to LF (+) (Superior Inferior)
Augmented unipolar limb leads (frontal plane):
 Lead aVR: RA (+) to [LA & LF] (-) (Rightward)
Lead aVL: LA (+) to [RA & LF] (-) (Leftward)
 Lead aVF: LF (+) to [RA & LA] (-) (Inferior)
Unipolar (+) chest leads (horizontal plane):
Leads V1, V2, V3: (Posterior Anterior)
Leads V4, V5, V6:(Right Left, or lateral) of chest electrodes

V1: right 4th intercostal space
V2: left 4th intercostal space
V3: halfway between V2 and V4
V4: left 5th intercostal space, mid-clavicular line
V5: horizontal to V4, anterior axillary line
V6: horizontal to V5, mid-axillary line

  • Check laboratory data (cardiac enzymes, ABGs, electrolytes, etc). Enzymes evaluate resolution/extension of infarction. Existence of hypoxia show necessitate for supplemental oxygen. Electrolyte imbalance, hypo/hyperkalemia for example, unfavorably affects cardiac rhythm/contractility.

  • Look out for dependent or general edema. May signify heart failure, renal or vascular injury.

  • Monitor response to increased activity. Physical activity augments the demands placed on the heart; fatigue and exertional dyspnea are frequent problems with reduced cardiac output conditions. Close monitoring of patient’s response to increased activity serves as a guide for most favorable succession of activity.

  • Note for chest pain. This signifies an imbalance between oxygen supply and demand.

  • Review urine output. Find out how often the patient urinates. Oliguria can echo decreased renal perfusion. Diuresis is anticipated with diuretic therapy.

Therapeutic Interventions (Tx)
  • Give medication as prescribed, noting reaction and inspecting for side effects and toxicity. Make clear with physician parameters for halting medication particularly the following: digitalis therapy, diuretics, vasodilator therapy, antidysrhythmics, ACE inhibitors, and inotropic agents.

  • Limit fluids and sodium as prescribed for patients with increased preload. This reduces extracellular fluid volume.

  • Retain hemodynamic parameters at prescribed levels. Close monitoring of these parameters directs titration of fluids and medications for patients in the acute setting.

  • Sustain optimal fluid balance. Giving of fluid increases extracellular fluid volume to elevate cardiac output.

  • Keep up adequate ventilation and perfusion, as in the following:
1)     Put patient in semi- to high-Fowler’s position. This lessens preload and ventricular filling.
2)     Put patient in supine position. This promotes venous return, increases diuresis.
3)     Give humidified oxygen as ordered. The deteriorating heart may not be able to compensate with increased oxygen demands.

  • Maintain physical and emotional rest, as in the following:
1)     Limit activity. This decreases oxygen demands.
2)     Offer quiet, relaxed milieu. Emotional stress adds to cardiac demands.
3)     Systematize nursing and medical care. This permits rest periods.
4)     Check progressive activity within restriction of cardiac function.

  • Check sleep patterns; administer sedative as prescribed. Rest is essential for conserving energy.

  • Offer bedside commode. Have patient keep away from activities provoking a vasovagal response, Give stool softeners as considered necessary. Use of commode lowers works getting to bathroom or having a great effort to use bedpan. Vasovagal maneuver grounds vagal stimulation. Rebound tachycardia subsequently occurs, which more compromises cardiac function or output.

  • Offer little, easily digested meals. Restrict caffeine intake. Huge meals may augment myocardial workload and root vagal stimulation, leading to bradycardia or ectopic beats. Caffeine is a direct cardiac stimulant that can rise up the heart rate. Note: New guidelines propose no need to limit caffeine in regular coffee drinkers.

  • If arrhythmia takes place, verify patient response, document, and report if significant or symptomatic.
1.     Have antiarrhythmic drugs readily accessible.
2.     Care for arrhythmias according to medical orders or procedure and evaluate reaction.
Either tachyarrhythmias or bradyarrhythmias can lower cardiac output and myocardial tissue        perfusion.

  • Have emergency apparatus or medications accessible. Abrupt coronary occlusion, lethal dysrhythmias, infarct, and unremitting pain are conditions that may lead to cardiac arrest, requiring urgent life-saving managements.

Educative (Edx)
  • Clarify progressive activity program and signs of overexertion.
  • Explain diet restrictions especially regarding fluid and sodium.
  • Give details on symptoms and management for reduced cardiac output related to respective etiological factors.
  • Give explanation about the drug regimen, purpose, dose, and possible side effects.

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