Acute Bronchitis

 Infection of the lower respiratory tract the major bronchi

Etiology
 Viral
 Bacterial agents
 Exposure to irritants
Two Types of Acute Bronchitis
Infectious Bronchitis
 Occurs most during winter
 Often caused by virus
 It may be caused by bacteria Chronic Obstructive Pulmonary Disease (COPD)
Irritative Bronchitis  Pulmonary disease that causes chronic obstruction of
 Also called industrial or environmental bronchitis airflow from the lungs
 Exposure to various mineral and vegetable dust  A progressive and irreversible condition characterized by
Clinical Manifestation diminished inspiratory and expiratory capacity of the
 Productive cough – common sign lungs
 Wheezing  Includes Chronic Bronchitis, and Emphysema
 Dyspnea and Tachypnea Key Points for COPD
 Pleuritic chest pain  Happens gradually
 Diffuse rhonchi and crackles  Inability to fully exhale
Diagnostic Evaluation  Irreversible
 Based on signs – productive cough  Limited airflow
 Chest X-ray
 Culture and sensitivity
Nursing Diagnosis
 Ineffective airway clearance related to sputum
productions and inflammation of lower airways
Nursing Interventions
 Hydration and humidity
 Increase fluid intake
 Avoid beverages like caffeine or alcohol
 Avoid cough suppressants, antihistamines, and
decongestants
Nursing Interventions
 CPT
Etiology of COPD
 Bronchodilators
 Cigarette smoking
 Antibiotics (7-10 days)
 Air pollution, occupational exposure
 Analgesics
 Allergy, autoimmunity
 Corticosteroids
 Aging, genetic predisposition
 Expectorants
 Alpha1 anti trypsin deficiency (genetic)
Health Teachings
 Completion of the course of antibiotics
Chronic Bronchitis (Blue Bloater)
 Seek medical attention for shortness of breath and
 Chronic inflammation of the lower respiratory tract
worsening condition
characterized by excessive mucous secretion that limits the
 Inform the patient that a dry cough may persist after ability to completely exhale the air that leads to
bronchitis Hyperinflation.
 Majority recover from bronchitis without antibiotic  Less oxygen is getting into the blood and more carbon
treatment dioxide is staying in the blood.
 Patients will have cyanosis due to a decreased oxygen
level.
 The body increases RBC production and cause blood to
shift elsewhere which increases pressure in the pulmonary
artery leading to pulmonary hypertension.
Pulmonary Emphysema (Pink Puffer)
 Destruction of alveoli, narrowing of small airways and
trapping of air resulting to loss of lung elasticity and
breakdown of alveolar walls.
 The alveoli sacs lose their ability to inflate and deflate
due to an inflammatory response in the body resulting to
air trapped in the sacs and this causes major
hyperinflation of the lungs
 Hyperinflation causes the diaphragm to flatten Complications
 In order to fully exhale, the patient starts to  Heart failure
hyperventilate and use accessory muscles to get the air  Pneumothorax (spontaneous
out and leads to the barrel chest look  Risk for pneumonia
Clinical Manifestation  Lung cancer
 Lack of energy Diagnostic Evaluation
 Unable to tolerate activity (shortness of breath)  Spirometry
 Nutrition poor (weight loss due to energy used breathing  ABG
especially with emphysema  Chest X-ray
 Gases abnormal (High PCO2, and Low PO2 <90)-  Alpha antitrypsin assay
Respiratory Acidosis Incentive Spirometer
 Dry or productive cough (constant productive with chronic  A device that measures how deeply you can inhale
bronchitis) (breathe in)
 Accessory muscle usage during breathing, abnormal lung  It helps you take slow, deep breaths to expand and fill
sounds: diminished, coarse crackles (chronic bronchitis) or your lungs with air
wheezing  Helps prevent lung problems, such as pneumonia
 Modification of skin color from pink to cyanosis in lips,  Made up od a breathing tube, an air chamber, and an
mucous membranes, nail beds (“blue bloaters”) indicator
 Anteroposterior diameter increased (barrel chest)  The breathing tube is connected to the s=air chamber and
 Gets in the Tripod Position has a mouthpiece at the end.
 Extreme dyspnea Indications
 Most commonly used after surgery
 Increased risk of airway or breathing problems
 People who smoke or have lung disease

How do I use an incentive spirometer?

 Sit up as straight as possible, do not bend your head
forward or backward
 Hold the incentive spirometer in an upright position
 Place the target pointer to the level that you need to reach.
 Put the mouthpiece in your mouth and close your lips tightly
around it, do not block the mouthpiece with your tongue
 Inhale slowly and deeply through the mouthpiece to raise
the indicator. Try to make the indicator rise up to the level
of the goal marker.
Nursing Interventions
 Assess lung sounds and sputum production and obtain a
culture if ordered
 Keep the patient in orthopneic position
 Keep oxygen saturation (88%-93%)
 Given oxygen as prescribed 1-2 liters
 Monitor effort of breathing and teach about pursed-lip
and diaphragmatic breathing
Pursed-lip Breathing
 Used for when patient starts to get dyspneic
 Similar to like blowing out a birthday candle
Diaphragmatic Breathing
 Uses abdominal muscles for breathing rather than accessory
muscles
 Administer medications as needed: bronchodilators,
corticosteroids, mucolytics
 O2 therapy 1-3 LPM (safest is 2 LPM)
 CPT – percussion, vibration, postural drainage
 Bronchial hygiene inhalation – Steam inhalation, Aerosol
inhalation
Education for COPD
 Diet: HIGH CAL, HIGH CHON, LOW CHO
 Avoid large heavy meals
 Avoiding sick people, irritants, hot humid (smothering or
very cold weather
 Avoid smoking, alcohol, environmental pollutants
 Avoid powerful odors, extreme temperature, pets,
fireplace and feather pillows
 REST
 Increase fluid intake
 Good oral care
 Stop smoking or being around people who smoke
 Vaccination up-to-date: annual flu shot and Pneumovax
every 5 years
 Pursed lip and diaphragmatic breathing techniques
Pharmacotherapy
Corticosteroids
 Decreases inflammation and mucous production in airway
 Route: oral, IV, inhaled
 Used in combination with bronchodilator like Symbicort
 Other corticosteroids: Prednisone, Solu-medrol, Pulmicort
 Side effects: easy bruising, hyperglycemia, risk of
infection, bone problems (long term use)
 Rinse mouth after using inhaled corticosteroids
 Monitor blood sugar and signs of infection
Phosphodiestrace-4 inhibitors
 “Roflumilast”
 Used for chronic bronchitis and it works by decreasing
COPD exacerbation
 Side effects: can cause suicidal thoughts and weight loss.
