RESPIRATORY SYSTEM

ANATOMY
 Comprised of the upper airway and lower airway structures.
 UPPER RESPIRATORY SYSTEM- filter, moisten and warms air during respiration.
1. Nose- Serves as passageway for air to pass to and from the lungs. It filters impurities and humidifies and warms
the air as it inhaled.
2. Paranasal Sinuses- prominent function of the sinuses is to serve as resonating and chamber in speech.
3. Pharynx- throat, is a tube-like structure that connects the nasal oral cavities to the larynx.
4. Larynx- voice organ is a cartilaginous epithelium lines structures that connects the pharynx and the trachea; the
major function is for vocalization
5. Trachea (windpipe )- serves as the passage between the larynx and the bronchi.
 LOWER RESPIRATORY SYSTEM- enables the exchange of gases to regulate serum Pa02, PaC02, and
pH.
1. Lungs- paired elastic structures enclosed in the thoracic cage, which is the airtight chamber with distensible walls.
2. Pleura- serous membrane that line the lungs and wall of the thorax
3. Bronchi and Bronchioles
4. Alveoli
 basic gas-exchange unit of the respiratory system in the alveoli.
 Alveolar strech receptor- responds to the inspiration by sending signals to inhibit inspiratory neurons in the
brain stem to prevent lung over distension.
 Oxygen and carbon dioxide are exchange across the alveolar capillary membrane by process of diffusion.
 Neural control of respiration are located in the medulla. The respiratory center in the medulla is stimulated by
the concentration of carbon dioxide in the blood.
 Chemoreceptors, a secondary feedback system, located in the carotid arteriesand aortic arch respond to
hypoxemia. These chemoreceptors are stimulate to the medulla.

Disorder of the Upper Respiratory System

RHINITIS- A group of disorder charaterized by inflammation and irritation of the mucous membrane of the nose.
ALLERGIC RHINITIS
 Further classified as seasonal rhinitis( occurs during pollen season), or perennial rhinitis (occurs
throughout the year)
 Commonly associated with exposure to airborne particles such as dust, dander, or plant pollens in people who
are allergic to these substance.

CLINICAL MANIFESTAIONS:
 Rhinorrhea ( excessive nasal drainage, runny nose)
 Nasal Congestion
 Sneezing
 Pruritus of the nose, the mouth, throat, eyes and ears

MANAGEMENT
 Antihistamine
 Costicosteriod Nasal Spray
 Desensitizing immunizations

NURSING INTERVENTIONS:
 instruct the pt. with allergic rhinitis to avoid or reduce exposure to allergens and irritants
 instruct the pt. in correct administrations of nasal medications
 to achieve maximal relief, the pt. is instructed to blow the nose before applying any medication into the nasal
cavity.

VIRAL RHINITIS (COMMON COLD)

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  Most frequent viral infection in the general population caused by coronavirus
 Highly contagious because virus is shed for about 2 days before the symptoms appear and during the first part
of the symptomatic phase.

CLINICAL MANIFESTATIONS:
 low grade fever
 nasal congestion
 rhinorrhea and nasal discharge
 halitosis, sneezing
 tearing, watery eyes
 “scratchy” or sore throat
 General malaise, chills
 headaches and muscle aches

MANAGEMENT:
 symptomatic therapy
 adequate fluid intake and rest
 prevention of chilling
 warm salt-water gargles to soothe the sore throat
 NSAIDS to relieve aches and pain
 Antihistamines are used to relieve sneezing, rhinorrhea, and nasal congestions
 inhalation of steam or heated, humidified air

ACUTE PHARYNGITIS
 A sudden painful inflammation of the pharynx, the back of the throat that includes the posterior third of the
tongue, soft palate and tonsils.
 Common referred to us sore throat

CLINICAL MANIFESTATIONS:
 Fiery-red pharyngeal membrane and tonsils
 swollen lymphoid follicles
 enlarged and tender cervical lymph nodes
 fever
 malaise
 sore-throat

PHARMACOLOGIC THERAPY
 Penicillin is the treatment of choice
 Cephalosporin
 Macrolides
 Gargles with benzocaine may relieve symptoms

NURSING INTERVENTION:
 liquid or soft diet is provided during acute stage
 cool beverages, warm liquids, and flavored frozen desserts such as popsiccles are often soothing
 warm saline gargles or throat irrigations
 increase oral fluid intake
 ice collar can relieve sever sore throat
 CBR during febrile stage
 instruct the pt. about the preventive measures

CHRONIC PHARYNGITIS
 Is a persistent inflammation of the pharynx. It is common in adults, who work in dusty sorroundings, use their
voice to excess, suffer from chronic cough, or habitualy used alcohol and tobacco.
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 Three types of chronic pharyngitis are:
1. Hyperthropic- characterized by general thickening and congestion of the pharyngeal mucous membrane
2. Athropic- late stage of the first type ( the membrane is thin, whitish, glistening and at times winkled)
3. Chronic Granular (“clergyman’s sore-throat)- characterized by numerous swollen lymph follicles on the
pharyngeal wall.

CLINICAL MANIFESTAIONS:
 constants sense of irritation or fullness in the throat
 mucus that collects in the throat
 difficulty swallowing

MANAGEMENT:
 Nasal sprays or medications containing ephedrine sulfate or phenyleprine hydrochloride
 Antihistamine decongestant medications
 Acetaminophen

NURSING MANAGEMENT:
 Instruct the pt. to avoid contact with others until the fever subsides to prevent the spread of the infection,
 avoidance of alcohol, tobacco, secondhand smoke, and exposure to cold or to environment or occupational
pollutants

TONSILITIS AND ADENOIDITIS

 The tonsils are composed of lymphatic tissue and are situated on each side of the oropharynx
 The adenoids or pharyngeal tonsils consist of lymphatic tissue near the center of the posterior wall of the
nasopharynx
 Acute inflammation or infection that is ussually caused by GABHS (group A beta- hemolytic streptoccoccus)

CLINICAL MANIFESTAIONS:
 sore-throat, fever, snoring and difficulty swallowing
 enlarged adenoids may cause mouth breathing , earache, draining ears, frequent head colds, bronchitis, foul-
smelling breath, voice impairment, and noisy respiration

MANAGEMENT:
 Penicillin (first-line therapy) or cephalosporins
 Tonsillectomy or adenoidectomy is indicated if the pt. has had repeated episodes of tonsilitis despite antibiotic
therapy

NURSING INTERVENTION (post-op)

 in the emmidiate post-op period, the most comfortable position id prone, with the pt. head turned to the side to
allow drainage from the mouth and pharynx
 apply ice collar to the neck
 assess for post-op bleeding such as frequent swallowing
 instruct the pt. to refrain from coughing and too much talking
 ice chips maybe given to the pt.
 provide soft adequate diet
 Alkaline mouthwashes and warm saline solutions are useful in coping with the thick mucus and halitosis that
may be present after surgery
 Milk and milk products (ice cream and yogurt) maybe restricted
 instruct the pt. to avoid vigorous tooth brushing or gargling
 instruct pt. to avoid smoking and heavy lifting or exertion for 10 days

PERITONSILLAR ABSCESS (quinsy)

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  most common major suppurative complication of sore-throat/tonsilitis. This collection of purulent exudate
between the tonsillar capsule and the sorrounding tissues, including the soft palate, may develop after an acute
tonsillar infection that progress to a local cellulitis and abscess.

CLINICAL MANIFESTAIONS:
 severe sore-throat, fever trismus (inability to open the mouth ) and drooling.
 Severe pain, raspy voice
 odynophagia (a severe sensation of burning, squeezing pain while swallowing)
 dysphagia (difficulty of swallowing)
 otalgia (pain in the ear) tender and enlarged cervical nodes
 airway obstruction may occur

MANAGEMENT:
 Antimicrobal agents (penicillin)
 corticosteroid therapy
 needle aspirations are performed to decompress the abscess

NURSING INTERVENTION:
 assist in performing intubation, crico-thyroidotomy, or tracheotomy to treat airway obstruction
 assist when needle aspiration is needed
 gentle gargling after the procedure with a cool normal saline gargle may relieve discomfort
 provide cool liquids
 instruct the pt. to refrain from or rase smoking
 it is also important to reinforce the need for good oral hygiene

LARYNGITIS
 An inflammation of the larynx, often occur as aresult of voice abuse or exposure to dust, chemicals, smoke
and other pollutants
 most common cause is virus, bacterial invasion maybe secondary

CLINICAL MANIFESTATIONS:
 hoarseness of voice ---initial sign
 aphonia (complete loss of voice)
 severe cough
 throat feels worse in the morning and improves when the pt. is in warmer climate

MANAGEMENT:
 instruct the pt. to rest the voice and avoid irritants (smoking)
 inhaling cool steam or an aerosol is provided
 administer anti-bacterial therapy as ordered
 topical corticosteroid may be given by inhalation
 increased oral fluid intake

CANCER OF THE LARYNX

ETIOLOGY:
 most tumors of the larynx are squamous carcinoma
 men >women , age 60-70
 cigarette smoking and alcohol consumption are associated with laryngeal cancer

CLINICAL MANIFESTATIONS:
 hoarseness of voice for more than two weeks
 persistent cough and sore throat
 dyspnea
 pysphagia
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  pain radiating to ear and burning sensation to throat
 weight loss
 enlarged cervical lymph nodes
 unilateral nasal obstruction

DIAGNOSTIC PROCEDURE
 Virtual endoscopy
 Optical Imaging
 CT Scan or MRI
 Direct laryngoscopic examination

MANAGEMENT:
 Radiation Therapy
 Chemotherapy
 Surgery:
1. Partial Laryngectomy- a portion of the larynx is moved, along with one vocal cord and the tumor
COMPLICATIONS: Change in voice quality or hoarseness of voice
2. Total Laryngectomy- Laryngeal structures are removed, including the hyoid bone, epiglottis, cricoid
cartilage, and two or three rings of the trachea. COMPLICATIONS: permanent loss of voice, salivary leak,
wound infection, stomal stenosis, and dysphagia
NURSING INTERVENTION:
 arrange for clients with laryngectomies to meet with members of support groups
 establish a method for communication before a surgery
 maintain airway; have suction equipment at bedside
 Observe for signs of hemorrhage or infection
 taech about tracheostomy and stoma care
 assist with period of grieving

DISORDER OF THE LOWER RESPIRATORY SYSTEM

CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)

 Refers to a disease characterized by airflow limitations that is not fully reversible. The airflow limitations is
generally progressive and is normally associated with an inflammation response of the lungs due to irritants,
COPD includes Chronic Bronchitis and Pulmonary Emphysema.
 DIAGNOSTIC CRITERIA: Cough for three months for two consecutive years
 CHRONIC BRONCHITIS: chronic inflammation of the lower respiratory system characterized by
excessive mucous secretion, cough, and dyspnea associated with recurring infections of the lower respiratory
tract characterized by three primary symptoms: chronic cough, sputum production, and dyspnea excretion.

