acute biologic crises

8/4/2019 Acute Biologic Crises

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ACUTE BIOLOGIC CRISES

HIGH RISK ADULT:

RESPIRATORY DISORDERS

1. PULMONARY EMBOLISM

Occurs when a pulmonary embolus [thrombotic (bloodclot) or nonthrombotic (fat) emboli] lodges in thepulmonary artery system.

This blockage obstructs blood flow to the lung tissuesupplied by the affected vessel.

2 types:1. Thrombotic emboli mainly originate from the deep veinsof the legs, right ventricle of the heart, or pelvis.

2. Nonthrombotic emboli mainly originate from fat releaseafter skeletal injuries, amniotic fluid, air, and foreign bodies.

The Virchows Triad- Three conditions and risk factors that can predispose apatient or that can precipitate the formation of venousthrombi.1. Venous stasiseg. atrial fibrillation, heart failure immobility, polycythemia,pregnancy, varicose veins2. Vessel wall injuryeg. infection, trauma3. Coagulation problems

Pathophysiologic ChangesEmbolus lodge in the pulmonary vasculature-Pulmonaryembolism (decreased/nonperfusion of alveoli distal toocclusion)-Infarction ofpulmonary vessel


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decreased C02-bronchoconstriction-shunting of blood toventilated areas of the lungs- increased pulmonaryresistancehypoxiarelease of mediators at the injurysiteincrease right ventricular

workloadvasoconstrictionright ventricular failurepulmonary hypertensionventricular failure decreasedcardiac output decreased blood pressureshockdeathClinical Manifestations

Shortness of breath and/or tachypnea- a responseto the hypoxia that develops from impairedgas exchange

Cough

Hemoptysis occurs when an infarction at or near theperiphery of the lung begins to hemorrhage

Chest pain generally comes from an infarction of thepulmonary vessel near the area in which the pleuralnerves innervate. Usually worsen when the patienttakes a deep breath.

Tachycardia a response to the decrease inoxygenation and impaired gas exchange

Jugular vein distention a result of pulmonaryhypertension and the decreased effectiveness of theright ventricle

Hypotension observed with large pulmonaryembolism and is related to the decrease in cardiacoutput after ventricular dysfunction.


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Diagnosis Chest radiograph excludes other reasons that may

cause the same clinical manifestations. May showpulmonary artery distention, an elevation of the

diaphragm, and small infiltrates or pleural effusions.

ABG analysis can reveal respiratory alkalosis, lowpartial pressure of oxygen, and low partial pressureof carbon dioxide

Electrocardiogram involve transient nonspecific STsegment and T wave changes.

Management The best treatment for pulmonary embolism isPREVENTION.

When patients are at risk for developing pulmonaryembolism, prophylacticmeasures should beinstituted such as intravenous or subcutaneousheparin (Lovenox) or oral anticoagulants such aswarfarin (Coumadin).

The goal of therapy is to prevent thrombi formation,

limit thrombi growth, and encourage breakdown ofexisting thrombi. Management of hypoxia may require supplemental

oxygen, intubation and mechanical ventilation.

Heparin Therapy started with a bolus (usually based on patients

weight) and a continuous infusion adjusted every 4-6hours, depending on the institutions protocol.

Activated partial thromboplastin time (apt) should bemaintained at 1.5-2.0 times the normal value.

generally continued for 7-14 days while the patient ison bedrest

reversal agent (antidote) is protamine sulfate. The reversal agent for warfarin (Coumadin) is vitamin

K or fresh frozen plasma.


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Surgical intervention is rarely used and is considered alast resort.

Pulmonary embolectomy

is the removal of a clot from the larger vessel of thepulmonary vasculature. This surgery carries a high riskof death and is only used in those patients who do notrespond or have contraindications to otherinterventions.

Nursing Responsibilities The main nursing goal is to prevent the development of

deep venous thrombosis (DVT) that may lead to athrombotic pulmonary embolism.

Interventions should include early ambulation, use ofpneumatic stockings, support hose, and passive range-of-motion exercises. All of these improve venous bloodflow and increase circulation.

Other nursing interventions include the following:

Signs and symptoms of DVT are monitored in the lowerextremities (calf pain or tenderness, redness, swelling,

warmth, pain on dorsiflexion of foot [Homans sign]). IfHomans sign is positive, DO NOT retest it; doing somay dislodge the clot.

Prescribed oxygen therapy is maintained, and thepatient is asked to cough and deep breath every 2hours

Signs and symptoms of respiratory distress or

a worsening of pulmonary status (heart failure,pulmonary edema) are monitored, and the physician isnotified of any developments.

ABG analysis is monitored and pulse oximetry iscontinuously taken.


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Patient is positioned for comfort and maximaloxygenation, as well as to promote the expulsion ofsecretions.

Signs and symptoms of bleeding are monitored whenanticoagulant or thrombolytic therapy is in progress.(eg. blood in stool or urine, pale mucous membranes,petechiae, echymosis, complaints of back or flankpain).

2. ACUTE RESPIRATORY DISTRESS SYNDROME

A clinical syndrome characterized by a sudden andprogressive pulmonary edema, increasing bilateralinfiltrates, hypoxemia refractory to oxygensupplementation and reduced lung compliance.

A syndrome with inflammation and increasedpermeability of the alveolar capillary membrane thatoccurs as a result ofan injury to the lungs.

This inflammation causes noncardiogenic pulmonaryedema with severely impaired gas exchange.

Etiologic Factors Related to ARDS:

1. Aspiration (gastric secretions, drowning,hydrocarbons)2. Drug ingestion and overdose3. Hematologic disorders4. Prolonged inhalation of high concentrations of oxygen,

smoke, or corrosive substances5. Localized infection (bacterial, fungal, viral pneumonia)6. Metabolic disorders ( pancreatitis, uremia)7. Shock (any cause)8. Trauma ( pulmonary contusion, multiple fractures,head injury)


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9. Fat or air embolism10. Systemic sepsis

Pathophysiology

lung injury immune system initiates an inflammatoryresponse activation of neutrophils, macrophages, andendotoxins into the lungs and the release of mediatorsincreased alveolomembrane permeability fluid enters intothe lung tissue Acute Respiratory Distress Syndromealveolar collapsenarrowing ofairways pulmonary vasoconstrictionhypoxia pulmonary hypertension

hyperventilation right ventricular dysfunctionrespiratory failure decreased cardiac output

Clinical Manifestations:

1. Rapid onset ofsevere dyspnea2. Anxiety3. Labored breathing and tachypnea

Assessment: Intercostal retractions and crackles

In patients with ARDS, PaO2 will be low, despiteoxygen administration, pCO2 will decrease as a resultofhyperventilation.

Medical Management:

- The main goals in the treatment of ARDS include improvingand maintaining oxygenation, maintaining fluid andelectrolyte imbalances, providing adequate nutrition, andpreventing respiratory and metabolic complications.

1. Primary focus of management includes identification andtreatment of the condition.2. Supportive Therapy: Intubation and mechanicalventilation to maintain adequate gas exchange


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3. Circulatory support, adequate fluid volume and nutritionalsupport.-Fluid restriction is generally observed to prevent further

leakage of fluid into the alveoli and to decrease pulmonaryedema, but fluid restriction can also cause a decrease incardiac output and blood pressure.

4. Supplemental oxygen is used as the patient begins theinitial spiral of hypoxemia. Oxygen toxicity may develop ifhigh concentrations of oxygen are used for longer than 24-48 hours.

5. Positive end-expiratory pressure (PEEP)- generally leads

to improved gas exchange and allows for lowerconcentrations of oxygen to be used.

6. Hypovolemia must be carefully treated.

7. Intravenous crystalloid solutions are administered.

8. Pulmonary artery pressure catheters are used to monitorpatients fluid status

Nursing Management:

1. Positioning is important.- Nurse should turn the patient frequently to improveventilation and perfusion in the lungs and enhance secretiondrainage.- Prone positioning is an intervention that mayimprove oxygenation by decreasing edema and atelectasis,thereby providing an improved distribution of oxygen

throughout the lungs.

2. Nurse must closely monitor rapid changes in oxygenationwith changes in position.

3. The nurse should explain all procedures and deliver carein calm, reassuring manner.


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4. Rest is essential to reduce oxygen consumption

Nursing Diagnosis:

Impaired gas exchange r/t inadequate respiratory centeractivity, chest wall movement, airway obstruction, fluidsin the lungs

RESPIRATORY FAILURE

Respiratory failure is a sudden and life-threatening

deterioration of the gas exchange function of the lung.

Exists when the exchange of oxygen for carbon dioxide inthe lungs can not keep up with the rate of oxygenconsumption and carbon dioxide production by the cells ofthe body.

ACUTE RESPIRATORY FAILURE (ARF)

Defined as a fall in arterial oxygen tension and a risein arterial carbon dioxide tension.

The ventilation and/or perfusion mechanisms in thelung are impaired.

Respiratory system mechanisms leading to ARF include:1 . A l v e o l a r h yp ove n t i l a t i o n2 . D i f f u s i o n ab n o rma l i t i e s3. Vent i lat ion-perfusion mismatching4 . S h u n t i n g

Pathophysiology


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Common Causes of Acute Respiratory Failure:

1. Decreased Respiratory Drive

May occur with severe brain injury, large lesions of thebrain stem (multiple sclerosis), use of sedativemedications, and metabolic disorders such ashyperthyroidism.

This disorders impair the normal responseofchemoreceptors in the brain to normal respiratorystimulation

2. Dysfunction of the Chest Wall

The impulses arising in the respiratory center travelthrough nerves that extend from the brain stem downthe spinal cord to receptors in the muscles ofrespiration. Thus, any disease ofthe nerves, spinalcord, muscles or neuromuscular junction involvedin respiration seriously affects ventilation and may leadto ARF

3. Dysfunction Of Lung Parenchyma

Pleural effusion, hemothorax, pneumothorax, andupper airway obstruction are conditions that interferewith ventilation by preventing expansionof the lung.