Bronchodilator
 Theophylline (most commonly)
 A bronchodilator used long term in patients who have
severe COPD
 Remember: Narrow therapeutic range of 110 to 20
mcg/mL
 Increases risk of digoxin toxicity and decreases the
effects of lithium and Dilantin
Short-acting Bronchodilators
 Relaxes the smooth muscle of the bronchial tubes and are
used in emergency situations where quick relief is needed
 Albuterol (beta 2 agonist)
Long-acting Bronchodilators
 Relaxes the smooth muscle of the bronchial tubes
 Used over a longer period of time
 Taken once or twice a day
 Beta 2 agonist: salmeterol, anticholinergics: Spiriva
 Patient education: use bronchodilator inhaler BEFORE
steroid inhaler (wait 5 minutes in between)
Nursing Considerations
 Always administer the bronchodilator FIRT and then 5
minutes later the corticosteroids
 Avoid consuming products with caffeine while taking this
medication, Caffeine has the same properties as
Theophylline, which can increase the toxic effects of the
medication
 Stop smoking as it interferes with the drug effectiveness
 Check the HR – it may cause tachycardia
Anti-cholinergic
 Ipratropium - bronchodilator that also is short-acting and
relaxes airway
 Tiotropium – a bronchodilator that is long-acting
 These drugs can cause dry mouth – sugarless candy can
help
Anti-histamine Steroids
 Benadryl (Diphenhydramine)  Betamethasone, and methylprednisone
 Observe for drowsiness and dizziness  Rinse mouth after inhalation to prevent oral thrush
 Avoid driving and operating electrical machines to Anti-microbials
prevent accidents  If infection is present
Anti-microbials Leukotriene antagonist
 If infection is present  Prevent bronchoconstriction, decrease mucosal edema and
 Prevent bronchoconstriction, decrease mucosal edema and mucous production
mucous production  Ex: Montelucast
 Ex: Montelucast
Pleurisy
Asthma  Inflammation of both parietal and visceral pleura
 Abnormal bronchial hyperactivity to certain substances Clinical Manifestation
resulting mucosal edema and mucous production  Pleuritic pain
 It is reversible  Intercostal tenderness
 ALLERGY – the strongest factor for the development of  Pleural friction rub
asthma  Evidence of infection
 Status Ashmaticus – severe, persistent asthma that does Nursing Dx:
not respond to conventional therapy  Ineffective breathing pattern r/t stabbing chest pain
Ss and Sx Diagnostic Exam
 Dyspnea – IM  Chest X-ray
 Increased bronchial sounds  Sputum Exam
 Cough  C and S
 Distress at rest  Pleural Biopsy
 Wheezing Management
 Tachycardia 1. Pain relief using both pharmacologic and non-
Lab Data pharmacologic
 CXR 2. Intercostal Nerve Block
 Pulse oximetry - Necessary when pain causes hypoventilation
 Elevated Immunoglobulin - Inform the Px that he will experience prick of the
 ABG analysis needle and slight sensation of pressure
Nursing Dx: - Place the Px in sitting position, bend forward,
 Ineffective breathing pattern r/t bronchospasm and hug a pillow
Interventions - Prone with a pillow under chest
 Assess precipitating factors and eradicate this source - Ask the Px to identify the site of pain
 Instruct patient to avoid 3 E’s (exercise in cold weather,
environmental factors like dust, emotional factors) Pneumothorax
 Orthopneic position and do purse lip breathing  Is the accumulation of air in the pleural space
 Liberal fluid intake  Caused by trauma as a result, a laceration oof lung
 O2 as ordered parenchyma, tracheobronchial tree.
 Administer medications – bronchodilators and Types of Pneumothorax
corticosteroids Spontaneous Pneumothorax
Collaborative Management in COPD  Onset of air in the pleural space with the deflation of the
 REST affected ling in the absence of trauma
 Increase fluid intake Open Pneumothorax
 Good oral care  Air enters the chest during inspiration and exit during
expiration
 Avoid smoking, alcohol, environmental pollutants. These
inhibit mucociliary function
 Diet: HIGH CAL, HIGH CHON, LOW CHO
 O2 therapy 1-3 LPM (safest is 2 LPM)
 CPT – percussion, vibration, postural drainage
 Bronchial hygiene inhalation
 Steam inhalation
 Aerosol inhalation
 Medimist inhalation
Pharmacotherapy
 Expectorants/mucolytic
 Antitussives
Antihistamines
 Benadryl (Diphenhydramine)
 Observe for drowsiness and dizziness. Avoid driving and
operating electrical machines to prevent accidents
Tension Pneumothorax  Hydrothorax
 Air can enter the pleural space but not leave the
chest/lungs. Air trapping and ipsilateral ling is
compressed.