CLINICAL MNAIFESTATIONS:
 blue bloater
 usually insidious,developing over a period of years
 prescence of productive cough lasting at least 3months a year for 2 succesive years
 production of thick, gelatinous sputum, greater amounts produced during superimposed infections
 wheezing and dyspnea as disease progresses

EMPHYSEMA
 Complex lung disease characterized by destruction of the alveoli, enlargement of distal airspaces, and a
breakdown of alveolar walls. These are slowly progressive deterioration of lung function for many years
before the development of illness.
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2 TYPES:
1.Panlobular Emphysema- destruction of respiratory bronchiole, alveolar duct and alveolus
 all air spaces within the lobule are essentially enlarged, but there is little inflammatory disease
 hyperinflated (hyperexpand) chest, marked dyspnea on exertion, and weight loss typically occur
 Negative pressure is required during inspiration to move air into and out of the lungs
 Expiration becomes active and requires muscular effort

2.Centrilobular (centroacinar) Emphysema -pathologic changes takes place mainly in the center of the
secondary lobule, preserving the peripheral portions of the acinus
 There is derangement of ventilation- perfusion rations, producing chronic hypoxemia, hypercapnia,
polycythemia, and episodes of right-sided heart failure.
 Leads to central cyanosis and respiratory failure, and pt. also develop peripheral edema

CLINICAL MANIFESTATIONS:
 Pink puffer
 Dyspnea, decreased exercise tolerance
 Cough may be minimal, except with respiratory infection
 Sputum expectoration
 Barrel chest- increased anteroposterior diameter of chest due to air trapping with diaphragmatic flattening
Diagnostic Procedure for COPD
 Spirometry • used to evaluate airflow obstruction
 ABG Ievels - decreased Pao2z pH, and increased CO2
 Chest X-ray - in late stages, hyperinflation, flattened diaphragm, increased retrosternal space, decreased
vascular markings, possible bullae
 Alpha-l-antitrypsin assay useful in identifying genetically determined deficiency in emphysema

Medical Management for COPD

 Smoking cessation
 Bronchodilators to relieve bronchospasm
 Inhaled and systemic corticosteroids
 Alpha 1-antitrypsin augmentation therapy
 Antibiotic agents, Mucolytic agents Antitussive agents, vasodilators and narcotics

Surgical Management
 Bullectomy - surgical removal of enlarged airspaces that do not contribute to ventilation but occupy space in
the thorax
 Lung Volume Reduction Surgery - removal of a portion of the diseased lung parenchyma

Nursing Interventions For COPD

 Pulmonary rehabilitation to reduce symptoms, improve quality of life and increased physical and emotional
participation in everyday activities
 Pursed-lip breathing helps slow expiration, prevents collapse of small airways, and helps the patient co the
rate and depth of respiration
 Instruct the patient to coordinate diaphragmatic breathing with activities such as walking, bathing, bending,
climbing stairs
 Provide small frequent meals and offer liquid nutritional supplements to improve caloric intake an( weight
loss
 Administer low flow of oxygen (l-2L/min)
 Administer bronchodilator as prescribed
 Adequately hydrate the patient
 Instruct the patient to avoid bronchial irritants
 If indicated, perform CPT in the morning and at night as prescribed
 Encourage alternating activity with rest periods
 Teach relaxation technique or provide a relaxation tape for patient
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  Enroll patient in pulmonary rehabilitation program where available
 Monitor respiratory status, including rate and pattern of respiration, breath sounds, and signs and symptoms of
acute respiratory distress.

BRONCHIAL ASTHMA
 Chronic inflammatory disease of the airways that causes airway hyperresponsiveness, mucosal edema, and
mucus production is reversible and diffuse airway inflammation that leads to airway narrowing
Clinical Manifestations
Three most common symptoms of asthma:
1. Cough
2. Dyspnea
3. Wheezing
o Chest tightness, diaphoresis, tachycardia

Pharmacologic Therapy
o There are two general classes of asthma medications:
1. Quick relief medications for immediate treatment of asthma symptoms and exacerbations
 Short-acting beta2-adrenergic agonists (albuterol [Proventil Ventolin], levalbuterol [Xopenex], and
pirbuterol [Maxair])
2. Long acting medications to achieve and maintain control of persistent asthma
 Corticosteroids
 Long-acting beta2-adrenegic agonists
 Leukotriene modifiers (inhibitors)
 Antiieukotrienes, Montelukast (Singulair), zafirlukast (Accolate), and zileuton (Zyflo)

Nursing Interventions
o Assesses the patients respiratory status by monitoring the severity of symptoms, breath sounds peak flow,
pulse oximetry, and vital signs
o Administer medications as prescribed and monitor the patient's responses to those medications
o Administer fluids if the patient is dehydrated emphasize adherence to prescribed therapy, preventive
measures, and the need to keep follow-up appointments with health care providers.

BRONCHIECTASIS
 A chronic, irreversible dilation of the bronchi and bronchioles
Etiology
o Airway obstruction
o Diffuse airway injury
o Pulmonary infections and obstruction of the bronchus or complications of long-term pulmonary infections
o Generic disorders such as cystic fibrosis
o Abnormal host defense (eg, ciliary dyskinesia or humoral immunodeficiency)
o Idiopathic causes

Diagnostic Procedure
・ CT scan 一 reveals bronchial dilation

Clinical Manifestations
o Chronic cough with copious amount of purulent sputum
o Hemoptysis
o Clubbing of the fingers
o Repeated episodes of pulmonary infection

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Management
o Smoking cessation
o Chest physiotherapy
o Bronchoscopy to remove mucopurulent sputum
o Antimicrobial therapy based on result of culture and sensitivity of the sputum
o Influenza and pneumococcal vaccines
o Bronchodilators
o Surgical interventions for patients who continue to expectorate large amount of sputum and hemoptysis
despite adherence to treatment regimen

Nursing intervention
o Assess the patient in alleviating the symptoms and in dearing pulmonary secretions
o Encourage the patient in smoking cessation
o Educate the patient and his family in performing postural drainage
o Instruct the patient to avoid exposure to people with upper respiratory or other infection
o Assess nutritional status and ensure adequate diet

OCCUPATIONAL LUNG DISEASES

o Asbestosis is diffuse interstitial fibrosis of the lung caused by inhalation of asbestos dust and particles. Found in
workers involved in manufacture, cutting and demolition of asbestos-containing materials
o Silicosis is a chronic pulmonary fibrosis caused by inhalation of silica dust
Exposure to silica dust is encountered in almost any form of mining because the earth's crust is
composed of silica and silicates (gold, coal, tin, copper mining); also stone cutting, quarrying, manufacture of
abrasives, ceramics, pottery, and foundry work
o Sarcoidosis
o Granulomatous disease in which clumps of inflammatory epithelial cells occur in many organs, primarily in
lungs.
o Lymph node enlargement seen on chest X-ray

ClinicaI Manifestations
o Chronic cough; productive in silicosis
o Dyspnea on exertion; progressive and irreversible in asbestosis
o Susceptibility to lower respiratory tract infections
o Bibasal crackles in asbestosis

Management
o There is no specific treatment; exposure is eliminated, and the patient is treated symptomatically
o Give prophylactic isoniazid (INH) to patient with positive tuberculin test, because silicosis is associated with
high risk of TB
o Persuade people who have been exposed to asbestos fiber to stop smoking to decrease risk of lung cancer
o Keep asbestos worker under cancer surveillance; watch for changing cough, hemoptysis, weight loss, melena
Bronchodilators may be of some benefit if any degree of airway obstruction is present

Nursing Interventions
o Administer oxygen therapy as required
o Administer or teach self-administration of bronchodilators as ordered
o Encourage smoking cessation
o Advise patient on pacing activities to prevent fatigue
o Provide information to healthy workers on prevention of occupational lung disease

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PENETRATING TRAUMA
Pneumothorax- Pneumothorax occurs when the parietal or visceral pleura is breached, and the pleural space
is exposed to positive atmospheric pressure
Simple/Spontaneous Pneumothorax
o Occurs when air enters the pleural space through a breach of either the parietal or visceral pleura. Most
commonly, this occurs as air enters the pleural space through the rupture of a bleb or a bronchopleural fistula

Traumatic Pneumothorax
o A traumatic pneumothorax occurs when air escapes from a laceration in the lung itself and enters the pleural
space or from a wound in the chest wall, it may result from blunt trauma (eg, rib fractures), penetrating chest
or abdominal trauma (eg, stab wounds or gunshot wounds), or diaphragmatic fear

Open Pneumothorax
o One form of traumatic pneumothorax. It occurs when a wound in the chest wall is large enough to allow air to
pass freely in and out of the thoracic cavity with each attempted respiration

Tension Pneumothorax
o Occurs when air is drawn into the pleural space from a lacerated lung or through a small opening or wound in
the chest wall. It may be a complication of other types of pneumothorax. The air that enters the chest cavity
with each inspiration is trapped, this causes the lung to collapse and the heart, the great vessels, and the
trachea to shift toward the unaffected side of the chest (mediastinal shift)

Clinical Manifestations
o Hyperresonance; diminisher breath sounds
o Reduced mobility of affected half of thorax
o Tracheal deviation away from affected side in tension pneumothorax
o Clinical picture of open or tension pneumothorax is one of air hunger, agitation, hypotension, cyanosis
and profuse diaphoresis
o Mild to moderate dyspnea and chest discomfort may be present with spontaneous pneumothorax

MANAGEMENT:

Spontaneous Pneumothorax
o Treatment is generally nonoperative if pneumothorax is not too extensive.
o Observe and allow for spontaneous resolution for less than 50% pneumothorax in otherwise healthy person.
o Needle aspiration or chest tube drainage may be necessary to achieve re-expansion of collapsed lung if
greater than 50% pneumothorax
o Surgical intervention by pleurodesis or thoracotomy with resection of apical blebs is advised for patients with
recurrent spontaneous pneumothorax
Tension Pneumothorax
o Immediate decompression to prevent cardiovascular collapse by thoracentesis or chest tube insertion to let air
escape
o Chest tube drainage with underwater-seal suction to allow for full lung expansion and healing

Open Pneumothorax
o Close the chest wound immediately to restore adequate ventilation and respiration
-Patient is instructed to inhale and exhale gently against a closed glottis (Valsalva maneuver) as a pressure
dressing (petroleum gauze secured with elastic adhesive) is applied. This maneuver helps to expand collapsed
lung.
o Chest tube is inserted and water-seal drainage set up to permit evacuation of fluid/air and produce re-
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 expansion of the lung
o Surgical intervention may be necessary to repair trauma