These conditions, which may cause respiratory failure,usually are produced by an underlying lung disease,pleural disease, trauma and injury.

Other diseases and conditions of the lung that leadto ARF pneumonia, status asthmaticus, lobar atelectasis, pulmonary embolism pulmonary edema


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4. Other Factors

In the postoperative period, esp. after major thoracic

or abdominal surgery, inadequate ventilation andrespiratory failure may occur. Causes ofARF during this period include the effects of

anesthetic agents, analgesics, and sedatives; they maydepress respiration and lead to hypoventilation.

Clinical Manifestations:

Early signs are those associated with impaired oxygenation

Restlessness fatigue headache dyspnea air hunger tachycardia tachypnea central cyanosis diaphoresis

respiratory arrest

Physical findings use of accessory muscles, decreased breath sounds

Medical Management Objectives of treatment are to correct the underlyingcause and to restore adequate gas exchange in the lung.

Intubation and mechanical ventilation

Nursing Management:

Assist with intubation


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Assess respiratory status by monitoring patients levelof response, arterial blood gases, pulse oximetry andvital signs

Implement strategies to prevent complications: turningschedule, mouth care, skin care, ROM

CHRONIC RESPIRATORY FAILURE

Defined as deterioration in the gas exchange functionof the lung that has developed insidiously or haspersisted for a long period after an episode of ARF.

Patients develop a tolerance to the worseninghypoxemia and hypercapnia.

Patient with chronic respiratory failure may developAcute respiratory failure seen in COPD patientswho develops an exacerbation or infection that causesadditional deterioration of the gas exchangemechanism.

2 Causes of Chronic Respiratory Failure:1 . C O P D2 . N e u r o m u s c u l a r D i s e a s e s

Mechanical ventilation

* is a form of artificial ventilation that takes over all or partof the work performed by the respiratory muscles andorgans.

* It is initiated when the patients ability to oxygenate andexchange carbon dioxide is impaired.


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* Indicated for the following reasons: Hypoxemia Aspiration

Atelectasis Pulmonary Edema Pulmonary Embolism Respiratory Distress To reduce intracranial pressure To stabilize the chest wall Respiratory Muscle Fatigue Acute Respiratory Distress Syndrome Over sedation

*The main goal of mechanical ventilation is to support gasexchange until the disease process or condition is resolved.

Positive pressure ventilation is the most common form of mechanical ventilation

used in the acute care setting. This form of ventilation forces oxygen into the lungs,

either through an endotracheal tube or a tracheostomytube, mimicking respiration.

Modes of Ventilation there are various modes of ventilation that may be used

to ventilate and oxygenate the patient. these modes are ways in which ventilation is triggered;

they allow the patient some or all control over his orher breathing.

1. Controlled ventilation (CV) delivers a preset volume or pressure at a preset

rate. This mode takes away all control of breathing from the

patient. it is primarily used for patients who have no

respiratory effort at all.


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2. Assist-control ventilation (ACV) delivers a preset volume or pressure whenever

the patient initiates a breath. If the patient does not initiate a breath by a preset

time, the ventilator will give one. This mode is usedprimarily for the patient with normal breathing but whohas weak respiratory muscles or who cannot achieve anadequate volume on his or her own.

3. Synchronized intermittent mandatory ventilation (SIMV) delivers a preset volume at a preset rate and is

synchronized with patients effort. This mode allows for spontaneous breathing between

ventilated breaths and prevents competition betweenthe patient and the ventilator. When a spontaneousbreath occurs, it is at the patients own rate and tidalvolume.

SIMV is the most common mode used and allows forweaning from the ventilator.

4. Pressure-controlled ventiation (PCV) delivers a positive pressure breath until a

maximum amount of pressure is reached; then thebreath stops. The maximum pressure limit is preset and helps

prevent barotraumas (damage from the pressure) tothe lungs.

The amount of volume that is delivered varies, basedon airway resistance and lung compliance. Usually themaximal pressure limit is set to achieve a goal tidalvolume that is designed by the physician.

5. Inverse-ratio ventilation (IRV) is used when the inspiratory time is increased

and the expiratory time is decreased. With IRV the inspiration-expiration (I/E) ratios used

most are 1:1 and 2:1. This mode of ventilation allowsfor a longer period for gas exchange toimprove


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oxygenation. This mode is generally used in patientswith ARDS.

This type of ventilatory mode creates an abnormalbreathing pattern for the patient; consequently the

patient may become uncomfortable and anxious.

6. Constant positive airway pressure (CPAP) provided positive pressure during spontaneous

breaths; the ventilator will not initiate any breaths. This mode increases oxygenation by opening any

closed alveoli that may occur at end-expiration. CPAP generally ranges from5-10 cm water

pressure. Greater than 10 cm water pressure may

increase intrathoracic pressure to the point that itaffects the patients venous return, decreasing cardiacoutput and blood pressure. CPAP at this level may alsocause a pneumothorax to occur

7. Positive end-expiratory pressure (PEEP) adds positive pressure during expiration of each

ventilated breath. Ventilator settings must be individualized to each

patient to allow for optimal gas exchange. Settings are generally based on arterial blood gas

(ABG) measurements and arterial oxygen saturationlevel.

VENTILATOR SETTING / DESCRIPTION / RANGES

1. VT ( Tidal Volume) Amount of oxygen delivered to patient with each

preset ventilated breath. 5-15ml/kg (average 10ml/kg)

2. Respiratory rate Number breaths per minute that ventilator is set

to deliver.


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4-20 breaths/min

3. FIO2 (Fraction of Inspired Oxygen) Percentage of oxygen delivered by ventilator with

each breath. 21%-100%

4. I/E Ratio (Inspiratory to Expiratory) duration of I/E time 1:2 (unless IRV is used)

5. Sensitivity Determined how fast ventilator will delivered

during inspiration High: increase airway pressure Low: decrease airway pressure

6. Pressure Limits Regulates maximum amount of pressure the

ventilator will generate to deliver preset ventilator. Ventilated breath is stopped when pressure limit is

reached.

Barotrauma occurs when high airway pressures cause

overdistention of the alveoli, rupture and leakage ofair.

Barotrauma can cause pneumothorax, subcutaneous

emphysema, or crepitus. Air can leak under the mediastinum or into the

pericardium or peritoneum, causing problems withorgans located in these areas.

A patient needing long-term ventilatory management willneed a tracheostomy placed at some point.


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Endotracheal tubes (oral or nasal) are not intended forlong-term management and may lead to otherproblems such as mucosal breakdown, skin ulcerations(lips), sinusitis, and vocal cord paralysis or damage (or

both).

The following are practices performed for patientsreceiving mechanical ventilation:

The respiratory status is assessed every 4 hours andmore frequently when a change in conditionoccurs. Close attention is paid to breathing sounds andthe amount ofpatient effort.

Signs of hypoxia are assessed. These signs includerestlessness, anxiety, increased heart rate and bloodpressure, increased respiratory rate, and oxygensaturation via pulse oximetry less than 90%.

Endotracheal or tracheostomy tube placement ismaintained by properly securing the tube andpreventing inadvertent extubation by staff or

patient. Placement is maintained until extubation.

The endotracheal tube is repositioned per institutionalpolicy to prevent pressure sores.

Secretions are suctioned to maintain an openairway. Amount, color, and consistency of thesecretions are noted, as well as how thepatient tolerated the procedure.

Ventilator settings and alarms are verified dehydration.Unlike patients with DKA, patients with HHNC do notdevelop ketoacidosis, but the reason for this is notknown.

Contributing factors include:


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The limitation on ketogenesis by hyperosmolarity the lower levels offree fatty acids available for

ketogenesis

the availability of insulin in amounts sufficient to inhibitketogenesis but not sufficient to prevent hyperglycemia the hepatic resistance to glucagon in these patients.

Management: refer to DKA

THYROTOXIC CRISIS (THYROID STORM)

A severe form of hyperthyroidism marked by suddenrelease of thyroid hormone into the blood stream

Precipitating Factors

Stress such as injury, infection, thyroidal and non-thyroid surgery, tooth extraction, insulin reaction,diabetic acidosis, pregnancy, digitalis intoxication,abrupt withdrawal of anti-thyroid medications, extreme

emotional stress, or vigorous palpation of the thyroid.

Clinical Manifestations

1. High fever2. Diaphoresis3. Cardiopulmonary symptoms:

extreme tachycardia, HPN, arrhythmias, CHF,pulmonary edema

4. CNS symptoms: increasing feeling oftremulousness to severeagitation, psychosis with developing apathy,irritability, coma , heat intolerance5. GI disturbance:

weight loss, diarrhea, abdominal pain


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The cause of high BP in 0.9% to 2.2% of patients withHPN

One form of HPN that is usually cured by surgery

Clinical Manifestations

Typical triad ofsymptoms: Headache, Diaphoresis, Palpitations

HPN may be intermittent or persistent

Tremor, flushing and anxiety

Hyperglycemia may result from conversion of liver andmuscle glycogen to glucose

Clinical picture is usually characterized by:

1. Acute, unpredictable attacks, lasting seconds orseveral hours

2. Pat ient is anxious, tremulous and weak3. Headache, vertigo, blurring of vision, tinnitus, air

hunger, and dyspnea4. Polyuria, nausea, vomit ing, d iarrhea,

abdominal pain5 . F e e l i n g o f imp e n d i n g d oom6 . P a l p i t a t i o n s an d t a c h y c a r d i a7 . B P a s h i g h a s 350 /200 mm Hg

Assessment/Diagnostic Findings:

Signs of sympathetic nervous system over activity: 5 Hs (HPN, headache, hyperhidrosis (excessive

sweating), hypermetabolism, and hyperglycemia)

Medical Management: Pharmacologic Therapy


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1. Close monitoring of ECG changes and carefuladministration of alpha-adrenergic blocking agents,muscle relaxants to lower BP quickly.