Causes of Pneumothorax and Pleural Effusion

 Trauma
Pleural Effusion  Thoracic Surgery
 Accumulation of fluids in the pleural space  Positive pressure ventilation
Types of Pleural Effusion  Thoracentesis
 Hemothorax  CVP line Pressure
 Emphysema
Assessment Pleural Effusion and Pneumothorax
 Sudden sharp chest pain (pleuritic pain)
 Cough
 Dyspnea
 Dullness or flatness to percussion (over areas to fluid)
 Absence of breath
 Increase RR
 Chest tightness
 Chest asymmetry
 SOB
Collaborative Management
 High Fowlers position
 Pain mammnagemnet
 O2 therapy (high flow 10-15lpm)
 Chest x-ray
 Pyothorax/Empyema  UTZ
Accumulation of Pus in the pleural cavity  Thoracentesis/ chest tube
 ABG analysis
 Monitor shock
 Pleurodesis
 Apply petroleum gauze to sucking chest wound
 Maintain the patency of the tubes
Tension Pneumothorax
Management
 Thoracentesis/CTT
 Chest tube drainage with underwater seal suction
Spontaneous Pneumothorax
 Needle aspiration or CTT
 Pleurodesis
 Thoracotomy – resection of the apical blebs
 Massive Empyema
Thoracentesis  Hemoptysis
 Rusty/ colored purulent sputum
 Recurring episodes of pleural effusion) when cancer
metastasis in the pleural space), Pneumonia, Bronchitis
 Dyspnea
 Chest shoulder, arm pain
Diagnostic Evaluation
1. Chest x-ray, fluoroscopy and tomography – lung
cancers may be partly or completely hidden by other
structures
2. Cytologic Examination – Malignant cells (confirmatory
test)
3. CT – Sensitive in detecting small nodules and
metastatic lesions
4. Lympnode biopsy/ mediastinoscopy – to establish
lymphatic spread
5. PFT – to determine if patient will have adequate
pulmonary reserve to withstand surgical procedure
6. Needle Biopsy
Collaborative Management
Improving Breathing Patterns
Lung Cancer (Bronchogenic Cancer)  Maintain patent airway
 Refers to the malignant tumor of the lung arising within  Administer O2 and Aerosol therapy
the wall or epithelial lining of the bronchus  DBE
 The lungs is the common site of metastasis from cancer  Expectorant
Predisposing  Provide humidifier/vaporizer
 Cigarette smoking  Rest
 Asbestos Improving Nutritional Status
 Exposure to radiation, arsenic, nickel, chlomethyl ethers,  High calories
mustard gas  High chon foods
 Air pollution Controlling Pain
 Emphysema  Administer pain reliever NSAID
Types of Lung Cancer Surgery
Squamous/Epidermoid Pneumonectomy – removal of the lung
 Most common type of lung cancer  Position on semi-fowlers, turned on affected side. To
 With good prognosis promote lung expansion and prevent flooding of the
Adenocarcinoma remaining lung with blood from the affected part
 With good prognosis  Avoid full side lying position – to prevent mediastinal shift
Small Cell/Oat Cell Carcinoma  No chest tube after surgery
 With poor prognosis Lobectomy – removal of lobe
Large Cell/Undifferentiated Carcinoma Segmentectomy – removal of segment
 With poor prognosis Wedge Resection – removal oof an entire tumor regardless of
Staging the segment
 Refers to anatomic extent of tumor, lympnode involvement Decortication – stripping off fibrinous membrane enclosing the
and metastatic spread lung
 Is done by tissue diagnosis, lympnode biopsy, and Thoracoplasty – removal of ribs
mediastinoscopy For Lobectomy, Segmentectomy, Wedge Resection, Decortication,
Clinical Manifestation Thoracoplasty
 Hacking cough, non-productive then thick purulent blood-  Chest tube will be in place post op
tinged sputum  Position on semi fowlers or on the unaffected side to allow
 Dyspnea, wheezing expansion of the affected lung
 Chest pain (poorly localized and aching) Chemotherapy
 Chest tightness  The treatment of choice for small cell carcinoma
 Chronic RTI  The cancer has almost always spread to distant arts of
 Hoarseness the body
 Hypoxia  Without chemo, the survival is 4 months with small cell
 Edema around the neck carcinoma
 Pleural Effusion Radiation Therapy
 Paraneoplastic Syndrome  Given to those people who refuse surgery, who has
 Late Signs: weakness, anorexia, weight loss, anemia another condition
Warning Signs of Lung Cancer  It partially shrinks or slows the growth of cancer
 Any change in respiratory pattern  Useful in controlling the complications of cancer
 Persistent cough – first and most common symptom
Prevention Anti TB Drugs
 Quit smoking INZ(Isoniazid)
 Early detection  Maybe used at any age and among pregnant women
 Chest x-ray once a year  SE: peripheral neuritis, hepatoxicity
 Administer Vit. B6
Pulmonary Tuberculosis (PTB)  Monitor SGPT and SGOT
 Infectious disease cause by mycobacterium tuberculosis  Used as prophylaxis for 6 months to 1 year
 It usually infected the lung but it can occur in any part of Streptomycin
the body  SE: ototoxity, nephrotoxicity
Classification of TB Rifampicin
Class 1  SE: red orange color to body secretion, hepatoxicity, N/V,
 Exposure; no infection thrombocytopenia
Class 2 Ethambutol
 Infection; no disease  SE: optic neuritis, skin rash
 +PPD reaction but no clinical evidence of active PTB  Ophthalmologic exam at regular basis
Class 3
 Disease clinically active KEY POINTS
Class 4  Evaluate the effectiveness of anti TB drugs – AFB
 Disease, not clinically active  Anti TB drugs must be taken in combination
Class 5  Should be taken to an empty stomach
 Suspected disease, diagnosis pending  Advise the client not to take alcohol