Nursing Intervention
o Apply petroleum gauze to sucking chest wound
o Assist with emergency thoracentesis or thoracostomy
o Position patient upright if condition permits to allow greater chest tubes
o Maintain patency of chest tubes
o Assist patient to splint chest while turning or coughing and administer pain medications as needed
o Monitor oximetry and ABG levels to determine oxygenation
o Provide oxygen as needed

“PLEURAL CONDITION”

PLEURAL EFFUSION
 Collection of fluid (transudate or exudate) in the pleural space
 Maybe a complication of heart failure, pulmonary infection or nephrotic syndrome
 Usually caused by underlying disease

Clinical Manifestations
o Dyspnea
o Difficulty lying on flat
o Coughing/fever
o Chills
o Pleuritic chest pain

Diagnostic Procedure
o CT scan
o Lateral Decubitus X-ray

Management
o Treatment of underlying disease
o Thoracentesis or chest tube drainage is performed
o Surgical pleurectomy for pleural effusion caused by malignancy
o Pleuroperitoneal shunt 一 fluids from the pleural space is drain into

Nursing Intervention
o Assist in thoracentesis
o Record the amount of fluid aspirated and send it to the laboratory
o Administer medications as ordered such as analgesics am
o Assist the patient in a comfortable position

HEMOTHORAX
o Blood in pleural space as a result of penetrating or blunt chest trauma
o Accompanies a high percentage of chest injuries
o Can result in hidden blood loss
o Patient may be asymptomatic, dyspneic, apprehensive, or in shock
Management
o Assist with thoracentesis to aspirate blood from pleural space
o Assist with chest tube insertion and set up drainage system for complete and continuous removal of blood and
air
o Auscultate lungs and monitor for relief of dyspnea
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 o Monitor amount of blood loss in drainage
o Replace volume with I.V. fluids or blood products

PLEURISY (PLEURITIS)
 Inflammation of both layers of the pleurae (parietal and visceral)
 May develop in conjunction with pneumonia or an upper respiratory tract infection, TB or collagen disease
 When the inflamed pleural membranes rub together during respiration (intensified on inspiration), the result is
severe, sharp, knifelike pain
Clinical Manifestations
o Pleuritic pain during deep breath, coughing or sneezing
o Pain is limited in distribution rather than diffuse
o Pleural friction rub can be heard with stethoscope

Diagnostic Procedures
o Chest X-ray
o Sputum Analysis
o Thoracentesis
o Pleural Biopsy
Management
o Treatment of underlying condition causing pleurisy
o Topical applications of heat or cold
o Indomethacin for pain relief
o Intercostal Nerve Block if pain is severe
Nursing Interventions
o Instruct the patient in heat/cold application for pain relief
o Instruct the patient to turn onto the affected side to splint the chest wall and reduce the stretching of the
pleauare
o Teach the patient to use hands or pillow to splint the ribcage while coughing

EMPYEMA THORACIS

o Accumulation of purulent fluid in the pleural space

o Occur as complication of bacterial pneumonia, lung abscess or chest trauma
o Patient is acutely ill and has signs and symptoms similar to acute respiratory infection
o Diagnosis is established by chest CT
o Main objective is to drain the fluid in the pleural cavity
o Thoracentesis is done if fluid is not too thick
o Tube Thoracostomy is done to patients with loculated or complicated pleural effusions
o Open chest drainage via thoracotomy is done to remove thickened pleura, pus and debris
o Nursing intervention: provide care specific to the method of drainage of the pleural fluid

INFECTIOUS DISEASES OF THE LOWER RESPIRATORY TRACT

PNEUMONIA
 Inflammation of the lung parenchyma caused by various microorganisms, including bacteria, mycobacteria,
fungi and viruses
Community-Acquired Pneumonia
o Occurs either in the community setting or within the first 48 hours after hospitalization or institutionalization
Hospital-Acquired Pneumonia
o Also known as nosocomial pneumonia, is defined as the onset of pneumonia symptoms more than 48 hours
after admission in patients with no evidence of infection at the time of admission

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Aspiration Pneumonia
o Refers to the entry pulmonary consequences resulting from entry of endogenous or exogenous substances into
the lower airway

Clinical Manifestation
o Sudden onset, rapidly rising fever of 38.3°C to 40.5°C
o Cough productive of purulent sputum
o Pleuritic chest pain aggravated by deep respiration/coughing
o Dyspnea, tachypnea accompanied by respiratory grunting, nasal flaring use of accessory muscles of
respiration fatigue
o Rapid, bounding pulse
o Orthopnea
o Rusty, blood-tinged sputum
o Poor appetite, diaphoresis

Diagnostic Procedure
o Chest X-ray shows presence/extent of pulmonary disease typically consolidation.
o Gram stain and culture and sensitivity test of sputum may indicate offending organism
o Blood culture detects bacteremia (bloodstream invasion) occurring with bacterial pneumonia

Management
Administration of the appropriate antibiotic as determined by the results of a Gram stain
o S. pneumonia 一 macrolide antibiotic (azithromycin, clarithromycin, or erythromycin) / Pseudomonas
infection 一 anti pneumococcal, antipseudomonal beta-lactam
o Treatment of viral pneumonia is primarily supportive
o Oxygen therapy if patient has inadequate gas exchange

Complications
o Shock and respiratory failure
o Pleural Effusion

NURSING INTERVENTIONS
 Encourage coughing and deep breathing after chest physiotherapy, splinting the chest if necessary
 Maintain semi-Fowlers position
 Promote hydration (2-3 L/day) to liquefy secretions
 Suction if necessary
 Instruct client to cover nose and mouth when coughing
 Teach the need to continue entire course of antimicrobial therapy which is usually seven to ten days
 Teach the patient about proper administration of antibiotics and potential side effects
 Teach that findings are expected to be less within 48 to 72 hours of initial therapy
 Nutritionally enriched drinks or shakes maybe helpful in maintaining nutrition
 Teach effective coughing techniques to minimize energy expinditure, plan rest period

PULMONARY TUBERCULOSIS
 Tuberculosis (TB) is an infectious disease that primarily affects the lung parenchyma. It also may be
transmitted to other parts of the body, including the meninges, kidneys, bones and lymph nodes
 The primary infectious agent ,M. tuberculosis, is an acid-fast aerobic rod that grows slowly and is sensitive to
heat and ultraviolet lights spread from person to person by airborne transmission.
Clinical Manifestations
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 Fatigue, anorexia, weight loss, low-grade fever, night sweats
 Some patients have acute febrile illness, chills, and flu-like symptoms
 Cough (insidious onset) progressing in frequency and producing mucoid or mucopurulent sputum
 Hemoptysis, chest pain, dyspnea (indicates extensive involvement)

Diagnostic Evaluation
 Sputum smear/Sputum culture confirms a diagnosis of TB
 Chest X-ray to determine presence and extent of disease
 Tuberculin skin test (purified protein derivative [PPD] or Mantoux

Classification
Data from the history, physical examination, TB test, chest x-ray, and microbiological studies are use to
classify TB into one of five classes. A classification scheme provide public health officials with a systematic
way to monitor epidemiology and treatment of the disease.
Class 0: no exposure; no infection
Class 1: exposure; no evidence of infection
Class 2: latent infection; no disease (eg, positive PPD reaction but no clinical evidence of active TB)
Class 3: disease; clinically active
Class 4: disease; not clinically active
Class 5: suspected disease, diagnosis pending

Management
 Pulmonary TB is treated primarily with antituberculosis agents for 6 to 12 months
 The initial phase consists of a multiple-medication regime of INH, rifampin, pyrazinamide, and ethambutol
and is administered daily for 8 weeks
 Continuation phase of treatment include INH and rifampicin and lasts for an additional 4 or 7 months
 Vitamin B (pyridoxine) is usually administered with INH to prevent IHN-associated peripheral neuropathy

FIRST-LINE ANTITUBERCULOSIS MEDICATIONS

Commonly
Adult Daily Dosage Most Common Side Effects
Used Agents
Isoniazid 5 mg/kg (300 mg Peripheral neuritis, hepatic enzyme elevation,
(INH) maximum daily) hepatitis, hypersensitivity

Rifampicin 10 mg/kg (600 mg Hepatitis, febrile reaction, purpura (rare), nausea,

maximum daily) vomiting

Pyrazinamid 15-30 mg/kg (2.0 g Hyperuricemia, hepatotoxicity, skin rash, arthralgias,

e maximum daily) GI distress

Nursing Intervention
 Instructs the patient to increase fluid intake and about correct positioning to facilitate airway drainage
 Discuss the medications schedule and side effects of the drugs
 Instructs the patient to take the medication either on an empty stomach or at least 1 hour before meals

13
 because food interferes with medication absorption
 Patients taking INH should avoid foods that contain tyramine and histamine because it may result in
headache, flushing, hypotension, lightheadedness, palpitations, and diaphoresis
 Monitors for side effects of anti-TB drugs
 Encourage rest and avoidance of exertion
 Provide nutritional plan that allows for small, frequent meals
 Instruct the patient about important hygiene measures, induding mouth care, covering the mouth and nose
when coughing and sneezing, proper disposal of tissues, and hand washing

ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)

 Severe form of acute lung injury. This clinical syndrome is characterized by a sudden and progressive
pulmonary edema, increasing bilateral infiltrates on chest x-ray, hypoxemia unresponsive to oxygen
supplementation regardless of the amount of Positive End-Expiratory Pressure (PEE) and the absence of an
elevated left atrial pressure
 Patients often demonstrate reduced lung compliance

Clinical Manifestations
 Typically develops over 4 to 48 hours
 Severe dyspnea, severe hypoxemia
 Arterial hypoxemia that does not respond to supplemental oxygen
 Chest x-ray are similar to those seen with cardiogenic pulmonary edema
 Increased alveolar dead space
 Severe crackles and rhonchi heard on auscultation
 Labored breathing and tachypnea

DIAGNOSTICS
 Clinical presentation and history of findings
 Hypoxemia on ABG despite increasing inspired oxygen level
 Chest x-ray shows bilateral infiltrates
 Plasma Brain Natriuretic Peptide (BNP)
 Echocardiography
 Pulmonary Artery Catheterization

Management
 Treatment of the underlying condition
 Optimize oxygenation
 Intubation and mechanical ventilation
 Sedation may be required
 Paralytic agents may be necessary
 Antibiotics, as indicated
 PEEP usually improves oxygenation
 Supportive drugs includes surfactant replacement therapy, pulmonary antihypertensive agents and antisepsis
agent