2. Long-acting alpha blocker to prepare patient for surgery

3. Beta-adrenergic blocking agents for patients with cardiacdysrhythmias

Surgical Management

Adrenalectomy- surgical removal of the tumor

HEPATIC FAILURE (Hepatic Coma)

An end stage of liver disease, usually arises as acomplication of conditions that cause liver dysfunctionalthough it can be idiopathic

Also called Hepatic coma because the patients neurologicstatus gradually deteriorates

Represents the most advanced stage of hepaticencephalopathy

A life threatening crisis may occur if the serum ammonialevel rises, causing cerebral ammonia intoxicationCauses:1.Cirrhosis2. Hepatitis3. Drug or toxin-induced damage4. Fattyliver 5. Portal HPN6. Surgically-created portal systemicshunts that bypass the liver and allow toxins into the


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The pupil is comatose and does not react to stimuli. Pupilsare dilated and lack corneal and deep tendon reflexes.Extremities are flaccid andmay assume flexion or extensionposturing, decebrate rigidity. The EEG is markedly

abnormal.Assessment and Diagnostic Findings:1. Elevatedarterial ammonia blood levels2. The encephalogram showsgeneralized slowing and an increase in amplitude of brainwaves and the appearance of characteristic triphasicwaves3.Occasionally, fetor hepaticus, a characteristic breath odorlike freshly mowed grass, acetone, or old wine, may benoticed.4. In a more advanced stage, there are grossdisturbances of consciousness and the patient is completelydisoriented with respect to time andplace5. With further

progression of the disorder, the patient lapses into frankcoma and may have seizures.Intervention:1. Anti-infectiveagents to decrease bacterial action in the colon.2.Ammonia detoxicants to reduce ammonia. Lactulose(Duphulac) is administered3. Cleansing enemas with dilutedacetic acid or neomycin4. Discontinuation of anyprecipitating substance: Dietary proteins, sedatives, diuretictherapy, analgesics5. IV administration of glucose tominimize protein breakdown6. Oxygen administration7.

Correction of any electrolyte imbalance8. Promote rest,comfort and quiet environmentNursing Diagnosis:1. Alteredthought process2. Potential impaired skin integrity3.Impaired skin integrityRENAL DISORDERRENAL FAILURE

Renal Failure is a systemic disease and is a final commonpathway of many different kidney and urinary tract diseases.

Results when the kidneys are unable to remove the bodysmetabolic wastes or perform their regulatory functions

The substances normally eliminated in the urine accumulatein the body fluids as a result of impaired renal excretion and


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lead to a disruption inendocrine and metabolic functions andfluid and electrolyte, an acid-base disturbances.ACUTE RENAL FAILURE

Acute renal failure is a sudden and almost complete loss ofkidney function over a period of hours to days.Categories of Acute Renal Failure:1. Prerenal Condition(hypoperfusion of kidney).Occurs as a result of impaired blood flow that leads tohypoperfusion of the kidney and a dropin the GFR. Commonclinical situations are volume-depletion states (hemorrhageor gastrointestinal losses), impaired cardiac performanceandvasodilation (sepsis or anaphylaxis)

2. Intrarenal. Intrarenal causes of acute renal failure are the result ofactual parenchymal damage to the glomeruli or kidneytubules. Conditionssuch as burns crush injuries, andinfections, as well as nephrotoxic agents, may lead to acutetubular necrosis and cessation of renal function.Severetransfusion reaction may also cause intrarenal failure.Medications may also predispose a patient to intrarenaldamage, esp. nonsteroidalanti-inflammatory drugs and ACE

inhibitors3. Post renal conditions. Postrenal causes of acute renal failure are usually theresult of an obstruction somewhere distal to the kidney.PHASES OF ACUTE RENAL FAILURE:1. Initiation period begins with the initial insult and ends when oliguriadevelops.2. Period of Oliguria accompanied by a rise in the serum concentration of

substances usually excreted by the kidney (urea, creatinine,uric acid,organic acids and the intracellular cations potassium and magnesium3. Period of diuresis The patient experiences a gradual increase in urinaryoutput, which signals that glomerular filtration has started torecover.Laboratory values start rising and eventually begin a


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downward trend.Uremic symptoms may still be present. Thepatient must be closely monitoredfor dehydration during thisphase; if dehydration occurs, the uremic symptoms arelikely to increase.

4. Period of Recovery signals the improvement of renal function. Laboratoryvalues return to the patients normal level.ClinicalManifestations:1. May appear critically ill and lethargic2.Persistent nausea, vomiting and diarrhea3. The skin andmucous membranes are dry due to dehydration4. Uremicfetor breath have the odor of urine5. CNS manifestations:drowsiness, headache, muscle twitching, andseizuresAssessment and Diagnostic Findings:1. Changes in

urine. The urinary output varies (from scanty to normalvolume). Hematuria may be present and urine has low-specific gravity.Patients with prerenal azotemia have adecreased amount of sodium. Those patients with intrarenalazotemia usually have urinary sodium levelsgreater than 40mEq/L.2. Increased blood urea nitrogen and creatinine levels(Azotemia)3. Hyperkalemia4. Metabolic acidosis5. Calciumand Phosphorus AbnormalitiesAnemia due to reduced erythropoietin production, uremicgastrointestinal lesions, reduced Rbc lifespan, and blood

lossPrevention:1. Renal function must be monitored closelyif patient has been taking nephrotoxic antibiotic agents orhas been exposed to environmental toxins.Blood should bedrawn for determining baseline and monitoring serum BUNand creatinine levels by 24 hours after initiation ofmedication therapyMedical Management:1. Prerenalazotemia is treated by optimizing renal perfusion.2.

Postrenal failure is treated by relieving the obstruction3.Overall, medical management includes maintaining fluidbalance, avoiding fluid excesses, or performing dialysis4.The elevated potassium levels may be reduced byadministering ion-exchange resins (sodium polystyrenesulfonate kayexalate)5. Diuretics are used formanagement of volume status6. Low-dose dopamine is


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often used to dilate the renal arteries7. Atrial natriureticpeptide inhibits sodium and water absorption and dilatesthe afferent arteriole, thus improving blood flow to theglomerulus8. Correction of acidosis and elevated phosphate

levels. When severe acidosis is present, the arterial bloodgases or serum bicarbonate levelsmust be monitoredbecause patient may require sodium bicarbonate therapy ordialysis. Patients elevated phosphate level may becontrolled withphophate-binding agents (aluminumhydroxide).9. Nutritional Therapy. Dietary proteins arelimited to about 1 g/kg during the oliguric phase. High-carbohydrate meals to meet caloric requirements.Foods andfluids containing potassium and phosphorus are

restricted.Nursing Management:1. Monitoring fluid andelectrolyte balance. Hyperkalemia is the most immediatelife-threatening imbalance seen in acute renal failure.2.Reducing metabolic rate. To reduce catabolism and thesubsequent release of potassium and accumulation ofendogenous waste products. Bedrest is indicated and feverand infection are prevented or treated promptly.3.Promoting pulmonary function.Patient is assisted to turn,cough and take deep breaths frequently to prevent

atelectasis and respiratoryinfection.4. Preventing Infection.Asepsis is essential with invasive lines and catheters5.Providing skin care. Meticulous skin care is important.Massaging bony prominences, turning the patient frequently,and bathing the patient withcool water are comforting andprevent skin breakdown6. Providing support. The patientand family will need assistance, explanation and supportduring this time.CHRONIC RENAL FAILURE

CRF is a progressive, irreversible deterioration in renalfunction in which the bodys ability to maintain metabolicand fluid and electrolytebalance fails, resulting in uremia orazotemia (retention of urea and other nitrogenous wastes inthe blood)Pathophysiology:As renal function declines, theend products of protein metabolism (which are normally


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excreted in urine) accumulate in the blood. Uremiadevelopsand adversely affects every system in the body.4 Stages of Chronic Renal Disease:Stage 1Reduced renal reserve. Characterized by a 40 to 75% loss of

nephron function. The patient usually does not havesymptoms because theremaining nephrons are able to carryout the normal functions of the kidney.Stage 2Renal Insufficiency. Occurs when 75 to 90% of nephronfunction is lost. At this point, the serum creatinine and bloodurea nitrogen rise, the kidneyloses its ability to concentrateurine and anemia develops. The patient may report polyuriaand nocturia.