Etiologic Agent:  TB is no longer contagious 2-3 weeks after starting the
 Mycobacterium Tuberculosis therapy or after 2 negative sputum culture
 Constitutional Symptom
 Pulmonary Signs:
- Indicates extensive involvement
 Extra Pulmonary TB
Clinical Manifestation
 Initially asymptomatic
 Cough
 Fatigue
 Anorexia
 Wight loss
 Low grade fever
 Night sweats
 Hemoptysis
 Dyspnea
 Chest pain
Reservoir
 Man, Diseased cattle
MOT
 Airborne-droplet infection: 1-5 micron in diameter
IP: 4-12 weeks
POC
 A person who excretes tubercle bacilli is communicable
Factors that determine the risk of exposure
 Number of infectious cases in the community
 Population density
Pneumonia
 Family size
 Inflammatory disease that involves the terminal airways
 Duration of exposure
and the alveoli of the lungs
 Environmental condition
 Bacterial, Viral, And Fungal
Client Education Guide
Classification of Pneumonia
 TB is infectious; curable and treatable by medication
1. Community Acquired Pneumonia
 Cover the nose and mouth when coughing, sneezing, or - Streptococcus pneumonia
laughing 2. Nosocomial Pneumonia
 Wash hands after any contact with body substances, - Due to gram negative bacilli and staphylococci
mask or soiled tissues 3. Pneumonia in Immunocompromised person
 Patient should wear surgical mask when advise. Health Clinical Manifestation
care workers – n95 Hypertrophy of Mucous Membrane
 Take anti TB drugs regularly  Increased sputum production
 Primary anti TB drugs  Wheezing
 Dyspnea
  Cough Obstructive Atelectasis
 Rakes  Due to obstruction of the airways supplying a lung
 Rhonchi segment or lobe
Increased Capillary Permeability
 Increased fluids ISC
 Consolidations
 Hypoxemia
Inflammation of the Pleural
 Chest pain
 Pleural effusion
 Dullness
 Diminished breath sounds
Protective Mechanism
 Increase WBC
 Fever
Collaborative Management
 Promote rest
 Provide adequate
 Incentive spirometry
 O2 therapy
 Semi fowlers
 Bronchial hygiene measure
 Oral hygiene
 Humidifier
 Splint chest when coughing
 Antibiotics
 Flu vaccine-annual, Pneumu Vaccine-q 5 years

Atelectasis
 Is a complete or partial collapse of the entire lung or lobe
of the lung.
 The alveoli are deflated down to little or no volume in
which they are filled with liquid
Types of Atelectasis
Adhesive Atelectasis
 Occurs due to the decrease or absence of pulmonary
surfactant produced by type II pneumocytes
 It is most commonly seen in the neonate with RDS.

Acute Atelectasis
 The lung has collapsed and airlessness
 Most common type of atelectasis
Chronic Atelectasis
 Characterized by a complex mixture of airlessness,
Compressive Atelectasis infection, widening of the bronchi, destruction and scarring.
 Due to compression by a space-occupying process.
 Result from tumor, enlarged heart, diaphragm elevation
or fluids in the pleural space
Causes of Atelectasis
 Foreign body, tumor, retained secretions, pain, alteration Two Layers of Pericardium
in small airway function, prolong supine positioning, Visceral Pericardium
increase abdominal pressure, reduce lung volumes due  Thin serous inner layer which surrounds the heart
too neurologic disorders Parietal Pericardium
 Postoperative patients such as upper abdominal, thoracic  Outer layer, and serves to prevent over distension of the
and open heart surgery heart
 Impaired cough reflex in post operative patients
 Muscular and neurologic disorders and bed ridden
Clinical Manifestation
 Respiratory distress, tachycardia, tachypnea increased
work of breathing / DOB
 Pain and Fever
 Central Cyanosis
 Decrease SaO2 and decreased breath sounds
 Crackles
Diagnostics
 Chest X-ray – suggest atelectasis
 Low oxygen saturation less than 90% Layers of the Heart
Nursing Diagnosis Epicardium
 Ineffective Airway Clearance r/t foreign body, tumor in  Outermost layer, a smooth outer surface of the heart
an airway, retained secretions, compression of the lungs Myocardium
 Ineffective Breathing pattern r/t disease process  Thick middle layer
Medical Management  Responsible for the heart’s ability to contract
 Frequent turning Endocardium
 Early ambulation  Innermost layer of the heart
 DBE, coughing  It lines the chambers and covers the heart valves of the
 Incentive spirometer heart
 CPT (postural drainage and chest percussion)
 Bronchodilators
 Bronchoscopy
 Endotracheal intubation or mechanical ventilation
 Thoracentesis/Chest Tube insertion
Nursing Interventions
 Position frequently from supine to upright
 Encourage early mobilization
 Encourage to do DBE and coughing
 Reinforce appropriate technique for incentive spirometer
 Perform CPT
 Suctioning PRN
Chambers of the Heart
HEART Right Atrium
 Pump blood through the arteries, capillaries and veins  Receives deoxygenated blood from the body by way of
 Creates blood pressure, circulates oxygen, nutrients and the superior vena cava (SVC) and inferior vena cava (IVC)
other substance Right Ventricle
Location & Size  Receives blood from the RA and ejects this blood into the
 Weighs 300g or size of the fist lungs via pulmonary artery
 Cone like in appearance Left Atrium
 Located in mediastinum  Receives oxygenated blood from the lungs by way of
 Enclosed by pericardium four pulmonary veins
Left Ventricle
 Receives blood from the left atrium and ejects blood into
systemic arterial circulation
Valves of the Heart
Atrioventricular Valves