Nursing Intervention
 Requires close monitoring in the intensive care unit
 Assess the patients status frequently to evaluate the effectiveness of the treatment
 Turn the patient frequently to improve ventilation and perfusion in the lungs and enhance drainage secretions
 Res is essential for patient to limit oxygen consumption and reduce oxygen needs
14
  Adequate nutritional support is vital, 35 to 45 kcal/kg/day is required to meet caloric requirements
 Identify problems with ventilation that may cause anxiety reaction to the patient
PULMONARY EMBOLISM
 Refers to the obstruction of the pulmonary artery or one of its branches by a thrombus (or thrombi) that originates
somewhere in the venous system in the right side of the heart
 Often associated with trauma, surgery (orthopedic, major abdominal, pelvic, gynecologic, pregnancy, heart
failure, age older than 50 years, hypercoagulable states, and prolonged immobility

Clinical Manifestations
o Dyspnea is the most frequent symptom
o Chest pain (sudden and pleuritic), may be substernal and any mimic angina pectoris or a myocardial
infarction.
o Petechiae over the chest
o Anxiety, fever, tachycardia and apprehension
o Cough, diaphoresis, hemoptysis, and syncope. The most frequent sign is tachypnea

Diagnostic Procedures
o Chest x-ray - shows infiltrates, atelectasis, elevation of the diaphragm on the affected side
o ECG 一 shows sinus tachycardia, PR-interval depression and nonspecific T-wave changes
o Arterial blood gas analysis - shows hypoxemia and hypocapnia
o Ventilation-perfusion (V/Q.) scan
o Pulmonary angiography is considered the best method to diagnose PE
o Spiral computed CT scan of the lung

Management
o Treatment goal is to dissolve the existing emboli
o Improve respiratory and vascular status, anticoagulation therapy, thrombolytic therapy, and surgical
intervention
o Stabilize the cardiopulmonary system
o Nasal oxygen is administered immediately to relieve hypoxemia, respiratory distress, and central cyanosis
o Intravenous infusion lines are inserted to establish routes for medications or fluids that will be needed
o Hypotension is treated by a slow infusion of dobutamine (Dobutrex), which has a dilating effect on the
pulmonary vessels and bronchi, or dopamine (Intropin)
o Small doses of IV morphine or sedatives are administered to relieve patient anxiety, to alleviate chest
discomfort, to improve tolerance of the endotracheal tube, and to ease adaptation to the mechanical
ventilator
o Anticoagulant therapy (heparin, warfarin sodium
o Coumadin has traditionally been the primary method for managing PE
o Thrombolytic therapy (urokinase, streptokinase, alteplase) is used in treating PE, particularly in patients
who are severely compromised
o Surgical embolectomy is performed if the patient has massive PE.

Nursing Intervention
o Monitor oxygen therapy and assess the patient for hypoxia
o Watch patient for signs of discomfort and pain
o Assess patient for bleeding related to anticoagulant or thrombolytic therapy
o Advise patient of the possible need to continue taking anticoagulant therapy
o Monitor for potential complication of cardiogenic shock or right ventricular failure
o Encourage ambulation and active/passive leg exercises to prevent venous stasis
o Advise the patient not to sit or lie in bed for prolonged periods, not to cross the legs, and not to wear
15
 constrictive clothing

CARDIOVASCULAR NURSING

THE HEART
 Hollow, muscular organ
 Weight approximately 300 g
 It occupies the space between the lungs (mediastinum) and rests on the diaphragm
 The heart pumps blood to the tissues supplying them with oxygen and other nutrients.

THREE LAYERS OF THE HEART

o Endocardium-lines the inside of the heart and valves
o Myocardium-made up of muscle fibers and is responsible for the contraction
o Epicardium- Exterior layer of the heart in which pericardium can be found
- Outermost
- Essential coronary arteries are located

Pericardium- thin layer of fibrous tissue that contains pericardial fluid that lubricates the lining of the heart, it
consists of two layers:
o Adhering to the epicardium is the visceral pericardium.
o Enveloping the visceral pericardium is the parietal pericardium, which supports the heart in the mediastinum.

"The pumping action of the heart is accomplished by the rhythmic relaxation and contraction"

Systole- refers to the events in the heart during, contraction of the two top chambers (atria) and two lower chambers
(ventricles)

Diastolic- is characterized by relaxation of the lower chambers which allows the ventricles to fill in preparation for
contraction 2 CHAMBERS UPPER
 ATRIUM
 Collecting/ Receiving chamber LOWER
 VENTRICLES
 Pumping/ Contracting chamber

Apical impulse (also called the point of maximal impulse [PMI]) located at the 15th intercostal space (ICS), left
mid-clavicular line.

MECHANICAL PROPERTIES OF THE HEART

CARDIAC OUTPUT
 Volume of blood (liters) ejected by the heart each minute 5 L/min
 During exercise the total cardiac output may increase fourfold, to 2 L/min,
 Cardiac Output = Heart Rate x Stroke Volume
・ CO = HR x SV

PULSE RATE/ HEART RATE

 Number of times the ventricles contract each minute
16
 60-100 beats/min
 Controlled by the ANS

STROKE VOLUME
 Volume of blood ejected by the left ventricle during each systole
 Affected by 3 factors:
o Preload
o Contractility
o Afterload
PRELOAD
 Degree of myocardial stretch at the end of diastole & just before contraction
 Determined by the amount of blood returning to the heart from venous & pulmonary system

STARLING'S LAW
 The more the heart is filled during diastole, the more forcefully it contracts
 The higher the preload, the higher the stroke volume.

CONTRACTILITY
 Force generated by the contracting enhanced by myocardium
 Catecholamines, sympathetic activity and with medications such as the 3 D's
 Digoxin, Dopamine, Dobutamine
 The higher the contractility, the higher the stroke volume.

AFTERLOAD
 Pressure or resistance that the ventricles must overcome to eject blood through the semi-lunar valves
 Directly proportional to the BP & Diameter of blood vessels
 The higher the afterload, the lower the stroke volume.
HEART SOUNDS

 The first heart sound (SI) is heard as the atrioventricular valves close and is heard loudest at the apex of the heart.
 The second heart sound (S2) is heard when the semilunar valves close and is heard loudest at the base of the heart.
 A third heart sound (S3) may be heard if ventricular wall compliance is decreased and structures in the ventricular
wall vibrate heart; this can occur in conditions such as congestive heart failure or valvular regurgitation. However, a
third heart sound may be normal in individuals younger than 30 years.
 A fourth heart sound (S4) may be heard on atrial systole if resistance to ventricular filling the is present; this is an
abnormal finding, and causes include cardiac hypertrophy, disease, or injury to the ventricular wall.

CARDIAC ELECTROPHYSIOLOGY:
Automaticity: ability to initiate an electrical impulse by itself
Excitability: ability to respond to an electrical impulse
Conductivity: ability to transmit an electrical impulse from one cell to another

SINOATRIAL (SA) NODE

 Location: Junction of Superior vena cava & Right Atrium
 Function: Pacemaker of heart
 Initiates 60-100 bpm

ATRIOVENTRICULAR (AV) NODE

 Location: Interatrial septum
 Delays the electric impulse to allow ventricular filling of 0.8 milliseconds
 40-60 beats/min

17
BUNDLE OF HIS
 Location: Interventricular septum
 Branches out into:
Right main Bundle Branch
Left main Bundle Branch

PURKINJE FIBERS
 Location: Walls of ventricles
 Ventricular contractions
 Fastest conduction is: 20 - 40 beats/min
 It can function as a back up pacemaker if all other facemaker fail

FACTS
 ''The parasympathetic impulses, which travel to the heart through the Vagus nerve, can slow the cardiac rate,
whereas sympathetic impulses increase it."

 Baroreceptors are specialized nerve cells located in the aortic arch and in both right and left internal carotid
arteries. The baroreceptors are sensitive to changes in blood pressure.

 Hypotension can result in less baroreceptor stimulation, which prompts a decrease in parasympathetic inhibitory
activity in the SA node, allowing for enhanced sympathetic activity. The resultant vasoconstriction and increased
heart rate elevate the blood pressure.

ELECTRICAL CONDUCTION THROUGH THE HEART

P WAVE
 The P wave represents atrial muscle depolarization. It is normally small, smoothly rounded, and no wider than
0.12 second

QRS COMPLEX
 The QRS complex represents ventricular muscle depolarization
 Normal QRS width is 0.04 to 0.10 second.
 Atrial repolarization happens simultaneously.

TWAVE
 The T wave represents ventricular repolarization
 T waves are not normal more than 5 mm

PR INTERVAL
 The PR interval is measured from the beginning of the P wave to the beginning of the QRS complex and
represents the time required for the impulse to travel through atria, AV junction, and Purkinje system. The normal PR
interval is 0.12 to 0.20 seconds.

QT INTERVAL
 It represents the total time for ventricular depolarization and repolarization.
 QT interval is usually 0.32 to 0.40
 If QT interval becomes prolonged, the patient may be at risk for a lethal ventricular dysrhythmia called torsades
de pointes.

PP INTERVAL
 The duration between the beginning of one P wave and the beginning of the next P wave
 Used to calculate atrial rate and rhythm
18
RR INTERVAL
The duration between the beginning of one QRS complex and the beginning of the next QRS complex; used to
calculate ventricular rate and rhythm

U WAVE
 The part of an ECG that may reflect Purkinje fiber repolarization: usually it is not seen unless a patient's serum
potassium level is low (Hypokalemia)

CORONARY ARTERY DISEASE

 Coronary artery disease (CAD) is the most prevalent type of cardiovascular disease in adults.
 Most common cause of cardiovascular disease is atherosclerosis- (abnormal accumulation of fats)

CLINICAL MANIFESTATIONS
 Symptoms and complications according to the location and degree of narrowing of the arterial lumen, if
impediment to the blood flow has occurred, inadequate supply to cardiac cells will lead to a condition known as
ischemia.