Stage 3Renal Disease. Edema, metabolic acidosis, and hypocalcemiaoccur. Patient may exhibit overt uremia with cardiovascular,gastrointestinal, andneurologic complications.Stage 4End-stage renal Disease(ESRD). The final stage of CRF occurs when there is lessthan 10% nephron function remaining. All of thenormalregulatory, excretory, and hormonal functions of thekidney are severely impaired. ESRD is evidenced by elevated

creatinine and blood ureanitrogen levels as well aselectrolyte imbalances. Once the patient reaches this point,dialysis is usually indicated.Signs And Symptoms Of CRF:1.Neurologic

Weakness and fatigue; confusion; inability to concentrate;disorientation; tremors; seizures; asterixis; restlessness oflegs; burning of soles of feet; behavior changes.2.Integumentary

Gray-bronze skin color; dry, flaky skin; pruritus;ecchymosis; purpura; thin, brittle nails; coarse, thinning hair3. Cardiovascular

HPN; pitting edema (feet , hands, sacrum), periorbitaledema; pericardial friction rub; engorged neck veins;


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pericarditis; pericardial effusion;pericardial tamponade;hyperkalemia; hyperlipidemia4. Pulmonary

Crackles; thick, tenacious sputum; depressed cough reflex;

pleuritic pain; shortness of breath; tachypnea; kussmaul-type respirations; uremicpneumonitis; uremic lung5.Gastrointestinal

Ammonia odor to breath (uremic fetor); metallic taste;mouth ulcerations and bleeding; anorexia; nausea andvomiting; hiccups; constipation or diarrhea; bleeding fromGIT6. Hematologic

Anemia; thrombocytopenia7. ReproductiveAmenorrhea; testicular atrophy; infertility; decreasedlibido8. Musculoskeletal

Muscle cramps; loss of muscle strength; renalosteodystrophy; bone pain; bone fractures; footdropAssessment And Diagnostic Findings:

Glomerular Filtration Rate. Decreased GFR can be detectedby obtaining a 24-hour urine analysis for creatinineclearance. As GFR decreases,the creatinine clearance valuedecreases, whereas the serum creatinine and BUN levelsincrease.Sodium and Water Retention. The kidney is unable toconcentrate or dilute the urine normally in ESRD. Somepatients retain sodium and water,increasing the risk for

edema, CHF, and HPN.Acidosis. With advanced renal disease, metabolic acidosisoccurs because the kidney is unable to excrete increasedloads of acid.


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Anemia. Anemia develops as a result of inadequateerythoropoietin production, the shortened life span of RBCs,nutritional deficiencies, andthe patients tendency to bleed,particularly from GIT

Calcium and Phosphorus Imbalance. The bodys serumcalcium and phosphate levels have a reciprocal relationshipin the body; as one rises,the other decreases.14Complications:1. Hyperkalemia. Due to decreasedexcretion, metabolic acidosis, catabolism, and excessiveintake (diet, medications, fluids)2. Pericarditis. Due toretention of uremic waste products and inadequate

analysis3. Hypertension. Due to sodium and water retentionand malfunction of the rennin-angiotensin-aldosteronesystem4. Anemia. Due to decrease erythropoietin, decreasedRBC life span, GIT bleeding and blood loss during dialysis.5.Bone disease and metastatic calcifications. Due to retentionof phosphorus, low serum calcium levels, abnormal vitaminD metabolism, andelevated aluminum levelsMedicalManagement:1. Pharmacologic Therapy

Antacids. Hyperphosphatemia and hypocalcemia are treatedwith aluminum based antacids that bind dietary phophorusin the GIT

Antihypertensive and Cardiovascular agents. HPN ismanaged by intravascular control and a variety ofhypertensive medications. CHF andpulmonary edema mayrequire treatment with fluid restriction, low sodium diets,diuretics, inotropic agents such as digitalis, or

dobutamine,and dialysis.Anticonvulsants. If seizures occurs. The onset of seizure isrecorded along with the type, duration and general effect onthe patient. IntravenousDiazepam or phenytoin is usuallyadministered to control seizures. The side rails must bepadded to protect the patient


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Erythropoietin. Anemia associated with CRF is treated withrecombinant human erythropoietin (Epogen)2. NutritionalTherapy> Includes careful regulation of protein intake, fluid

intake to balance fluid losses, sodium intake to balancesodium losses and some restriction of potassium3. Dialysis>Hyperkalemia is usually prevented by ensuring adequatedialysis treatments with potassium removal and carefulmonitoring of all medications for their potassiumintakeNursing ManagementNursing Diagnoses:1. Fluidvolume excess r/t decreased urine output, dietary excesses,and retention of sodium and water 2. Altered nutrition; lessthan body requirements r/t anorexia, nausea and vomiting,

dietary restrictions, and altered oral mucous membranes3.Knowledge deficit regarding condition and treatmentregimen4. Activity intolerance r/t fatigue, anemia, retentionof waste products, and dialysis procedure5. Self-esteemdisturbance r/t dependency, role changes, changes in bodyimage, and sexual dysfunction Nursing Care:1. Directedtoward assessing fluid status and identifying potentialsources of imbalance2. Implementing a dietary program toensure proper nutritional intake within the limits of the

treatment regimen3. Promoting positive feelings byencouraging increased self-care and greater independenceCARDIOVASCULAR DISORDERSANGINA PECTORIS-literally translates as pain in the chest. This symptom occursas a result of myocardial ischemia. Anginal chestpain istransient, lasting only 3-5 minutes and is usually relievedwhenever the precipitating event is discontinuedor

nitroglycerin is administered. The most common cause ofangina is preexisting cardiovascular disease, whichnarrowsor occludes the arteries that feed the heart muscle.Numerous disorders occur along thepathophysiologiccontinuum of cardiovascular disease; these includeatheorsclerosis, angina, cerebrovascular accident,myocardial infarction (MI), and heart failure.The coronary


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arteries, which arise from the ascending aorta immediatelyon exiting the heart, normally supplies the myocardium withadequateoxygen and nutrient-rich blood to meet metabolicdemands. In the atherosclerotic heart, arteries are

chronically dilated beyond narrowed or partially obstructedareas to meet the hearts metabolic demands at rest. Thuswhen the myocardium requires more oxygen during times ofincreased work, the coronary arteries cannot increase flowbecause they are already maximally dilated. An oxygendeficit is created as a result of the oxygen supply being lessthan the cellular demands.The oxygen imbalance createdwith angina can be quite precarious, and many factors canadversely affect this relationship. The demand for oxygen is

increased whenever anyone of the following is increased:heart rate, afterload (hypertension), wall ension (ventricularvolume or pressure), myocardial wall thickness(hypertrophy), or contractility. All of these factors make theheart work harder. Conversely, the oxygen supplyisdecreased whenever any of the following occur:hypotension, anemia, respiratory insufficiency, ortachycardia, which allows minimal time for diastolic filling.Inthe absence of adequate oxygen and glucose, cellular

metabolism shifts from the efficient oxidativephosphorylation, which yields a large amountof adenosinetriphosphate (ATP) to the inefficient glycolysis; this actionnot only yields a very small amount of ATP but it also yieldslactic acid as aby-product. This acidic environment activateschemical nociceptors, which transmit pain impulses to thebrain, and the individual experienceschest pain. At this pointthe damage is reversible; in other words, if the flow ofoxygen and glucose-rich blood is restored, no permanent

damageresults. However, if the oxygen deficit continues andthe lactic acid is allowed to build up, cellular metabolism andfunction can be altered to thepoint of irreversible cell deathor myocardial infarction (MI).Types of Angina1.Stable angina


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(classic or exertional angina).The primary differentiatingfactor about this type of angina is that it is predictable andoccurs intermittently over an extended period. It occurswiththe same pattern of onset, duration, and intensity each

time. Further, the same precipitating activity (most oftenphysical in nature) usuallybrings on stable angina. The painis relieved either when the precipitating event isdiscontinued or when nitroglycerin is administered intheprescribed fashion. If the pain is unrelieved by either restor nitroglycerin, the patient may then be at risk for an MI.As previously discussed,stable angina is a result ofatherosclerotic plaque that has narrowed the arteries. Thechronically dilated vessel is unable to dilate further tomeet

metabolic demands.2. Unstable angina(progressive, crescendo, preinfarction angina, acutecoronary insufficiency)This type is potentially life-threatening because it signifiesadvanced ischemic heart disease. This type of angina ismost often unpredictable.Moreover, unstable angina attackstend to occur with increasing frequency, intensity and

duration. No precipitating event is necessary. In fact,theseattacks are brought on at times of complete rest. Anindividual previously diagnosed with stable angina canprogress to unstable angina;alternatively, unstable anginamay be the first clinical manifestation in an individual withCAD.3.Prinzmetals angina(variant angina)

The least common type of angina. It is unpredictable inonset, duration, and intensity and occurs almost exclusivelyat rest. Vasospasm of one or more of the coronary arteriesis the underlying cause, which can occur with or withoutassociated atherosclerosis.Clinical Manifestations


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The cardinal symptom of angina is chest pain or discomfort.However, many patients describe feeling vague sensationsof discomfort, tightness,

15pressure, heaviness, aching or squeezing. Otherscomplain of heartburn or indigestion during an attack. Themost common location is substernal;however, the pain ordiscomfort may radiate to the neck, jaw, back, shoulders,left arm, or occasionally the right arm.When asked todemostrate or point to the location of the pain, typically

patients will clench one or two fists over the substernalregion whenexperiencing myocardial ischemia. This displayis known as theLevines sign. Other associated sighs and symptoms include pallor,diaphoresis,cold skin, shortness of breath, weakess,dizziness, anxiety, and feelings of impending doom.When anindividual complains of chest pain,the source of pain should be considered cardiac until proven

otherwise. However, it is prudentto consider both cardiac andnoncardiac causes of chest pain as possible differentials.Electrocardiogram(ECG) remains the gold-standard for a first-line,noninvasive tool for diagnosis.Percutaneous transluminal coronary angioplasty (PTCA) involves the passage of an inflatable balloon catheter into

the stenotic coronaryvessel, which is then dilated, resulting

in compression of the atherosclerotic plaque and widening ofthe vesselCoronary artery bypass grafting (CABG) done by harvesting either a saphenous vein from the legor the left internal mammaryartery and thenused to bypassareas of obstruction in the heartNursing Responsibilities


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In caring for patients with angina, the focus of the nursesrole is two-fold. The first priority is appropriate treatment ofthe acute attack to alleviatediscomfort and, if possible, toavert untoward sequelae. The second priority is geared

toward extensive education that not only empowersthepatient to become an active participant in his or her wellbeing but also imparts practical tools with which the patientcan effectively manage thecondition at home to achieve thehighest level of wellness and independent functioning.Duringan acute anginal attack, it is imperative that the nurseperforms a rapid and focused physical assessment andhealth history. Frequent vitalsigns and continuous cardiacmonitoring are essential parts of the ongoing assessment.