 Allow blood to flow from the atria into the ventricles
 Effective in preventing backflow of blood into the atria
 Tricuspid
 Mitral/Bicuspid
Semilunar Valves
 Prevent backflow pf blood into the ventricles
 Aortic valve and pulmonic valve
  Aortic valve – lies between the LV and the aorta
 Pulmonic valve – lies between RV and pulmonary artery Two Basic Myocardial Cell Groups
Veins Myocardial Working Cells
 Blood vessel that carries blood towards the heart  Primary function is both contraction and relaxation
 SUPERIOR VENA CAVA – drains blood from the head to Specialized Peacemaker Cells
the neck  Generation and conduction of electrical impulses
 INFERIOR VENA CAVA – collects blood from the lower  Controlling the heart rate and the rhythm of the heart
portion of the body Primary Cardiac Cell Characteristics
 Automaticity
 Excitability
 Conductivity
 Contractility

1. Sinoatrial (SA) Node

 Located in the upper portion of the Right Atrial wall of
Cardiac Cycle the heart
Systole  Natural peacemaker of the heart
 Contraction and emptying of the atria and ventricles  Capable of generating impulses travel through the muscle
Diastole fibers of both atria resulting in depolarization
 Relaxation and filling of atria and ventricle  Firing rate of 60-100 bpm
Two Heart Sounds Internodal Pathways
LUB  Distribute the electrical impulse from SA node throughout
 The first, loudest and longest sound caused by ventricular the atria to the Av node
systole closing the AV valves  The transmission of impulses from the SA node to the Av
DUB nide and to the rest of atrial myocardium brings atrial
 The second sound caused by the closure of aortic and systole
pulmonary semilunar valves 2. Atrioventricular (AV) Node
Cardiac Output  Located on the floor of the right atrium just above the
 The volume of blood ejected from the left ventricle into tricuspid valve
the aorta per minute  The electrical activity is delayed approximately 0.05sec
 CO=SV x HR  Intrinsic firing rate of 40-60 bpm
 Normal – 5-6 L/Minute AV JUNCTION
ANS influences on Cardiac Activity  Region where the Av node joins the bundle of His
SNS  AV Junction tissue contain fibers that can depolarize
 Responsible for preparation of the body for physical spontaneously forming an electrical impulse that can
activity (Fight or Flight) spread to the heart chambers
 Releases Norepinephrine 3. Bundle of His
PNS  The conduction pathway that leads out of the AV Node
 Regulates the calmer (REST and Digest)  Has the ability to initiate electrical activity at an intrinsic
 Releases Acetylcholine firing rate of 40-60 bpm
Chemoreceptors  Called as Bundle Branches (right and left)
 Medulla Oblongata and special receptors are found in  Two main branches (left and right) conduct electrical
the carotid and aortic bodies activity form the Bundle of His down to Purkinje Network
 A decrease pH or increase in paCO2 level causes a Purkinje’s Network
reflex SNS response that result in tachycardia,  Possessed the intrinsic ability to serve as peace maker
vasoconstriction, and increased myocardial contractility  Intrinsic firing rate of PF is 20-40 bpm
 Decreased paCO2 and increased pH leads to
vasodilation
 Diagnostic Test
Coronary Artery Disease  Blood Test: Lipid profile: total cholesterol, LDL, HDL,
 Accumulation of fatty deposits or plaques triglycerides
(ARTHEROSCLEROSIS) along the innermost layer of the  ECG: ST segment depression, ST segment elevation
coronary arteries leading to restriction of blood flow to  Stress testing
the heart and inadequate oxygen supply to the heart  Cardiac catheterization/coronary angiography –
muscle. presence, location and extent of coronary lesion
Main Arteries of the Heart Goal/Planning
Left Coronary Artery  To maintain normal blood and oxygen supply to the heart
 Left circumflex artery – provides blood to left atrium and  To eliminate the signs and ss
side and back of the left ventricle  Patient can resume his/her ADL
 Left anterior descending artery – provides blood to the  Prevent further progression of CAD
front and bottom of the left ventricle and front of the Nursing Intervention
septum  Assess signs and symptoms and when to seek help
 Monitoring heart rate and blood pressure and oxygen
saturation
 Modifying lifestyle: Diet (low fat, low calorie), Exercise,
Smoking cessation, weight loss
 Educating patient about treatment, preventive measure,
medications, and management
 Education about procedures: EKG, stress test, heart cath,
lipid profile blood test
 Educate the patient about the significance and
Right Coronary Artery complications of CAD
 Provide blood to the right atrium and ventricle and to the Medical Management
bottom part of the left ventricle and back of the septum Antiplatelet
and branches off to:  Prevent clots from forming or growing which decrease the
 Right marginal artery and posterior descending artery chances of ischemia
Risk Factors  Aspirin and Plavix
 Age  Nursing Considerations:
 Gender  Watching for GI bleeding and monitor Thrombotic
 Race Thrombocytopenic Purpura (TTP)
 Heredity or family history Nitrates
 Stress  Causes vasodilation
 Diet  Sublingual, transdermal
 Sedentary lifestyle  Place one tab or one spray under the tongue for
 Smoking maximum of 3 doses
 Alcohol  Monitor their blood pressure
 Hypertension  SE: dizzy or hot flushing after taken.