MODIFIABLE FACTOR
 Hyperlipidemia
 Cigarette smoking, tobacco use
 Hypertension
 Diabetes mellitus
 Metabolic Syndrome
 Obesity
 Physical Inctivity

NON-MODIFIABLE RISK FACTORS

o Family history' of CAD (first-degree relative with cardiovascular disease at 55 years of age or younger for men
and at
65 years of age or younger for women)
/ Increasing age '4 More than 45 years for men
/ More than 55 years for women
o Gender (men develop CAD at an earlier age than women)
o Race (higher incidence of heart disease in African Americans than in Caucasians)

CLINICAL MANIFESTATION
o Possibly normal asymptomatic periods
o Chest pain
o Palpitations
o Dyspnea
o Syncope
o Excessive fatigue

SURGICAL PROCEDURES
 PTCA to compress the plaque against the walls of the artery and dilate the vessel
 Laser angioplasty to vaporize the plaque
 Atherectomy to remove the plaque from the artery
 Vascular stent to prevent the artery from dosing and to prevent restenosis
 Coronary Artery Bypass Grafting (CABG) to improve blood flow to the myocardial tissue at risk for ischemia or
infarction because of the occluded artery

19
MEDICATIONS
 Nitrates to dilate the coronary arteries and decrease preload and afterload
 Calcium channel blockers to dilate coronary arteries and reduce vasospasm
 Cholesterol-lowering medications to reduce the development of atherosclerotic plaques
 Beta-Blockers to reduce the BP in individuals who are hypertensive

*AII adults 20 years of age or older should have a fasting lipid profile (total cholesterol, LDL Z HDLZ and triglyceride
I performed at least once every 5 years and more often if the profile is abnormal"

*HDLZ (high density lipoprotein) is known as good cholesterol because it transports other lipoproteins such as LDL
to the liver, where they can be degraded and excreted. Because of this, a high HDL level is a strong protective factor
for heart disease.

♦Mediterranean diet another diet that promotes the ingestion of vegetables and fish and restricts red meat, is also
reported to reduce mortality from cardiovascular disease"

♦Cholesterol is present in all body tissues and is a major component of low-density lipoproteins, brain and nerve
cells, cell membranes, and some gallbladder stones

♦Increased cholesterol levels, LDL (Low density lipoprotein) levels, and triglyceride levels place the client at risk for
coronary artery disease

INSTRUCT THE CLIENT REGARDING DIET COMPOSED OF:

 Low-calorie
 Low-sodium
 Low-cholesterol
 Low-fat diet
 Increase in dietary fiber

VALUES
 Cholesterol: 140 to 199 mg/dL
 Low-density lipoproteins: Lower than 130 mg/dL
 High-density lipoproteins: 30 to 70 mg/dL
 Triglycerides: Lower than 200 mg/dL

HEART FAILURE (HF)

 HF is the inability of the heart to pump enough blood to meet the needs of tissues for oxygen and nutrients.
 Decreased heart contractility/ Pump failure
 Inadequacy of the heart to pump blood throughout the body
 Insufficient perfusion of body tissues (decreased cardiac output)

COMMON CAUSES OF HEART FAILURE

o Hypertension
o CAD
o Cardiomyopathy
o Substance abuse (Alcohol, Cocaine, Amphetamines)
o Valvular disease
o History of myocardial infarction
o Congenital defects
o Cardiac infections & inflammations
o Hyperkinetic conditions

ACC/AHA CLASSIFICATION OF HEART FAILURE

20
 STAGE A Patients at high risk for Developing left ventricular
Dysfunction but without structural heart disease or symptoms of heart failure
STAGE B Patients with left ventricular dysfunction or structural heart disease who have not developed symptoms of heart
failure
STAGEC Patients with left ventricular dysfunction or structural heart disease with current or prior symptoms of heart
failure
STAGE D Patients with refractory end-stage heart failure requiring specialized interventions

TWO MAJOR TYPES OF HEART FAILURE

 Systolic heart failure- alteration in ventricular contraction which is characterized by weakened heart muscle
 Diastolic heart failure- characterized by a stiff and non- compliant heart muscle making it difficult for the
ventricle to fill. The signs and symptoms of HF can be related to which ventricle is affected.

LEFT-SIDED HEART FAILURE

 Pulmonary venous blood volume and pressure increase, forcing fluid from the pulmonary capillaries into the
pulmonary, tissues and alveoli； causing pulmonary,,' interstitial edema and impaired Bas exchange.
 Pulmonary congestion occurs
 Signs and symptoms: Pulmonary/Lung (Left=Lung)
o Dyspnea, cough, pulmonary crackles/ rales, and low oxygen saturation levels,
o Orthopnea, difficulty breathing when lying flat.
o Frothy, pink (blood-tinged) sputum: pulmonary congestion (pulmonary edema)
 An extra heart sound, the S3, or "ventricular gallop/' may he detected on auscultation.
 The dominant feature in HF is inadequate tissue perfusion

Compensatory Mechanisms
Compensatory mechanisms act to restore cardiac output to near-normal levels.
Sympathetic nervous system stimulation
1.Arterial vasoconstriction
2.Increases afterload
3.Increased left cardiac workload
4.Increased heart rate
5.Improved stroke volume
6.Arterial vasoconstriction

Renin-angiotensin system activation

 A decrease in renal perfusion due to low cardiac output causes the release of renin by the kidneys.

 Renin promotes the formation of Angiotensin I, a benign, inactive substance.

 Angiotensin- converting enzyme (ACE) in the lumen of pulmonary blood vessels converts angiotensin I to
angiotensin

 II a potent vasoconstrictor, which then increase blood pressure and afterload.

 Angiotensin II also stimulates the release of aldosterone from the adrenal cortex, resulting in sodium and fluid
retention by the renal tubules and stimulation of antidiuretic hormone. These mechanisms lead to the fluid
volume overload commonly seen in HF.

COMMON NURSING DIAGNOSES

o Impaired gas exchange related to ventilation perfusion imbalance
o Decreased CO related to altered contractility, preload & afterload
o Activity intolerance related to an imbalance between 02 supply and demand
o Potential for pulmonary edema, pneumonia, dysrhythmias

21
MANAGEMENT
o Patients with orthopnea usually prefer not to lie flat. They may need pillows to prop themselves up in bed, or they
may sit in a chair and even sleep sitting up.
o Monitor vital signs and look for changes.
o Record fluid intake and output—weigh daily to assess for fluid overload.
o Position patient in semi-Fowler's position to oxygen as ordered because it ease breathing
o Administer oxygen as ordered because it helps to decrease workload of heart.
o Administer diuretic as prescribed.
o Tell the patient:
Eat foods low in sodium to avoid fluid retention.

RIGHT-SIDED HEART FAILURE

o Right side of the heart cannot eject blood and cannot accommodate all the blood that normally returns to it from
the venous circulation
o Increased venous pressure leads to Jugular vein distention and increased capillary hydrostatic pressure throughout
the venous system
o Edema of the lower extremities (dependent system edema)
o Hepatomegaly (enlargement of the liver)
o Ascites (accumulation of fluid in the peritoneal al cavity)
o Weight gain due to retention of fluid.

"Inability of the right heart to empty its blood volume results in blood backing up into the systemic circulation. LV
failure is the most common cause of right ventricular (RV) failure. Sustained pulmonary hypertension also causes RV
failure".

NURSING INTERVENTIONS
o Monitor heart rate and for dysrhythmias by using a cardiac monitor.
o Assess for edema in dependent areas and in the sacral, lumbar, and posterior thigh regions in the client on the bed
rest.
o Avoid the unnecessary IV administration of fluids.
o Monitor weight to determine a response to treatment.
o Assess for hepatomegaly and ascites, and measure and record abdominal girth.

PHARMACOLOGICAL MANAGEMENT:

1.Administer diuretics for symptom control 1.Furosemide, bumetanide, metolazone,

resulting in patient comfort by reducing blood hydrochlorothiazide, spironolactone-be aware of
volume electrolyte imbalance-these medications may alter
the K+ level
2.Administer ACE inhibitors to decrease afterload 2. Captopril, enalapril, lisinopril

3.Administer beta blocker, which help to raise 3.Metoprolol (Lopressor, Toprol)

ejection fraction, and decrease ventricular size Atenolol (Tenormin) Carvedilol (Coreg)

4.Metoprolol (Lopressor, Toprol) 4.Digoxin

Atenolol (Tenormin) Carvedilol (Coreg)

5.Administer vasodilator to reduce preload, 5.Nitroprusside,

relieve dyspnea Nitroglycerin ointment

22
ARTERIOSCLEROSIS
❖ Thickening or hardening of the arterial wall

ATHEROSCLEROSIS
o Type of arteriosclerosis where a fatty plaque as formed within the arterial wall.
o Leading contributor of CAD (coronary artery disease) and CVA (cerebrovascular accident)

VALVULAR HEART DISEASE

Valvular heart disease occurs when the heart valves cannot fully open (stenosis) or closes inwards causing a leak
insufficiency or regurgitation.

TYPES:
 Mitral Stenosis: Valvular tissue thickens and narrows the valve opening, preventing blood from flowing from the
left atrium to the left ventricle.
 Mitral Insufficiency, regurgitation: Valve is incompetent, preventing complete valve closure during systole.
 Mitral Valve Prolapse: Valve leaflets protrude into the left atrium during systole.
 Aortic Stenosis: Valvular tissue thickens and narrows the valve opening, preventing blood from flowing from the
left ventricle into the aorta.
 Aortic Insufficiency: Valve is incompetent, preventing complete valve closure during diastole.
MITRAL STENOSIS
 Usually due to rheumatic endocarditis
 Causing valve thickening by fibrosis and calcification
 Mitral valve opening narrows
 Left atrial pressure rises and dilates
 Pulmonary artery pressure increases
 Can cause right ventricular failure

CLINICAL MANIFESTATIONS
1. A low-pitched, rumbling, diastolic murmur is heard at the apex
2. Dyspnea on exertion
3. Orthopnea
4. Difficulty Breathing When Lying Flat
5. Paroxysmal nocturnal dyspnea
6. Shortness of Breath that occurs suddenly during sleep
7. Dyspnea and dry cough
8. Hemoptysis and pulmonary edema
9. Right sided heart failure may occur late
10. Atrial dysrhythmias

MEDICAL MANAGEMENT
o Patients with mitral stenosis may benefit from anticoagulants to decrease the risk for developing atrial thrombus
o Surgical intervention consist of valvuloplasty
o Percutaneous transluminal valvuloplasty
o Mitral valve replacement

NURSING MANAGEMENT
Place patient in a nigh Fowler's position to ease breathing

Monitor for:
 Pulmonary edema because it may be a complication of surgery
 Thrombus because of a valve.
 Arrhythmias because of an imitated heart- patient may feel palpitations, anxiety.