The most crucial part of the assessment focuses onthecurrent attack; emphasis must be placed on evaluatingthe pain itself and any precipitating events.The nurse mustask the following questions:

How severe is the pain? (scale of 1-10)

What does the pain feel like?

Where is the pain? Does it move or radiate? Is it diffused orwell localized?

Did the pain start suddenly or gradually?

How long does it last?

How frequently does it occur?

What makes the pain worse? What brings the pain on?

What makes the pain better? What resolves the pain?

Has the pain been increasingly worse with each attack?Another critical nursing function is prompt institution of


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.Circumstances that can cause an imbalance in supply anddemand of oxygen and nutrient-rich blood:

Physical exertion

Emotional stress

Weather extremes

Digestion after a heavy meal

Valsalva maneuver

Hot baths or showers

Sexual excitation

Pathophysiologic chaaracteristicsClinical ManifestationsThe hallmark of MI is severe, unrelenting chest pain. As withangina, the pain is typically described as crushing, pressure-filled, vise-like, tight,constricting, or squeezing. The mostcommon location of the pain is substernal, with radiation tothe neck, jaw, or left arm. Leass frequently, painis reportedin the shoulders, back, or right arm. In addition, a positiveLevines sign(one or two fists clenched over the chest area whenthepatient is asked to localize the pain) can contribute to thediagnosis.The major difference in the clinical presentation ofMI compared with that of angina is the onset, severity, andduration. Chest pain aassociatedwith MI usually has anabrupt onset and can occur during activity, rest, or evensleep. The pain described during MI is typically more severethananginal pain, lasting at least 20-30 minutes, and it isnot relieved with either rest or nitroglycerin.However, not allpatients will experience the same clinicalpresentation.During MI, associated clinical manifestationscan range from vague sensations of just not feeling well to


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the loss of consciousness or cardiacarrest. Often the skin isdiaphoretic with a pale or ashen appearance, which occursbecause of peripheral vasoconstriction as the body shunts

blood to the vital core. The initial surge of catecholaminescan contribute to a variety of signs and symptoms such astachycardia, hypertension,anxiety, palpitations,apprehension, and feelings of impending doom. Stimulationof the medulla is mediated via vasovagal reflexes and canresultin nausea and vomiting. Fever may be presentsecondary to the activation of the inflammatory process. As

the infarction progresses and thehearts pumping abilitybecomes impaired, cardiac output drops. Associated withdecreased cardiac output is hypotension, restlessness,dyspnea, jugular vein distention, oliguria, and confusion.Electrocardiogram capable of diagnosing MI in 80% of patients, making it anindispensable, noninvasive, and cost-effective tool.EvolvingMI will show ST elevation which indicates acute myocardialnecrosis. The development of Q wave may beobserved which

signifies further electrical abnormalities. It may be anindication of worsening ischemia and necrosis.Cardiac EnzymesDuring the infarction process, cell membranes rupture,allowing intracellular enzymes to spill out into the bloodstream. Blood sample drawn atcertain times during or afterMI can be sent to the laboratory where enzymes can bemeasured and interpreted to determine the presence ofaninfarction.Cardiac Enzyme Laboratory

FindingsEnzymeEarliest Rise (in hours)Peak (in hours)Returnto BaselineCreatinine kinase (CK)CK-MBMyoglobinTroponin12-64-80.5-1.01-618-3615-246-97-243-6 days3-4 days12hours10-14 daysTroponin 1is the newest cardiac marker and is a protein found only inmyocardial cells. It is a quick, rapid test that, if elevated,


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indicated MI.First-Line and Initial Treatment for MyocardialInfarction

Provide oxygen

Obtain a 12-lead ECG

Monitor vital signs and pulse oximetry

Monitor continuous cardiac rhythm with ST segmentmonitoring

Conduct history and physical examinations

Administer medications (thrombolytic therapy andanticoagulant therapyNursing Interventions:1.Bedrestmust be enforced.2. The nurse should assist with all positionchanges and personal hygiene to avoid any exertionaleffort.3. Monitor I&O particularlyurine outputbecause this is a reliable indictor of cardiac output andsystemic perfusion.4. Administer stool softener as ordered toprevent straining and vasovagal stimulation which can causeprecipitous bradycardiaCARDIAC FAILURECONGESTIVE HEART FAILURE (CHF)

Often referred to as cardiac failure, is the inability of theheart to pump sufficient blood to meet the needs of thetissues for oxygenation andnutrients.

CHF is most commonly used when referring to left-sided andright-sided failure

The incidence of CHF increases withagePathophysiology:Cardiac failure most commonly occurswith disorders of cardiac muscles that result in decreasedcontractile properties of the heart. Commonunderlying


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conditions that lead to decreased myocardial contractilityinclude myocardial dysfunction, arterial hypertension, andvalvular dysfunction.Myocardial dysfunction may be due tocoronary artery disease, dilated cardiomyopathy, or

inflammatory and degenerative diseases of themyocardium.Atherosclerosis of the coronary arteries is the primary causeof heart failure. Ischemia causes myocardial dysfunctionbecause of resulting hypoxia and acidosis (fromaccumulation of lactic acid). Myocardial infarction causesfocal myocellular necrosis, the death of myocardialcells, anda loss of contractility; the extent of the infarction isprognostic of the severity of CHF.Dilated cardiomyopathycauses diffuse cellular necrosis, leading to decreased

contractility. Inflammatory and degenerative diseases ofthemyocardium, such as myocarditis, may also damagemyocardial fibers, with a resultant decrease incontractility.Systemic or pulmonary HPN increases afterloadwhich increases the workload of the heart and in turn leadsto hypertrophy of myocardial musclefibers; this can beconsidered a compensatory mechanism because it increasescontractility.Valvular heart disease is also a cause of cardiacfailure. The valves ensure that blood flows in one direction.

With valvular dysfunction, valve hasincreasing difficultymoving forward. This decreases the amount of blood beingejected, increases pressure within the heart, and eventuallyleads topulmonary and venous congestion.Etiologic Factors :1. Increased metabolic rate (eg. fever, thyrotoxicosis)2.Hypoxia3. AnemiaVENTRICULAR FAILURELEFT-SIDED CARDIAC FAILURE

Pulmonary congestion occurs when the left ventricle cannot

pump the blood out of the chamber. This increases pressurein the left ventricleand decreases the blood flow from the leftatrium. The pressure in the left atrium increases, whichdecreases the blood flow coming from thepulmonary vessels.The resultant increase in pressure in the pulmonarycirculation forces fluid into the pulmonary tissues andalveoli; whichimpairs gas exchangeClinical Manifestations :1.


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Dyspnea on exertion2. Cough3. Adventitious breathsounds4. Restless and anxious5. Skin appears pale andashen and feels cool and clammy6. Tachycardia andpalpitations7. Weak, thready pulse8. Easy fatigability and

decreased activity toleranceRIGHT-SIDED CARDIAC FAILURE

When the right ventricle fails, congestion of the viscera andthe peripheral tissues predominates. This occurs because theright side of the heartcannot eject blood and thus cannotaccommodate all the blood that normally returns to it fromthe venous circulation.Clinical Manifestations:1. Edema ofthe lower extremities (dependent edema)

Amanuel/Pslidasan/Ksjuliano/MRCuenoNCM 104 1stsem S.Y. 2007-2008

172. Weight gain3. Hepatomegaly (enlargement of theliver)4. Distended neck veins5. Ascites (accumulation of fluidin the peritoneal cavity)6. Anorexia and nausea7. Nocturia(need to urinate at night)8. WeaknessMedical

ManagementThe basic objectives in CHF management arethe following:1. Reducing the workload on the heart2.Increasing the force and efficiency of myocardialcontraction3. Eliminating the excessive accumulation of bodywater by avoiding excess fluid, controlling the diet, andmonitoring diuretic and angiotensin-converting enzyme(ACE) inhibitor therapyPharmacologic Therapy:If the patientis in mild failure, usually an ACE inhibitor is prescribed. Adiuretic is added if there is no improvement or if there are

signs of fluidoverload. Next, digitalis is added if thesymptoms continue. If symptoms are severe, all threemedications are usually started immediately.ACE Inhibitors.Promote vasodilation and diuresis by decreasing afterloadand preload eventually decreasing the workload of theheart.Diuretic Therapy. A diuretic is one of the firstmedications prescribed to a patient with CHF. Diuretics


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promote the excretion of sodium and water through thekidneys.Digitalis. This medication increases the force ofmyocardial contraction and slows conduction through the AVnode. It improves contractility thus,increasing left

ventricular output.Dobutamine.(Dobutrex) is an intravenousmedication given to patients with significant left ventriculardysfunction. A catecholamine, it stimulates thebeta1-adrenergic receptors. Its major action is to increase cardiaccontractility.Milrinone (Primacor). A phosphodiesteraseinhibitor that prolongs the release and prevents the uptakeof calcium. This in turn, promotesvasodilation, causing adecrease in preload and afterload and decreasing the

workload of the heart.Other medications. Anticoagulantsmay be prescribed. Beta-adrenergic blockers maybeindicated in patients with mild or moderate failure.NutritionalTherapy:1. A low-sodium diet2. Avoidance of excessiveamount of fluidsNursing Management:1. Record intake andoutput to identify a negative balance (more output thaninput)2. Weigh patient daily at the same time3. Auscultatelung sounds daily to detect a decrease or an absence ofpulmonary crackles4. Determine the degree of jugular

distention5. Identify and evaluate severity of dependentedema6. Monitor pulse rate and BP, and make sure thepatient does not become hypotensive from dehydration7.Examine skin turgor and mucous membranes for signs ofdehydration8. Assess for symptoms of fluid overload(orthopnea, paroxysmal nocturnal dyspnea, and dyspnea onexertion)Nursing Process: The Patient With CardiacFailureAssessment

The focus of the nursing assessment for the patient withcardiac failure is directed toward observing for signs andsymptoms of pulmonary andsystemic fluid overload.HealthHistory

The nurse explores sleep disturbances, particularly sleepsuddenly interrupted by shortness of breath.