 Obesity Beta Blocker
 DM  Decrease myocardial oxygen demand by decreasing the
 High cholesterol heart rate, BP, myocardial contractility and calcium output
Pathophysiology  Propranolol, metropolol, atenolol, pindolol, esmolol
 Etiology/Risk Factors >>> LDL adhere to the artery  Monitor the HR, and BP
wall >>> Plaque formation/Atherosclerosis >>> Blood Calcium Channel Blockers
restriction into the heart >>> signs and symptoms of  Inhibit the calcium ions transportation into myocardial cells
Ischemia, MI to depressed inotropic and chronotropic activity
Signs and Symptoms of CAD decreasing cardiac work load
 Chest pain – STABLE and Unstable Angina  Promote vasodilation and reduces coronary vasospasm
 Shortness of Breath  Verapamil, Nifedipine, Diltiazem, Amlodipine,
 Very tired, feeling run down especially with activity Nicardipine
 Diaphoresis  Monitor HR and BP
 Nausea Ace Inhibitors
 Tachycardia  Ends in “pril”
 Lisinopril, ramipril
 Blocks the conversion of angiotensin I to angiotensin II
which caused vasodilation, lowers blood pressure,
decrease the workload on the heart
 SE: nagging dry cough
Statins (“tins)
 Simvastatin, atorvastatin
 Helps lower LDL, total cholesterol, triglycerides and
increase HDL
 Educate not to replace diet and exercise
 Notify doctor if they develop muscle pain or tenderness
 Monitor CPK (creatine kinase) levels if elevated
 Monitor liver function
Surgical Management
Percutaneous Transluminal Coronary Angioplasty
 A balloon tip catheter is placed in a coronary vessel
narrowed by plaque
 The balloon is inflated and deflated to stretch the vessel
and flatten the lesion
 Blood flows freely through the unclogged vessel to the
heart
Intra Coronary Stent
 A diamond mesh tubular device is placed in the coronary
artery
 Prevents re-stenosis (after PTCA) by providing skeletal
support
Intra Coronary Atherectomy
 A blade tip catheter is guided in a coronary vessel to the
site of the plaque
 The plaque is cut, shave, or pulverized then removed
Coronary Artery Bypass Graft
 A graft is surgically attached to the aorta and the other
end of the graft id attached to a distal portion of a
coronary vessel
 By passes by obstructive lesion in the vessel and returns to
adequate blood flow to the heart muscle supplied by the
artery
Angina Pectoris
Angina Pectoris/Myocardial Ischemia
 Insufficient blood flow resulting to inadequate oxygen
supply to the myocardium causing transient chest pain due
to obstruction or spasm of coronary arteries
Types of Angina Pectoris
Stable Angina
 The most common form of angina
 Characterized by burning, heavy, or squeezing feeling in
the chest
Unstable Angina
 Chest pains occur with increased frequency
 Requires hospital admission and more aggressive therapy
Prinzmetal’s or Vasospastic Angina
 Is uncommon pattern of episodic angina that occurs at rest
due to coronary artery
 Responds promptly to coronary vasodilators and calcium-
channel blockers
Intractable Angina
 Also called Refractory Angina
 Chronic incapacitating angina unresponsive to intervention
 Respond poorly invasive procedures such as angioplasty
or by pass surgeries
Nocturnal Angina
 Occurs only at night and possibly associated with REM
sleep
Angina Decubitus
  Paroxysmal chest pain that occurs in sitting or lying down  Avoid saturated fat (animal fats)
Post Infraction Angina  White meat (chicken without skin, turkey, fish are low in
 Occurs after MI, when residual ischemia may cause cholesterol)
episodes of angina  Read labels
Precipitating Factors of Angina
4 E’s Myocardial Infraction (MI)
 Exertion  Results from prolonged lack of blood flow to a portion of
 Emotion the myocardial tissue resulting to lack of oxygen, death
 Eating heavy meal or necrosis to the myocardial tissue
 Environment
Clinical Manifestations
Chest Pain
 Transient (temporary), paroxysmal substernal or pre
cordial pain, squeezing, burning, pressing, choking aching
or bursting left sternal chest pain
 Heaviness or chest tightness
 The patient often says, “it feels like gas or heartburn or
indigestion”
 Radiates down one or both arms, left shoulder jaw, neck
and back
 Precipitated by physical exertion
 Relieve by rest and Nitroglycerine
Assessment of Chest Pain
 Precipitating factors of Angina What happens to the heart muscle after an MI?
 Provocative Early Signs of an MI
 Quality  No physical changes to heart muscle yet (until about 6-8
 Region hours).