23
  Arterial Blood Gas (ABG) to monitor for oxygenation, acidosis, alkalosis.
 Weigh the patient daily to determine fluid balance

Explain to the patient:

 Signs and symptoms to look for and to report changes in condition.
 Restrict diet to low-sodium and low-fat foods

MITRAL REGURGITATION (INSUFFICIENCY)

 Mitral regurgitation involves blood flowing back from the left ventricle into the left atrium during systole. Often
the edges of the mitral valve leaflets do not dose during systole
 Most common cause is mitral valve prolapse and rheumatic heart disease

CLINICAL MANIFESTATIONS
 Dyspnea, fatigue, and weakness are the most common symptoms.
 Palpitations, shortness of breath on exertion, and cough from pulmonary congestion also occur.
 Systolic murmur is heard as a high- pitched, blowing sound at the apex

MANAGEMENT
o Angiotensin-converting enzyme (ACE) inhibitor
o Surgical intervention consists of mitral valvuloplasty (iez surgical repair of the valve) or valve replacement
o Patients with mitral regurgitation and heart failure benefit from afterload reduction (arterial dilation)
TIC REGURGITATION- Aortic regurgitation is the flow of blood back into the left ventricle from the aorta during
diastole
❖ Blood from the aorta returns to the left ventricle during diastole

ETIOLOGY:
 Inflammatory lesions that deform the leaflets
 Rheumatic endocarditis,
 Congenital abnormalities
 Syphilis
 Dissecting aneurysm
 In many cases it is idiopathic

CLINICAL MANIFESTATION
 Patients experience forceful heart beats especially in the head and neck
 Marked arterial pulsations that are visible or palpable at the carotid or temporal arteries
 Palpable at the carotid or temporal arteries
 Exertional dyspnea and fatigue
 A diastolic murmur is heard as a high-pitched, blowing sound at the third or fourth intercostal space at the left
sterna border.
 Widening of pulse pressure
 One characteristic sign of the disease is the water-hammer (Corrigan's) pulse

SURGICAL MANAGEMENT
o The treatment of choice is aortic valvuloplasty or valve replacement, preferably performed before left ventricular
failure occurs.
o Surgery is recommended for any patient with left ventricular hypertrophy regardless of the presence or absence of
symptoms

NURSING MANAGEMENT:

24
o Patient is advised to avoid physical exertion
o Vasodilators such as calcium channel blockers (eg. nifedipine [Adalat, Procardia))
o Ace inhibitors (eg. Captopril, enalapril, lisinopril, ramipril), or hydralazine

AORTIC STENOSIS
 Narrowing of the orifice between the left ventricle and the aorta.

SE-Degenerative calcifications caused by inflammatory changes that occur in response to years of normal mechanical
stress.

PATHOPHYSIOLOGY:
 Progressive narrowing of the valve orifice occurs, the left ventride contracts more forcefully and consumes more
energy. It compensates by thickening its walls or hypertrophies.
CLINICAL MANIFESTATION:
 Exertional dyspnea caused by increased pulmonary venous pressure
 Pulmonary edema may also occur
 Syncope and dizziness because decreased circulation to the brain
 Angina pectoris from increased demands of the left ventricle
 Loud rough systolic murmur heard over the aortic area
 Blood pressure is normal

TREATMENT:
 Surgical replacement of the aortic valve or Percutaneous valvuloplasty procedures

INEFECTIVE ENDOCARDITIS:

 Microbial infection of the endothelial surface of the heart, it usually develops in people with prosthetic heart
valves or structural heart defects

 Hospital acquired infective endocarditis occurs in patients with indwelling catheters

PATHOPHYSIOLOGY: A deformity or injury of the endocardium brought about by infectious organisms leads to
accumulation on the endocardium of fibrin and platelets. The infection may erode through the endocardium into
underlying structures (valves/leaflet) causing deformity.

ASSESSMENT:

 Cluster of petechia may be found on the body

 Small painful nodules (osiers node) may be present in the pads of fingers or toes
 Irregular red, purple, painless, flat macules (janeway lessions) may be present on the palms, fingers and toes
 Hemorrhage with pale centers in the eyes caused by emboli, (Roth Spot) caused by emboli may be observed in
the fundi of the eyes.
 Splinter hemorrhage (ie, Reddish Brown lines and streak) may be seen under the fingernails and toenails

PREVENTION
Antibiotic prophylaxis is recommended for high-risk patients immediately before and sometimes after the
following procedures
 Dental procedures
 Tonsillectomy or adenoidectomy
 Cystoscopy
25
  Surgery involving infected skin musculoskeletal tissue
 Bronchoscopy

MEDICAL MANAGEMENT:
o Antibiotic therapy is usually administered parenterally in a continuous IV infusion for 2 to 6 weeks, penicillin is
usually the medication of choice
o In fungal endocarditis, an antifungal agent, such as amphotericin B (eg, Abelcet, Amphocin, Fungizone), is the
usual treatment

Nurse Home Care Instructions for the Client with Infective Endocarditis___________________
o Teach the dient to maintain aseptic technique during setup and administration of intravenous antibiotics.
o Instruct the client to monitor intravenous catheter sites for signs of infection and report this immediately to the
physician.
o Instruct the client to record the temperature daily for up to 6 weeks and report fever.
o Encourage oral hygiene at least twice a day with a soft toothbrush and rinse well with water after brushing
o Client should avoid use of oral irrigation devices and flossing to avoid bacteremia.

MYOCARDITIS
o Myocarditis is an inflammation of the myocardium. It is usually diagnosed when it leads to significant cardiac
dysfunction. Myocarditis can cause considerable morbidity and mortality
o Infection could be bacterial, protozoal, fungal parasitic
o Viral myocarditis is the most common type
o Characterized by necrosis and cell injury associated with inflammation of the heart muscle

ASSESSMENT FINDINGS
o Non-specific symptoms: fatigue, dyspnea and palpitation
o If the disease has progressed, symptoms of heart failure present, such as tachycardia, pulmonary edema,
diaphoresis, neck vein distention, and cardiomegaly.
o In myocarditis, the ECG can show low-voltage QRS complexes, ST segment elevation, or heart block
o An S4 and systolic ejection murmurs may be heard on auscultation
o Patients may also sustain sudden cardiac death or quickly develop severe congestive heart failure

MEDICAL MANAGEMENT___________________________________________________________
o Patient are given specific treatment for the underlying cause if it is known (eg, penicillin for hemolytic
streptococci)
o Inotropic support of cardiac function with dopamine, or dobutamine may be used Netroprusside and
nitroglycerine may be used to decrease afterload
o Beta Blocker are avoided because they decrease the strength of ventricular contraction (have a negative
inotropic effect)
o Sedation may be necessary to decrease cardiac workload
o Intra-aortic balloon pulsation and left ventricular assists devices have been used to improve cardiac output
myocarditis

NURSING ALERT
 Patients with myocarditis are sensitive to digitalis. Nurses must closely monitor these patients for digitalis
toxicity, which evidenced by dysrhythmia, anorexia, nausea, vomiting, headache, and malaise

Pericarditis
 It refers to an inflammation of the pericardium, the membraneous sac enveloping the heartIt may be a primary
illness or it may develop during various medical and surgical disorders.

............................
PATHOPHYSIOLOGY
26
 The inflammation process of pericarditis may lead to an accumulation of fluid in the pericardial (pericardial
effusion) and increase pressure on the heart leading to cardiac tamponade.
 Prolonged episodes of pericarditis may lead to thickening and decreased elasticity of pericardium. These
conditions restrict the hearts ability to fill with blood (constrictive pericarditis)
 Restricted filling may result in increased systemic venous pressure

ASSESSMENTS
o Chest pain- located beneath the clavicle, in the neck or in the left scapular region, may worsen with deep
inspiration and may be relieved with a forward leaning or sitting position. (Tripod Position)

MEDICAL MANAGEMENT__________________________________________________________________________
o Administer therapy for treatment and symptom relief, and detect signs and symptoms of cardiac tamponade.
o Analgesics and nonsteroidal anti-inflammatory drugs (NSAIDs
o Indomethacin (Indocin) is contraindicated because it may decrease coronary blood flow
o A pericardial window, a small opening made in the pericardium
o May be performed to allow continuous drainage into the chest cavity.
o Surgical removal of the tough encasing pericardium (pericardiectomy) may be necessary to release both
ventricles from the constrictive and restrictive inflammation scarring.Most characteristic sign of pericarditis is a
creaky or scratchy friction rub heard most clearly at the left lower sternal border (pericardial friction rub)

PERICARDIOCENTESIS

 Procedure in which some of the pericardial fluid is removed

 Emergency resuscitation should be readily available
 The head of the bed is elevated to 45 to 60 degrees, placing the heart In proximity to the chest wall so that the
needle can be directly inserted into the pericardial sac
 Slow iv infusion is started in case it becomes necessary to administer emergency medications or blood
products
 Ultrasound imaging is used to guide placement of the needle into the pericardial space
 Desired effect
 Decrease in central venous pressure
 Increase in blood pressure
 Withdrawal of pulsus paradoxus
>10 mm Hg drop in blood pressure during inspiration
 Disappearance of prominent neck veins due to increased venous pressure

COMPLICATIONS OF PERICARDIOCENTESIS
o Coronary artery puncture
o Myocardial trauma
o Dysrhythmias
o Pleural laceration
o Gastric puncture

NURSING MANAGEMENT
o Patients with acute pericarditis require pain management with analgesics, positioning, and psychological support
caring for patients with pericarditis must be alert to cardiac tamponade
o After pericardiocentesis, the patient's heart rhythm, blood pressure, venous pressure, and heart sounds are
monitored to detect possible recurrence of cardiac tamponade

NURSING ALERT

27
o A pericardial friction rub is diagnostic feature of pericarditis. It has a creaky or Scratchy sound and is louder at
the end of exhalation.
o Nurses should monitor for the pericardial friction rub by placing the diaphragm of the stethoscope tightly against
the thorax and auscultating the left sternal edge in the fourth intercostal space, the site where the pericardium
comes into contact with the left chest wall.
o The rub may be heard best when a patient is sifting and leaning forward.

CARDIAC TAMPONADE
 A condition where the heart is unable to pump blood due to accumulation of fluid in the pericardial sac
(pericardial effusion)
 This condition restricts ventricular filling resulting to decreased cardiac output
 Acute tamponade happens when there sudden accumulation of more than 50 ml fluid in the pericardial sac

CAUSES
o Cardiac trauma
o Complication of Myocardial infarction
o Pericarditis

ASSESSMENT FINDING_______________________________________________________________
o BECICs Triad
1. Jugular vein distention
2. Hypotension
3. Distant/muffled heart sound
o Pulsus paradoxus
o 10 mm Hg drop in blood pressure during inspiration
o Increased Central Venous Pressure
o Decreased cardiac output
o Anxiety
o Dyspnea

LABORATORY FINDINGS_____________________________________________________________
o Echocardiogram= shows accumulation of fluid in the pericardial sac
o Chest X-ray

NURSING MANAGEMENT
o The client needs to be placed in a critical care unit for hemodynamic monitoring.
o Administer fluids intravenously as prescribed to manage decreased cardiac output.
o Prepare the client for pericardiocentesis to withdraw pericardial fluid if prescribed.
o Monitor for recurrence of tamponade following pericardiocentesis.
o If the client experiences recurrent tamponade or recurrent effusions or develops adhesions from chronic
pericarditis, a portion (pericardial window) or all of the pericardium (pericardiectomy) may be removed to allow
adequate ventricular filling and contraction.