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The nurse finds out about the number of pillows needed forsleep (indication of dyspnea)

Find out also the activities of daily living and the activitiesthat causes shortness of breathPhysical Examination

The lungs are auscultated at frequent intervals to detectcrackles and wheezes or their absence. The rate and depthof respiration are alsonoted.

The heart is auscultated for an S3

heart sound, a sign that the heart pump is beginning to failand that increased blood volume remains in theventriclewith each beat. HR and rhythm are also noted.

Jugular vein distention is also assessed. Distention greaterthan 3 cm above the sternal angle is considered abnormal.

Sensorium and level of consciousness must be evaluated

Dependent parts of the patients body are assessed forperfusion and edema.

The liver is examined for hepatojugular reflux.

Output is measured carefully to establish a baseline againstwhich to measure the effectiveness of diuretic therapy.Intake and output recordare maintainedNursingDiagnoses:1. Activity intolerance r/t imbalance betweenoxygen supply and demand secondary to decreased CO2.Excess fluid volume r/t excess fluid/sodium intake orretention secondary to CHF and its medical therapy3.Anxiety r/t breathlessness and restlessness secondary toinadequate oxygenation4. Non-compliance r/t to lack ofknowledge5. Powerlessness r/t inability to perform roleresponsibilities secondary to chronic illness and


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hospitalization.Potential Complications:1. Cardiogenicshock2. Dysrhythmias3. Thromboembolism4. Pericardialeffusion and pericardial tamponadePlanning And Goals:1.Promoting activity while maintaining vital signs within

identified range2. Reducing fatigue

183. Relieving fluid overload symptoms4. Decreasing theincidence of anxiety or increasing patients ability to manageanxiety5. Teaching the patient about the self-careprogram.6. Encouraging the patient to verbalize his ability tomake decisions and influence outcomes.NursingInterventions:1. Promoting Activity Tolerance

The patient is encouraged to perform an activity more slowlythan usual, for a shorter duration, or with assistanceinitially.

Barriers that could limit abilities to perform an activity areidentified

Pacing and prioritizing activities will maintain the patients

energy to allow participation in regular exercise.Vital signs should be taken before, during and immediatelyafter an activity to identify whether they are within thepredetermined range.2. Reducing Fatigue

The nurse and patient can collaborate to develop a schedulethat promotes pacing and prioritization of activities. Theschedule should alternateactivities with periods of rest and

avoid having two significant energy-consuming activitiesoccur on the same day or in immediate succession.3.Managing Fluid Volume

The nurse monitors the patients fluid status closely.Auscultating the lungs, comparing daily body weights,


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monitoring intake and output andassisting the patient toadhere to a low-sodium diet.

The nurse needs to position the patient or teach the patient

how to assume a position that shifts fluid away from theheart.

The nurse needs to assess for skin breakdown and institutepreventive measures4. Controlling Anxiety

The nurse should take steps to promote physical comfortand psychological support. A family members presenceprovides reassurance.Speaking in a slow, calm, and

confident manner is helpful. Stating specific, brief directionsfor an activity is helpful in decreasing anxiety.5. MinimizingPowerlessness

Patients need to recognize that they are not helpless andthat they can influence their direction, their lives, and theiroutcomes.

The nurse needs to assess for factors contributing to a

perception of powerlessness and intervene accordingly.Contributing factors may includelack of knowledge, hospitalpolicies, and lack of opportunities to make decisions.

Taking time to listen to patient encourages them to expresstheir concerns and questions

Provide the patient with decision-making opportunities

Provide encouragement and praiseExpected Outcomes:1.Demonstrates tolerance for increased activity2. Has lessfatigue and dyspnea3. Maintains fluid balance4. Is lessanxious5. Adheres to self-care regimen6. Makes decisionsregarding care and treatment7. Absence of complicationsCARDIOGENIC SHOCK


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Occurs when the heart cannot pump enough blood to supplythe amount of oxygen needed by thetissues.Pathophysiology:The heart muscle loses itscontractile power, resulting in a marked reduction in SV and

CO, sometimes called forward failure. The damagetomyocardium results in a decrease in CO, which in turnreduces arterial blood pressure and tissue perfusion in thevital organs (heart, brain,kidneys). Flow to the coronaryartery is reduced, resulting in decreased oxygen supply tothe myocardium, which in turn increases ischemiaandfurther reduces the hearts ability to pump. Theinadequate emptying of the ventricle also leads to increasedpulmonary pressures, pulmonarycongestion, and pulmonary

edema, exacerbating the hypoxia and resulting ischemia ofvital organs.Clinical Manifestations:1. Tissue hypoperfusion classic signs of cardiogenic shock manifested as cerebralhypoxia (restlessness, confusion, agitation), lowbloodpressure, rapid and weak pulse, cold and clammy skin,increased respiratory crackles, hypoactive bowel sounds,and decreased urinary output.2. Initially, arterial blood gasanalysis may show respiratory alkalosis.3. Dysrhythmias arecommonAssessment and Diagnostic Findings:1. The use of a

Pulmonary Artery catheter to measure left ventricularpressures and CO is important in assessing the severity ofthe problem andplanning management. The PA wedgepressure is elevated and the CO is decreased as the leftventricle loses its ability to pump.2. The systemic vascularresistance is elevated due to the sympathetic nervoussystem stimulation that occurs as a compensatory responseto thedecrease in blood pressure.3. The decreased bloodflow to the kidneys causes a hormonal response that causes

fluid retention and further vasoconstriction.4. The increasesin HR, circulating volume, and vasoconstriction occur tomaintain circulation to the brain, heart and lungs, however,the workloadof the heart is increased.5. Continued cellularhypoperfusion eventually results in organ failure. The patientbecomes unresponsive, severe hypotension occurs, andthepatient develops shallow respirations, cold, cyanotic or


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mottled skin, and absent bowel sounds.6. Arterial blood gasanalysis shows metabolic acidosis7. All laboratory resultsindicate organ dysfunction.Medical Management:1. Reduceany further demand on the heart2. Improve oxygenation

and restore tissue perfusion3. Diuretics, vasodilators, andmechanical devices (filtration and dialysis)4. Intravenousvolume expanders (normal saline, lactated Ringers solution,and albumin) are given for hypovolemia or low intravascularvolume.5. Strict bed rest to conserve energy6. Oxygenadministration is increased for hypoxemia7. Intubation andsedation may be necessary to maintain oxygenationbalance.Pharmacologic Therapy:

Most medication are administered IV because of thedecreased perfusion to the gastrointestinal system

191. Pressor agents are medications used to raise BP andincrease CO. Many pressor medications are catecholamines (norepinephrine and high-dose dopamine) to promoteperfusion to the heart and brain.2. Diuretics and vasodilators

may be administered to reduce the workload of the heart.3.Positive inotropic medications are given to increasemyocardial contractility4. Circulatory assist devices: Intra-aortic balloon pump to augment the pumping action of theheart. The device inflates during diastole, increasingthepressure in the aorta and therefore increasing perfusion. Itdeflates just before systole, lessening the pressure withinthe aorta beforeventricular contraction, decreasing theamount of resistance the heart has to overcome to eject

blood and therefore decreasing the amount of workthe heartmust complete to eject blood.Nursing Management:1. Nursemust carefully assess the patient, observe the cardiacrhythm, measure hemodynamic parameters, and record fluidintake and urinaryoutput.2. The patient must be closelymonitored for responses to the medical interventions and forthe development of complications3. The patient is always


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treated in intensive care environment because of thefrequency of nursing interventions and the technologyrequired for effective medical management.THROMBOEMBOLISM

The decreased mobility of the patient with cardiac diseasesand the impaired circulation that accompany these disorderscontribute to thedevelopment of intracardiac andintravascular thrombosis.Intracardiac Thrombus

Detected by an echocardiogram and treated withanticoagulants, such as warfarin.

A part of the thrombus may become detached and may becarried to the brain, kidneys, intestines, or lungs

The most common problem is pulmonary embolism. Thesymptoms of pulmonary embolism include chest pain,cyanosis, and shortness of breath, rapid respirations andhemoptysis. (see discussion on pulmonary embolism)

The pulmonary embolus may block the circulation to a partof the lung, producing an area of pulmonary infarction

Systemic embolism may present as cerebral, mesenteric, orrenal infarction

An embolism can also compromise the blood supply to anextremityPERICARDIAL EFFUSION AND CARDIAC TAMPONADEPathophysiology:Pericardial effusion refers to the escape offluid into the pericardial sac. Normally, the pericardial saccontains less than 50 ml of fluid, which theheart needs todecrease friction for the beating heart. An increase inpericardial fluid raises the pressure within the pericardial sacand compressesthe heart. This results in :


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Increased right and left ventricular-end diastolic pressures

Decreased venous return

Inability of the ventricles to distend adequatelyPericardialfluid may accumulate slowly without causing noticeablesymptoms. A rapidly developing effusion, however, canstretch the pericardiumto its maximum size and, because ofincreased pericardial pressure, and reduce venous return tothe heart, and decrease cardiac output. Theresult iscardiac tamponade.Clinical Manifestations:1. The patient may complain of afeeling of fullness within the chest. The feeling of pressure

may result from stretching of the pericardial sac2. Engorgedneck veins3. Shortness of breath4. A drop and fluctuation inBPAssessment and Diagnostic Findings:1. Pericardialeffusion is detected by percussing the chest and noting anextension of flatness across the anterior aspect of thechest2. Echocardiogram to confirm diagnosisMedicalManagement:1. Pericardial Fluid Aspiration(pericardiocentesis) performed to remove fluid from thepericardial sac2. Pericardiotomy. A portion of pericardium is

sliced to permit the pericardial fluid to drain into thelymphatic system.CARDIAC ARREST

Occurs when the heart ceases to produce an effective pulseand blood circulation. It may be due to a cardiac electricalevent, as when the HRis too fast or too slow or when thereis no heart rate at all.Clinical Manifestations:1. Loss ofconsciousness, pulse and BP2. Ineffective respiratory

gasping3. The pupils of the eyes dilate within 45 seconds.4.Seizures may or may not occur EmergencyManagement:Cardiopulmonary Resuscitation1. Airway maintain open airway2. Breathing provide artificialcirculation by rescue breathing3. Circulation promotingartificial circulation by external cardiac compression4.