 Severity  If the myocytes die cardiac enzymes are released: CK-
 Timing and Treatment MB (4 to 6 hours after MI), troponin (2-4 hour most
Subsequent Assessment regarded) myoglobin (1 hour after injury)
 Obtain 12 lead ECG Within 24-36 hours
 Assess patient knowledge on the disease  Inflammation sets in and neutrophils come on the scene
 Medical History and congregate at the damaged tissue site
 Drug Therapy  Complication is possible pericarditis
Clinical Manifestations  Within 24 hours the heart fails to pump efficiently
 Pallor resulting to cardiogenic shock and arrhythmias
 Diaphoresis Within 10 days
 Dyspnea  Granulation occurs when the macrophages come on the
 Faintness scene
 Palpitation  WBCs came to clean up the dead cells and other
 Dizziness components
Nursing Interventions  The new tissue formed and is weak. This increases the
 Assess the level of chest pain and its duration chance of cardiac rupture
 Place in comfortable position Within 2 months
 VS q5-10 minutes until anginal pain subsides  Scarring occurs, and the heart is affected in size and
 Administer oxygen and nitroglycerine as ordered functionality due to increased collagen
 Monitor relief of pain Etiology/Causes
To maintain C.O.  Thrombus formation – the most common causes of MI
 Instruct to avoid over fatigue  Severe CAD
 Stop activity immediately  Intramural hemorrhage
 Monitor BP and HR in response to drug therapy  Coronary Artery Spasm
 Institute continuous ECG  Coronary Artery Embolism
To decrease anxiety Degree of Damage to the Heart Muscle
 Minimize emotional outburst, worry and tension Myocardial Ischemia/Zone of Ischemia
 Verbalize fears and concerns  Temporary deprivation of oxygen and transient absence
 Maintain an optimistic outlook of blood supply and other nutrients to the heart
 Explain the reasons for hospitalization, diagnostic test and
therapies administered
 Teach relaxation techniques such as yoga, DBE
 Administer sedative and tranquilizer
Diet
 Low sodium, low fat and cholesterol, high fibers
  Inverted T wave – from the zone of ischemia
 Pathologic Q wave – develops due to area of
infraction/tissue necrosis and are permanent
Elevated Troponins
 Gold standard now used by most hospitals in assessing
for an MI
 Most specific test to detect MI
 Elevated Troponin T, I, C – sensitive as CK MB for the
detection of MI
Myocardial Injury/Zone of Injury  Usually drawn every 6 hours for 3 sets
 Inflamed and Damage to the heart muscle (myocardium) CK-MB
 Most commonly results from myocardial ischemia  It elevates 4-6 hours after injury
Myocardial Necrosis/Zone of Infraction  The most sensitive enzyme for determining for heart
 Death of myocardial tissue (MI) muscle damage
 Complete oxygen deprivation Elevated LDH 1 and LDH 2
 Irreversible damage  Sensitive isoenzyme that indicates myocardial damage
Classification MI according to the Heart Muscle involve Elevated WBC and ERS
Transmural (Q Wave) Infraction  Due to inflammatory process
 Necrosis occurs throughout the entire thickness of the heart Other Test
muscle  Echocardiogram
 Extends from endocardium to epicardium  Heart Catheterization
Sub Endocardial Infraction  Stress test with Myocardial Perfusion Imaging
 Necrosis is in the innermost layer of the heart lining Nursing Interventions
chambers  Monitoring & Assessing Cardiovascular System – 12-lead
 Affects the endocardial muscles EKG, and continuous bedside cardiac monitoring
Intramural Infraction  Semi fowlers
 Patchy areas of the myocardium associated with long  Oxygen via nasal cannula – at 2-4 L/Minute
standing angina pectoris  Working IV access
 Monitor lung sounds “crackles”
 Bedrest for 24-48 hours
 Collect cardiac enzymes as ordered by the physician
 Administering medications per MD order:
 Oxygen, Morphine sulphate, Meperidine (Demerol),
Thrombolytic Therapy Streptokinase (Streptase),
Urokinase, and Tissue plasminogen activator (Activase)
Morphine Sulfate
 Narcotic Agonist, Analgesics, DOC of MI
 Used relieve pain
 To improve hemodynamics by reducing pre load and
afterload and promotes venous pooling of blood in the
Clinical Manifestations periphery
 Chest Pain (intense, heavy) Nursing Considerations
 Radiating chest pain that goes to left arm, jaw, back  Best taken with Food
 Unrelieved by nitroglycerin or rest (chest pain)  Report nausea and vomiting and respiratory depression
 Sweating (cold)  Keep Naloxone HCL (antidote) at the bedside
 Hard to breathe (shortness of breath)  Instruct the patient to lie down during IV administration
 Increased heart rate, blood pressure or irregular heart  Contraindicated to patient with pancreatitis
rate Meperidine (Demerol)
 Nausea with vomiting  Narcotic Analgesic
 Going to be anxious and scared  Has Vagolytic effect resulting to increase myocardial
Clinical Manifestations oxygen demand
 Shock – hypotension, tachycardia-bradycardia,  Negative pain
tachypnea, lethargy, cold skin and diaphoresis,  Avoid alcohol
peripheral cyanosis and weak pulse  Keep the antidote Naloxone hydrochloride
 Anxiety and Apprehension  Supine position – prevent hypotension
 Oliguria Thrombolytic Therapy
 Fever  Streptokinase (streptase), Urokinase, Tissue plasminogen
 Suffocation, dyspnea, orthopnea, gurgling or bubbling activator (activase)
respiration  It dissolves obstructing thrombus
Diagnostic Evaluations  Detect for occult bleeding during and after thrombolytic
ECG changes therapy
 Elevation of ST segment – results from injury area or  Assess neurologic status changes
Acute MI
Anti-Thrombotic Agents  Ends in “pril”
 Prevent formation of clot  Lisinopril, Ramipril, Enalapril, Captopril
 Lovenox and Heparin  It work by allowing more blood to get to the heart muscle
 Monitor for bleeding (assess gums of mouth, stool (dark  It does this by blocking the conversion of Angiotensin I or
tarry), drop in blood pressure and increase in heart rate, Angiotensin II
blood in urine Beta Adrenergic Blocking Agent
 Watch platelet count which may start to decrease after  Ends with “lol”
several days  Decrease myocardial oxygen demand by decreasing the
Anti-Platelet heart rate, bp, myocardial contractility and calcium
 It decreases platelets aggregation and thrombus output
formation  Propanolol, Atenolol, Metoprolol, Esmolol, Nadolol,
 It prevents platelet from clumping and blood clots from Pindolol, Timolol