ANGINA PECTORIS
o Angina pectoris is a clinical syndrome usually characterized by episodes or paroxysms of pain or pressure in the
anterior chest
o The cause is insufficient coronary blood flow, resulting in a decreased oxygen supply when there is increased
myocardial demand for oxygen

PATHOPHYSIOLOGY
o Angina is usually caused by atherosclerotic disease and associated with a significant obstruction of at least one
major coronary artery
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TYPES OF ANGINA___________________________________________________________________
o Stable angina: predictable and consistent pain that occurs on exertion and is relieved by rest and/or nitroglycerin
o Unstable angina (also called pre-infarction angina or crescendo angina): symptoms increase in frequency and
severity; may not be relieved with rest or nitroglycerin
o Intractable or refractory angina: severe incapacitating chest pain
o Variant angina (also called Prinzmetal's angina): pain at rest with reversible ST-segment elevation; thought to be
caused by coronary vasospasm
o Silent ischemia: objective evidence of ischemia (such as electrocardiographic changes with a stress test), but
patient reports no pain

TRIGGERING FACTORS
o Exertion
o Exposure to cold
o Eating a heavy meal, which increases the blood flow to the mesenteric area for digestion, thereby reducing the
blood supply available to the heart musde;
o In a severely compromised heart, shunting of blood for digestion can be sufficient to induce anginal pain
o Stress or any emotion-provoking situation, causing the release of catecholamine's, which increases blood pressure,
heart rate, and myocardial workload

MANIFESTATIONS
o Heavy sensation in the upper chest that ranges from discomfort to agonizing pain
o Severe apprehension and a feeling of impending death.
o Retrosternal pain
o Pain radiates to the neck, jaw, shoulders, and inner aspects of the upper am-is, usually the left arm ''An important
characteristic of angina is that it subsides with rest or administering nitroglycerin. In many patients, anginal
symptoms follow a stable, predictable pattern."

ASSESSMENT AND DIAGNOSTIC FINDING

 ECG may show changes indicative of ischemia such as T-wave inversion
 Nuclear scan or invasive procedure (eg, cardiac catherization, coronary angiography).
 ST depression

MEDICAL MANAGEMENT
o The objectives of the medical management of angina are decrease the oxygen demand of the myocardium and to
increase the oxygen supply
o Percutaneous transluminal coronary angioplasty (PTCA)
Balloon-tipped catheter is used to open blocked coronary vessels and resolve ischemia. The purpose of PTCA
is to improve blood flow within the coronary artery by compressing and ''cracking^ the atheroma
o Intracoronary stents
A Stent is a metal mesh that provides structural support to vessel at risk of acute dosure.
o Atherectomy
Atherectomy removes plaque from a coronary artery by the use of a cutting chamber on the inserted catheter
of a rotating blade that pulverizes the plaque.
o CABG (Coronary Artery Bypass Graft)
Surgical procedure in which a blood vessel is grafted to an occluded artery so that blood can flow beyond the
occlusion

PHARMACOLOGIC MANAGEMENT
o Nitroglycerine causes dilation of the veins the result is venous pooling of blood throughout the body. As a result,
less blood returns to the heart, decreasing the cardiac workload
o Facts about nitroglycerine

29
 Can be given:
o Sublingual tablet
o Spray
o Topical agent,
o Intravenous I.V. administration

MEDICATIONS USED TO TREAT ANGINA

NITRATES
• Nitroglycerin (Nitrostat, Nitro-Bid): Short-term and long-term reduction of myocardial oxygen consumption
through selective vasodilation

Beta-Adrenergic Blocking Agents (beta- blockers)

o Metoprolol (Lopressor, Toprol) Reduction of myocardial oxygen consumption by blocking beta-adrenergic
o Atenolol (Tenormin) stimulation of the heart

Calcium Ion Antagonists (calcium channel blockers)

o Amlodipine (Norvasc) Negative inotropic effects; indicated in patients not responsive to beta-blockers;
o Diltiazem (Cardizem, Tiazac) used primary treatment for vasospasm
o Felodipine (Plendil)

Antiplatelet Medications
o Aspirin Prevention of platelet aggregation
o Clopiidogrel (Plavix)
o Glycoprotein agents:
o Abciximab (ReoPro)
o Tirofiban (Aggrastat)
o Eptifibatide (Integrilin)

Anticoagulants
o Heparin (unfractionated): Prevention of thrombus formation
o Low-molecular-weight heparins (LMWHs): Enoxaparin (Lovenox)
o Dalteparin (Fragmin)

MYOCARDIAL INFARCTION
 In an MI, an area of the myocardium is permanently destroyed, typically because plaque rupture and subsequent
thrombus formation result in complete occlusion of the artery.
 The ECG usually identifies the type and location of the MI, and other ECG indicators such as a Q wave and
patient history identify the timing. Regardless of the location, the goals of medical therapy are to prevent or
minimize myocardial tissue death and prevent complications

RISK FACTORS
Non-modifiable Risk Factor
o Age
Average age of a person having a first heart attack is 65.8 yrs (male) and 70. 4 yrs (female) - AHA 2003
o Family history
o Ethnic background
African-Americans has a higher risk for developing M.I.

Modifiable Risk Factor

o Hypertension
o Smoking
o Hyperlipidemia
30
o ObesityImpaired
o glucose tolerance (DM)
o Physical inactivity
o Stress

ASSESSMENT
SUBSTANTIAL CHEST PAIN
o The pain associated with an MI usually lasts longer than 30 minutes
o Radiating to the left arm, back or jaw
o Occurring w/o a cause usually in the morning
o Relieved only by opioids associated with nausea, diaphoresis, dyspnea, fear & anxiety, palpitations, fatigue,
shortness
of breath.
o Decreased left ventricular function
o Decreased cardiac output
o Cardiovascular system compensates by increasing heart rate (Frank-Starling law)

CG AND CARDIAC ENZYMES ASSESSMENTS

o T-wave in
o ST-segment elevation
o Abnormal Q wave
o Elevated CKMB assessed by mass assay is an indicator of acute MI
o An increase in the level of troponin in the serum can be detected within a few hours during acute MI.
o Enzymes that indicate Myocardial Infarction

ENZYMES TIME OF DESCRIPTION

ELEVATIO
MYOGLOBIN First 1-3 First enzyme to elevate due to decreased
TROPONIN I 2-4 hours Released at the mentioned time frame
AST (aspartate amino 8 hours Is also used for liver damage
CK-MB 24 hours Cardiac- specific isoenzyme; it is found mainly in
cardiac cells and therefore increases only when
LDH (Lactic Dehydrogenase) 72 hours there hastissue
Reflects been damage
breakdownto these cells
and hemolysis

MEDICAL MANAGEMENT
The goals of medical management are to minimize myocardial damage, preserve myocardial function, and
prevent complications this can be achieved by:
o Reperfusing the area with the emergency use of thrombolytic medications
o Reducing myocardial oxygen demand and increasing oxygen supply with medications, oxygen administration,
and bed rest

PHARMACOLOGIC THERAPY
o Drug of choice: Morphine I.V.
o Potent vasodilator: Increases oxygen supply to myocardial tissues
o Decreases oxygen demand
o (ACE) inhibitors decreases blood pressure thus decreasing the workload of the heart
o Thrombolytics dissolve (ie, lyse) the thrombus in a coronary artery (thrombolysis), allowing blood to flow
through the coronary artery again
o THROMBINS2 - The new MONA (Morphine, Oxygen, Nitroglycerin, Aspirin)"
o Thienopyridines: Antiplatelet drugs (Clopidogrel, Prasurgel)
o Heparin: Anticoagulant
o RAAS Inhibitors: ACE-Inhibitors (-pril) or ARBs (-sartan)
31
 o Oxygen
o Morphine
o Beta-blockers: -olol
o Invasive interventions
o Nitroglycerin: vasodilator
o Statin: reduces cholesterol levels (Atorvastatin, Rosuvastatin)
o Salicylate: aspirin/acetylsalicylic add (ASA)

Common Physical Presentation of the Patient with Acute Myocardial Infarction

1.General-Alert anxious, Restless often fatigued
2.Skin- Cool, clammy; diaphoretic
3.Heart- Cardiovascular S3 or S4 may or may not be present, dysrhytmias or murmurs; Jugular venous distention
may be seen in the presense of pump failure
4.Lungs- Dyspnea, tachypnea, rales (crackles) suggest pulmonary congestion and heart failure
5.Circulatory- Peripheral pulses may be pounding or thready, regular or irregular
6. Gastrointestinal- Nausea and vomiting

CARDIOMYOPATHY
A heart musde disease associated with cardiac dysfunction.
TYPES
o Dilated
o Hypertrophic
o Restrictive

DILATED CARDIOMYOPATHY
 Extensive damage to the myofibrils & interference with myocardial metabolism
 Normal ventricular wall thickness but dilation of both ventricles & impairment of systolic function
 Decreased CO- inadequate heart pumping
 Dyspnea on exertion fatigue and palpitation

CAUSES
o Alcohol abuse
o Chemotherapy

ASSESSMENT
o Fatigue, weakness
o HF (left side)
o Dysrhythmias
o Moderate to severe cardiomegaly

HYPERTROPHIC CARDIOMYOPATHY
 Asymmetric ventricular hypertrophy and disarray of myocardial fibers
 LVH leads to a stiff LV that result in diastolic filling abnormalities
 Obstruction in LV outflow
 50 % genetically inherited

32
ASSESSMENT

 Dyspnea
 Angina
 Fatigue, syncope； palpitations
 Mild cardiomegaly
 Ventricular dysrhythmias
 Sudden death common
 Heart failure

RESTRICTIVE CARDIOMYOPATHY
 Restriction or filling of the rigid ventricular walls
 The cause is unknown (ie, idiopathic) in most cases.
 Can be caused by endocrinal or myocardial disease and produce a clinical picture similar to constrictive
pericarditis
 Fibrosed walls cannot expand or contract
 Chamber is also narrowed

ASSESSMENT
o Dyspnea & fatigue
o HF (Right side)
o Mild to moderate cardiomegaly
o Heart block

SHOCK
 Inadequate organ perfusion to meet the tissue's oxygenation demand.
 Hypoperfusion can be present in the absence of significant hypotension
3 Types of Shock
1. Hypovolemic
2. Cardiogenic
3. Distributive - systemic vasodilation leading to decreased blood pressure and insufficient tissue
perfusion
 Neurogenic
 Anaphylactic
 Septic

TYPES OF SHOCK
HYPOVOLEMIC
 Occurs when there is a loss of fluid (blood, plasma) resulting in inadequate tissue perfusion; caused by:
Hemorrhage and Excessive bleeding
 Excessive diarrhea or vomiting
 Dehydration
 Fluid loss from fistulas or burns / Massive third spacing/edema

TREATMENT
 Primary problem/underlying cause must be treated
 Whole blood, plasma (fluid and blood) Replacement and electrolytes

MANAGEMENT:
 Major goals in the treatment of hypovolemic shock are to restore intravascular volume to reverse the sequence
of events leading to inadequate tissue perfusion, to redistribute fluid volume, and to correct the underlying cause of
33
the fluid loss as quickly as possible

CARDIOGENIC
 Occurs when pump failure causes inadequate tissue perfusion; caused by / Congestive heart failure
 Myocardial infarction
 Cardiac tamponade

MANAGEMENT
 The goals of medical management in cardiogenic shock are to limit further myocardial damage and preserve the
healthy myocardium and to improve the cardiac function by increasing cardiac contractility, decreasing
ventricular afterload, or both.