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Defibrillation restoring the heart beatMaintaining Airwayand Breathing

The first step in CPR is to obtain an open airway. Any

obvious material in the mouth and throat should beremoved. The chin is directed up andback or the jaw(mandible) is lifted forward. The rescuer looks, listen. andfeels for air movement. An oropharyngeal airway is insertedif available. Two rescue ventilations over 3 to 4 seconds areprovided using a bag or mouth-mask device. If the firstrescue ventilation enteredeasily, then the patient isventilated with 12 breaths per minute and the open airwayis maintained. Endotracheal intubation is performed

toensure an adequate airway and ventilation.RestoringCirculation

After performing ventilation, the carotid pulse is assessedand external cardiac compressions are provided when nopulse is detected.

1. Compressions are performed with the patient on a firmsurface (Cardiac board, floor)

2. The rescuer (facing the patients head) places the heel ofone hand on the lower half of the sternum, two fingerwidthsfrom the tip of thexiphoid and positions the other hand ontop of the first hand. The fingers should not touch the chestwall.

3. Using the body weight while keeping the elbows straight,the rescuer presses quickly downward from the shoulder

area to deliver a forcefulcompression to the victims lowersternum toward the spine.

4. The chest compression rate is 80 to 100 times/minuteFollow-up Monitoring1. After successful resuscitation, the patient is transferred

to an intensive care unit for close monitoring. Continuous


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electrocardiographic monitoringand frequent BP assessmentare essential until hemodynamic stability is reestablished.DYSRHYTHMIAS

Disorders of the formation and/or conduction of theelectrical impulse within the heart. This can causedisturbances of the heart rate, the heartrhythm, or both.Normal Electrical ConductionThe electrical impulse that stimulates and paces the cardiacmuscle normally originates in the sinus node, located nearthe vena cava in the rightatrium. Normally, the impulseoccurs at a rate between 60 and 100 times a minute in theadult. The impulse quickly travels from the sinus

nodethrough the atria to the atrioventricular (AV) nodecausing the atria to contract. The structure of the AV nodeslows the impulse, which allows timefor the atria to contractand the ventricles to fill with blood. From the AV node, theimpulse travels quickly along the right and left bundlebranchesand the Purkinje fibers, located in the ventricularmuscle. The electrical stimulation of the ventricles, in turn,causes the ventricles to contract(systole). Then theelectromechanical impulse completes the circuit and the

cycle begins again. In this way, sinus rhythm promotescardiovascular circulation. The electrical stimulus causes themechanical event of the heart.

Depolarization. The electrical stimulation: the mechanicalcontractionis called systole.

Repolarization. The electrical relaxation and mechanical

relaxationis called diastole.Influences on Heart Rate and Contractility

Heart rate is influenced by the autonomic nervous system,which consists of sympathetic and parasympathetic fibers.


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Stimulation of the sympathetic system increases heart rate.

Sympathetic stimulation also causes the constriction ofperipheral blood vessels and, therefore, an increase in BP

Parasympathetic stimulation slows the heart rate

Manipulation of the autonomic nervous system may increaseor decrease the incidence of dysrhythmiasTypes ofDysrhythmias1. Sinus Node DysrhythmiasA. Sinus Bradycardia

Occurs when the sinus node creates an impulse at a slower

than-normal rate.Etiology:1. Slower metabolic needs(sleep, athletic training, hypothyroidism)2. Vagal stimulation(vomiting, suctioning, severe pain, extreme emotions)3.Medications4. Increased intracranial pressure andMITreatment:1. Atropine 0.5 to 1.0 mg given quickly and IVas bolus medication of choice2. Catecholamines andemergency transcutaneous pacingB. Sinus Tachycardia

Occurs when the sinus node creates an impulse at a faster-than-normal rate.

It may be caused by acute blood loss, anemia shock,hypovolemia, hypervolemia, CHF, pain, hypermetabolicstate, fever, exercise, anxiety or sympathomimeticmedications.Treatment:1. Calcium channel blockers (ex.Diltiazem)2. Beta-blockers (ex. Propranolol)

C. Sinus Arrhythmia

Occurs when the sinus node creates an impulse at anirregular rhythm; the rate increases with inspiration anddecreases with expiration2. Atrial DysrhythmiasA. Premature Atrial Complex (PAC)


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This is a single ECG complex that occurs when an electricalimpulse starts in the atrium before the next normal impulseof the SA node.

The PAC may be caused by caffeine, alcohol, nicotine,stretched atrial myocardium

PACs are common in normal hearts. The patient may sayMy heart skipped a beat. A pulse deficit may exist.

If PACs are infrequent, no treatment is necessary.B. Paroxysmal Atrial Tachycardia

A term used to indicate a tachycardia characterized byabrupt onset and abrupt cessation and a QRS of normalduration.

Now called AV nodal reentry tachycardiaC. Atrial Flutter

Occurs in the atrium and creates impulses at an atrial ratebetween 250 and 400 times per minute

May cause serious signs and symptoms: chest pain,shortness of breath, and low blood pressure.Treatment:1. Ifpatient is unstable, electrical cardioversion is indicated2. Ifpatient is stable, diltiazem, verapamil, beta-blockers ordigitalis may be administered IV to slow the ventricular rate.D. Atrial Fibrillation

Causes a rapid, disorganized, and uncoordinated twitching ofatrial musculature.The most common dysrhythmias

Usually associated with advanced age, valvular heartdisease, cardiomyopathy, hyperthyroidism, pulmonary


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disease, moderate to heavyingestion of alcohol and theaftermath of open heart surgeryTreatment:

Treatment depends on its cause and duration and the

patients symptoms and instabilityIn some cases, AF converts to sinus rhythm within 24 hourswithout treatment

Both stable and unstable AF of short duration are treated thesame as stable and unstable atrial flutter

To prevent recurrence and to promote heart rate control

over a long period, quinidine, procainnamide, flecainide,sotalol, or amiodatone may beprescribed

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Anti-coagulation therapy is indicated if patient is elderly orhas hypertension, heart failure or a history of stroke.

Pacemaker or surgery is sometimes indicated for patientswho are unresponsive to medications3. Junctional DysrhythmiasA. Premature Junctional Complex

An impulse that starts in the AV nodal area before the nextnormal sinus impulse.

Causes include: digitalis toxicity, congestive heart failure,and coronary artery disease

Rarely produce any significant symptomsTreatment is the same as for frequent PACsB. Junctional Rhythm

Occurs when the AV node, instead of the SA node, becomesthe pacemaker of the heart.


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Junctional rhythm may produce signs and symptoms ofreduced cardiac output. If so, the treatment is the same asfor sinus bradycardia.

C. AV Nodal Reentry TachycardiaOccurs when an impulse is conducted to an area in the AVnode that causes the impulse to be rerouted back into thesame area over and over again at a very fast rate.

Factors associated with the development of AV nodal reentrytachycardia include caffeine, nicotine, hypoxemia, and stress

Signs and symptoms vary with the rate and duration of thetachycardia and the patients underlying condition. Usually ofshort duration,resulting only in palpitations. A fast rate mayreduce cardiac output, resulting in significant signs andsymptoms such as restlessness, chestpain, shortness ofbreath, pallor, hypotension and loss ofconsciousnessTreatment:

Treatment is aimed at breaking the reentry of the impulse.1.

Vagal maneuvers, such as carotid sinus massage, gag reflex,breath holding, and immersing the face in ice water increase parasympatheticstimulation, causing slowerconduction through the AV node and blocking the reentry ofthe rerouted impulse.

Because of the risk of a cerebral embolic event, carotid sinusmassage is contraindicated in patients with carotid bruits.2.If vagal maneuvers are ineffective, the patient may thenreceive a bolus of adenosine, verapamil, or diltiazem.3.Cardioversion is the treatment of choice if the patient isunstable or does not respond to the medications.4.Intravenous adenosine may be prescribed to cause aconversion to sinus rhythm.4. Ventricular DysrhythmiasA. Premature VentricularComplex (PVC)


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PVC is an impulse that starts in a ventricle before the nextnormal sinus impulse.

PVCs can occur in healthy people, esp. with the use ofcaffeine, nicotine, and alcohol.

Also caused by cardiac ischemia or infarction, increasedworkload on the heart (ex. Exercise, fever. Hypervolemia,CHF, and tachycardia),digitalis toxicity, hypoxia, acidosis,and electrolyte imbalances, esp. hypokalemia

In the absence of disease, PVCs are not serious. In the

patient with acute MI, PVCs may indicate the need for moreaggressive therapy.