NEUROGENIC
Neurogenic shock develops as a result of the loss of autonomic nervous system function below the level of the
lesion in the spinal cord which caused rapid vasodilation and subsequent pooling of blood within the peripheral
vessels

MANAGEMENT
 Treatment of neurogenic shock involves restoring sympathetic tone, either through the stabilization of a spinal
cord injury or, by positioning the patient properly.
 It is important to elevate and maintain the head of the bed at least 30 degrees to prevent neurogenic shock when a
patient receives spinal or epidural anesthesia. Elevation of the head helps prevent the spread of the anesthetic
agent up the spinal cord.

ANAPHYLACTIC
 Caused by an allergic/anaphylactic reaction that causes a release of histamine and subsequent systemic
vasodilation

MANAGEMENT:
 Treatment of anaphylactic shock requires removing the causative antigen (eg, discontinuing an antibiotic
agent), administering medications that restore vascular tone, and providing emergency support of basic life
functions.
 Epinephrine is given for its vasoconstrictive action (emergency drug).
 Diphenhydramine (Benadryl) is administered to reverse the effects of histamine, thereby reducing capillary
permeability.

SEPTIC
Similar to anaphylaxis; the body's reaction to bacterial toxins (generally gram-negative infections) results in the
leakage of plasma into tissue

MANAGEMENT
o Current treatment of sepsis and septic shock involves identification and elimination of the cause of infection.

TYPE MECHANISM
Hypovolemic Loss of blood or plasma
Cardiogenic Decreased pumping capability/contractility of heart
Distributive Systemic vasodilation
-Anaphylactic due to severe allergic reaction
-Septic due to severe infection
-Neurogenic due to loss of SNS and vasomotor tone

34
HYPERTENSION
❖ Hypertension is defined as a systolic blood pressure greater than 140 mm Hg and a diastolic pressure greater than
90 mmHg

TYPES OF HYPERTENSION
ESSENTIAL HYPERTENSION
o No known direct cause
o Risk factor
 Age > 60 yrs
 Family history of hypertension
 Excessive caloric consumption
 Physical inactivity
 Excessive alcohol intake
 Hyperlipidemia
 High salt intake or caffeine; reduced intake of potassium, calcium, or magnesium
 Smoking

SECONDARY HYPERTENSION
 Disease
 Renal vascular & parenchymal disease
 Primary aldosterone
 Pheochromocytoma
 Cushing's disease
 Coarctation of aorta
 Brain tumors
 Encephalitis

PHARMACOLOGIC THERAPY
 For patients with uncomplicated hypertension and no specific indications for another medication, the
recommended initial medications include diuretics, beta blockers and angiotensin-converting enzyme (ACE)

BETA-BLOCKERS
o First line drug therapy
o Reduce BP by decreasing CO
o Decrease sympathetic stimulation
o Inhibit release of renin from the kidneys

ANGIOTENSIN -CONVERTING ENZYME (ACE) INHIBITORS

o Lower BP by reducing peripheral vascular resistance w/o reflex increase in CO, HR or contractility.
 Captopril (Capoten)
 Enalapril (Vasotec)
 Lisinopril (Zestril)
o Decrease secretion of aldosterone

CENTRAL ALPHA ANTAGONIST

• Acts on CNS preventing reuptake of norepinephrine resulting in lower peripheral Vascular resistance & BP /
Clonidine (Catapres) / Does not decrease renal blood flow

35
CALCIUM-CHANNEL BLOCKER
 Verapamil (Isoptin)
 Amlodipine
 Diltiazem
 Nicardipine

DIURETICS (WATER PILL)

Thiazide
o Chlorothiazide (Diuril)
o Hydrochlorothiazide (Hydrodiuril)
Loop
o Furosemide (Lasix) / Bumetanide (Bumex)
Potassium - sparing
o Spironolactone (Aldactone)

NURSING INTERVENTIONS
• The objective of nursing care for patients with hypertension focuses on lowering and controlling the blood pressure
without adverse effects and without undue cost through:
 Adhere to the treatment regimen
 Implementing necessary lifestyle changes
 Taking medications as prescribed
 Scheduling regular follow-up appointments

THROMBOANGITIS OBLITERANS/ BUERGER'S DISEASE

 Buerger's disease is characterized by recurring inflammation of the intermediate and small arteries and veins of
the lower and upper extremities
Factors
o Men between 20-35 years of age
o Heavy smoking and chewing tobacco
CLINICAL MANIFESTATIONS
o Foot cramps, especially of the arch (instep claudication), after exercise . Pain is relieved by rest
o Intense rubor (reddish-blue discoloration) of the foot and absence of the pedal pulse

MEDICAL MANAGEMENT
o The main objectives are to improve circulation to the extremities, prevent the progression of the disease
o Vasodilators are rarely prescribed

RAYNAUD'S PHENOMENON
 Raynaud's phenomenon is a form of intermittent arteriolar vasoconstriction that results in coldness, pain, and
pallor of the fingertips or toes.
Factors:
o Raynaud's phenomenon is most common in women between 16 and 40 years of age, and it occurs more
frequently in cold climate

CLINICAL MANIFESTATION
o The characteristic sequence of color change of Raynaud's phenomenon is described as white, blue, and red.
o Numbness, tingling, and burning pain occur as the color changes.

36
o The manifestations tend to be bilateral and symmetric and may involve toes and fingers.

MEDICAL MANAGEMENT
o Avoiding the particular stimuli (E.g. cold, tobacco) that provoke vasoconstriction is a primary factor in
controlling Raynaud's phenomenon.
o Calcium channel blockers (Nifedipine [Procardia], amlodipine [Norvasc])
o Sympathectomy (interrupting the sympathetic nerves by removing the sympathetic ganglia or dividing their
branches) may help some patients.

NURSING MANAGEMENT
o Exposure to cold must be minimize
o Sweater should be available when entering air-conditioned rooms
 Avoid smoking and afl sources of nicotine like nicotine gum or patches.

VENOUS THROMBOEMBOLISM
❖ Deep vein thrombosis (DVT)
Virchow's triad
1. Vessel wall injury
2. Venous stasis (stasis of blood)
3. Altered blood coagulation

Risk Factors for Venous stasis

 Bed rest or immobilization
 Obesity
 History of varicosities
 Spinal cord injury
 Age (greater than 65 years)

ASSESSMENT
o Obstruction of the deep veins comes edema and swelling of the extremity because the outflow of venous blood is
inhibited
o Limb pain, a feeling of heaviness, functional impairment, ankle engorgement, and edema

PREVENTION
o Preventive measures include the application of graduated compression stockings
o In surgical patients is administration of subcutaneous unfractionated or low molecular- weight heparin (LMWH).
o Lifestyle changes as appropriate, which may include weight loss, smoking cessation, and regular exercise

MEDICAL MANAGEMENT
Anticoagulant therapy
o (Administration of a medication to delay the clotting time of blood, prevent the formation of a thrombus in
postoperative patients, and forestall the extension of a thrombus after it has formed)
o Oral Anticoagulant Warfarin (Coumadin)

Thrombolytic
o Alteplase (Activase, t-PA)

37
o Urokinase (Abbokinase)
o Streptokinase (Streptase)

NURSING MANAGEMENT
o If the patient is receiving anticoagulant therapy, the nurse must frequently monitor the aPTT, prothrombin time
(PT) and INR
o Elevation of the affected extremity, graduated compression stockings, and analgesic agents for pain relief are
adjuncts the therapy. They help improve circulation and increase comfort.
o Warm; moist- packs applied to the affected extremity reduce the discomfort associated with DVT
o The patient is encouraged to walk once anticoagulation therapy has been initiated. The nurse should instruct the
patient that walking is better than standing or sitting for long periods.

NURSING ALERT
• For ambulatory patients, graduated compression stockings are removed at night and reapplied before the legs are
lowered from the bed to the floor in the morning.

ANEURYSMS
❖ An aneurysm is a localized sac or dilation formed at a weak point in the wall of the artery.

CAUSES
o Congenital: Primary connective disorders (Marfan's syndrome)
o Mechanical (hemodynamic): Poststenotic and arteriovenous fistula and amputation related
o Traumatic (pseudoaneurysms): Penetrating arterial injuries, blunt arterial (pseudoaneurysms)
o Infectious (mycotic): Bacterial, fungal, spirochetal infections
o Pregnancy-related degenerative:
o Nonspecific, inflammatory variant
o Anastomotic (postarteriotomy) and graft aneurysms: Infection, arterial wall failure, suture failure, graft failure

TYPES
 Normal artery.
 False aneurysm—actually a pulsating hematoma. The clot and connective tissue are outside the arterial wall,
 True aneurysm. One, two, or all three layers of the artery may be involved.
 Fusiform aneurysm—symmetric, spindle shaped expansion of entire circumference of involved vessel.
 Saccular aneurysm—a bulbous protrusion of one side of the arterial wall.
 Dissecting aneurysm—this usually is a hematoma that splits the layers of the arterial wall.

MEDICAL MANAGEMENT
• Antihypertensive agents, including:
Diuretics,
Beta blockers,
Ace inhibitors,
Angiotensin II receptor antagonists, calcium channel blockers
These drugs are frequently prescribed to maintain the patient's blood pressure within acceptable limits to prevent
rupture of the aneurysms

SURGICAL MANAGEMENT
o Resection of the vessel and sewing a bypass graft in place

38
o Endovascular grafting, which involves the transluminal placement and attachment of a sutureless aortic graft
prosthesis across an aneurysm

39