The following are warning or complex PVCs (precursors ofventricular tachycardia) : (1) more than 6/minute (2)multifocal (having differentshapes), (3) two in a row (pair),and (4) occurring on the T wave (the vulnerable period ofventricular depolarization)Treatment:1. Lidocaine is themedication most commonly used for immediate short-term

therapyB. Ventricular Tachycardia

Defined as three or more PVCs in a row, occurring at a rateexceeding 100 beats/minute.

Ventricular tachycardia is usually associated with coronaryartery disease and may precede ventricular fibrillation.

Ventricular tachycardia is an emergency because the patientis usually unresponsive and pulseless.Treatment:1.Lidocaine is the initial choice2. Cardioversion maybeindicated if the medications are ineffective or if the patientbecomes unstable3. Immediate defibrillation


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Ventricular tachycardia in a patient who is unconscious andwithout pulse is treated in the same manner as ventricularfibrillation.C. Ventricular Fibrillation

A rapid but disorganized ventricular rhythm that causesineffective quivering of the ventricles.

This dysrhythmias is always characterized by the absence ofan audible heartbeat, a palpable pulse, and respirations.

Cardiac arrest and death are imminent if VF isuncorrectedTreatment:1. Immediate defibrillation and

activation of emergency services. Placing a call foremergency assistance takes precedence over initiatingCPR2. After a successful defibrillation, eradicating causesand administering anti dysrhythmics medication aretreatments to prevent the recurrence of VF.D. Idioventricular Rhythm

Also called ventricular rhythm, occurs when the impulsestarts in the conduction system below the AV node

Commonly causes the patient to lose consciousness andexperience other signs and symptoms of reduced cardiacoutput. In such cases,treatment is the same as for anybradycardia, including identifying the underlying etiology,administering IV atropine, and initiatingemergencytranscutaneous pacing.

Bed rest is prescribed so as not to increase cardiac workloadE. Ventricular Asystole

Commonly called flatline, ventricular asystole ischaracterized by absent QRS complexes, although P wavesmay be apparent for a shortduration.

There is no heartbeat, no palpable pulse, and no respiration.


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Without treatment, ventricular asystole is fatal.Treatment:1.CPR2. Rapid assessment to identify possible causes3.Intubation and establishment of IV access are the first

recommended actions4. Bolus of IV epinephrine and to berepeated at 3-5 minutes intervals5. Sodium bicarbonatemaybe administered IVNursing Process: The Patient With ADysrhythmiaAssessment

Major areas of assessment include possible causes of thedysrhythmias and the dysrhythmias effect on the heartsability to pump an adequateblood volume

When cardiac output is reduced, the amount of oxygenreaching the tissues and vital organs is diminished. Thisdiminished oxygen producesthe signs and symptomsassociated with dysrhythmias.

A health history is obtained to identify possible causes andpast incidences of syncope (fainting), lightheadedness,dizziness, fatigue, chestdiscomfort, and palpitations.

Psychosocial assessment is also performed to identify thepossible effects of dysrhythmia

Physical assessment is conducted to confirm the dataobtained from the history and to observe for signs ofdiminished cardiac output during thedysrhythmic event, esp.changes in level of consciousness. Skin may be pale andcool. Signs of fluid retention, such as neck veindistention,crackles and wheezes in the lungs may bedetected during auscultation.

The rate and rhythm of apical and peripheral pulses areassessed and any pulse deficit is noted.

The chest is auscultated for extra heart sounds, esp. S


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3and S4,measures BP and determines pulse pressures. A declining

pulse pressureindicates reduced cardiac output.Diagnosis:1.Potential/actual decrease in cardiac output2. Anxiety relatedto fear of the unknown3. Lack of knowledge about thedysrhythmias and its treatment.Potential Complications:Ischemic Heart DiseaseNursing Interventions:1. Monitoringand Managing the Dysrhythmias

Controlling the incidence or effect of dysrhythmias is oftenachieved by the use of ant-idysrhythmic medications

A constant serum blood level of the medication is maintainedto maximize beneficial effects and minimize adverse effects

If the patient is hospitalized, an ECG is initiated and rhythmstrips are analyzed to track dysrhythmias

BP, rate and depth of respirations, pulse rate and rhythmare evaluated regularly to determine the hemodynamic

effect of the dysrhythmias2. Minimizing AnxietyNurse must maintain a calm and reassuring attitude

Maximize the patients control and to make the unknownless threateningEvaluationExpected Outcomes:1. Cardiacoutput is maintained2. Anxiety is minimized3. The patientknows about dysrhythmias and its treatmentAdjunctive Modalities and Management1. Cardioversion andDefibrillation

Treatment for tachydysrhythmias.

Used to deliver an electrical current to stimulate a criticalmass of myocardial cells. This allows the sinus node torecapture its role as thehearts pacemaker.


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One major difference between cardioversion anddefibrillation has to do with the timing of the delivery ofelectrical current.

Defibrillation is usually performed as an emergencytreatment, whereas cardioversion is usually a plannedprocedure

Cardioversion involves the delivery of a timed electricalcurrent to terminate a tachydysrhythmia.

Defibrillation is the treatment of choice for ventricular

fibrillation and pulseless ventricular tachycardia.2. Pacemaker Therapy

An electronic device that provides electrical stimuli to theheart muscle.

Usually used when a patient has a slower-than-normalimpulse formation

May also be used to control tachydysrhythmias that do notrespond to medication therapyComplications ofPacemakers:1. Local infection at the entry site of the leadsor at the subcutaneous site2. Bleeding and hematoma at thelead-entry sites or at the subcutaneous sites for permanentgenerator placement3. Hemothorax from puncture of thesubclavian vein or internal mammary artery4. Ventricularectopy and tachycardia from irritation of the ventricular wallby the endocardial electrode5. Movement or dislocation ofthe lead placed transvenously (perforation of themyocardium)6. Phrenic nerve, diaphragmatic (hiccupping) orskeletal muscle stimulation may occur if the lead isdislocated or if the delivered energy is set high7. Rarely,cardiac tamponade occurs after removal of epicardial wires8.Dislodgement of the pacing electrode most common


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complication. Minimizing patient activities can help toprevent this complication.BURNSThere are 4 major goals relating to burns:1. Prevention2.

Institution of lifesaving measures for the severely burnedperson3. Prevention of disability and disfigurement throughearly, specialized, individual treatment4. Rehabilitationthrough reconstructive surgery and rehabilitativeprogramsPathophysiology:Burns are caused by a transfer ofenergy from a heat source to the body. Heat maybetransferred through conduction or electromagneticradiation.Burns are categorized as thermal (includingelectrical burns), radiation or chemical. Tissue destruction

results from coagulation, proteindenaturation, or ionizationof cellular contents. The skin and the mucosa of the upperairways are the sires of tissue destruction. Deeptissues,including the viscera, can be damaged by electricalburns or through prolonged contact.The depth of the injurydepends on the temperature of the burning agent and theduration of contact with the agent.Classification of Burns

Burn injuries are described according to the depth of theinjury and the extent of body surface area (BSA) injured.Characteristics of Burns according to DepthFactors to consider in the determination of depth :1. History of how the injury occurred2. Causative agent,such as flame or scalding liquid3. Temperature of theburning agent4. Duration of contact with the agent5.Thickness of the skinExtent of Body Surface Area InjuredRule of Nines

An estimation of the total BSA involved in a burn issimplified using the rule of ninesLund and Browder Method

A more precise method of estimating the extent of a burn


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Recognizes that the percentage of BSA of various anatomicparts, especially the head and legs, changes with growth.

By dividing the body into very small areas and providing an

estimate of the proportion of BSA accounted for by suchbody parts, one can obtaina reliable estimate of the totalBSA burned.

The initial evaluation is made on the patients arrival at thehospital.Palm Method

A method to estimate the percentage of scattered burns.

The size of the patients palm is approximately 1% of BSA.The size of the palm can be used to assess the extent ofburn injury.Local and Systemic Responses to Burns

Burns that do not exceed 25% of the total BSA produce aprimarily local response

Burns that exceed 25% BSA may produce both a local and asystemic response, which is considered a major burn injury.Overview of physiologic changes after a major burninjuryCardiovascular Response

Cardiac output decreases before any significant change inblood volume is evident. As fluid loss continuous andvascular volume decreases,cardiac output continuous to falland blood pressure drops. This is the onset of burn shock. Inresponse, the sympathetic nervous systemreleasescatecholamines, resulting in an increase in peripheralresistance (vasoconstriction) and an increase in pulse rate.Peripheralvasoconstriction further decreases cardiac output.

Prompt fluid resuscitation maintains the blood pressure inthe low-normal range and improves cardiac output. Despite


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adequate fluidresuscitation, cardiac filling pressures remainlow during the burn-shock period. If inadequate fluidresuscitation occurs, distributive shock willoccur.

Generally, the greatest volume of fluid leak occurs in thefirst 24 to 36 hours after the burn, peaking by 6 to 8 hours.

As the capillaries begin to regain their integrity, burn shockresolves and fluid returns to the vascular compartment.

As fluid is reabsorbed from the interstitial tissue into thevascular compartment, blood volume increases.

If renal and cardiac function is adequate, urinary outputincreases.

Patients with severe burns develop massive systemicedema. As edema increases in circumferential burns,pressure on small blood vesselsand nerves in distalextremities causes an obstruction of blood flow andconsequent ischemia. This complication is known ascompartmentsyndrome. The physician may need to perform

an esharotomy, a surgical incision into the eschar(devitalized tissue resulting from a burn), torelieve theconstricting effect of the burned tissue.Effects on Fluids, Electrolytes, and Blood Volume

Circulating blood volum

acute biologic crises

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