forming Nursing Consideration (Beta Blockers)
 Aspirin (ASA), Plavix, Dypiridamole, Clopidogril  Assess the PR before giving the drug
 Watch for signs and symptoms of GI bleeding, and  Best taken with food
Thrombotic Thrombocytopenic Purpura (TTP)  Do not give to clients with asthma and DM patients
Nursing Considerations  Observe for SE: NV, Mental Depression, Mild Diarrhea,
 Watch for signs and symptoms of GI bleeding, especially fatigue, impotence
of patient has a history  Glucagon – antidote for beta blocker poisoning
 Assess for ss and sx of bleeding ARBS Angiotensin II Receptor Blockers
 Avoid straining of stool  End in “sartan” like Losartan, Valsartan
 ASA with food  It blocks angiotensin II receptor which causes vasodilation
 Observe for tinnitus, ASA toxicity  Monitor sodium, K, and blood pressure
 ASA may cause Bronchoconstriction Statins (“tins)
Anti-Coagulants  Simvastatin, atorvastatin
 It prevents blood clotting  Helps lower LDL, total cholesterol, triglycerides and
 Inactivates thrombin and other clotting factors inhibiting increase HDL
conversion of fibrinogen to fibrin  Educate not to replace diet and exercise
 Examples: Heparin, Coumadin  Notify doctor if they develop muscle pain or tenderness
Heparin Sodium  Monitor CPK (creatine kinase) levels if elevated
 Assess for signs of bleeding  Monitor liver function
 Keep protamine sulfate at the bedside Calcium Channel Blockers
 If administered SC, do not aspirate and massage the site  Norvasc, Cardizem, Verapamil (Isoptin, Calan),
of heparin injection Amlodipine, Nicardipine, Nifedipine, Diltiazem
 Monitor PTT or APTT levels  Stops the transport of calcium to the myocardium and into
 Used for maximum of 2 weeks smooth muscle which cause vasodilation on the coronary
Warfarin Sodium (Coumadin) arteries to improve oxygen demand and supple
 Assess for signs of bleeding  Monitoring heart rate, orthostatic hygiene
 Keep Vit K. Antidote if bleeding occurs in coumadin  Educate about good oral hygiene
therapy Nursing Considerations
 Monitor prothrombin time  Assess HR and BP
 Minimize green leafy vegetables in the diet  Monitor hepatic and renal function
 Don’t give ASA and coumadin together to prevent  Administer 1hr before or 2 hrs after meal
bleeding  Prepare Glucagon 0 antidote for calcium channel blocker
Nitroglycerine overdose
 Promotes venous and arterial relaxation of coronary Surgical Management
vessel and prevention of coronary spasm Percutaneous Transluminal Coronary Angioplasty
 Causes vasodilation and increases blood flow to the heart,  A balloon tip catheter is placed in a coronary vessel
hence better blood flow to the area experiencing narrowed by plaque
ischemia  The balloon is inflated and deflated to stretch the vessel
 Ointment, sublingual, IV, or oral “Imdur” and flatten the lesion
 Relief of chest pain
Nursing Considerations
 Best taken before any strenuous activity
 Place a tablet under the tongue at the first sign of chest
pain
 Burning sensation is a sign of potency of the drug. Facial
flushing is a side effect
 Do not chew the tablet
 Keep the tablets in dark container
 Monitor the BP and HR
Ace Inhibitors
 Blood flows freely through the unclogged vessel to the
heart
Intra Coronary Stent
 A diamond mesh tubular device is placed in the coronary
artery
 Prevents re-stenosis (after PTCA) by providing skeletal
support
Intra Coronary Atherectomy
 A blade tip catheter is guided in a coronary vessel to the
site of the plaque
 The plaque is cut, shave, or pulverized then removed
Coronary Artery Bypass Graft
 A graft is surgically attached to the aorta and the other
end of the graft id attached to a distal portion of a
coronary vessel
 By passes by obstructive lesion in the vessel and returns to
adequate blood flow to the heart muscle supplied by the
artery
Shock
 Condition results from some type of cause that leads to
decreased tissue perfusion resulting to cell or tissue
hypoxia
Types of Shock
Septic Shock
 Occurs due to severe infection
Hypovolemic Shock
 Occurs due too severe fluid loss
Neurologic Shock
 Occurs due to severe damage to the neuro system
Cardiogenic Shock
 Occurs due to a weak heart
 The heart doe not pump enough blood throughout the
body that decrease cardiac output and this leads to a
decrease tissue perfusion and oxygen supply to the
organs/tissue’s cells
 Extensive Damage of the left ventricle (40% or greater)
due to MI
 NOTE: In cardiogenic shock, it is not an issue with a loss of
blood volume like in some of the other types of shock.
Blood volume is normal.
Anaphylactic Shock
 Occurs due to an allergic reaction
Heart’s Role
 The heart is the pump of the body
 It takes blood to the right side of the heart that has been
used and depleted of oxygen by the cells of the body
and pumps it to the lungs
 The lungs oxygenate and remove carbon dioxide from
the blood and sends it back to the heart via its left side.
 The heart is the main center piece in the body that plays
a role in tissue perfusion
 In Cardiogenic Shock, cardiac output falls, which
decreases tissue perfusion and CO
Left Ventricle
 The main pumping chamber of the heart
 Shoots the fresh oxygenated blood into the aorta to the
whole parts of the body
Cardiac Output and Cardiogenic Shock
Cardiac Output
 The amount of blood the heart pumps per minute
 It ranges from 4-6 or 4-8 liters of blood per minute
 CO= SV x HR
Stroke Volume
 The amount of blood pumped from the left ventricle each
beat (50-100 mL)
 Stroke volume is determined by the preload, afterload,
and contractility of the heart
Preload
 The amount the ventricle stretches at the end of diastole
or the amount the ventricles stretch once their filled with
blood
Afterload
 The pressure the ventricle must pump against to squeeze
blood out
 It’s the force the heart has to pump against to get blood
out of the ventricle
Contractility
 Is how well the muscle cells are contracting
 It’s how well the heart id contracting to pump blood
  Will help remove extra fluid volume via the kidneys
Cardiac Index  Monitor I and O, and blood pressure
 This is a more specific cardiac output measurement based  Watch potassium level – it causes “hypokalemia)
in the patient’s body size
 It’s calculated by taking the cardiac output and dividing it Vasopressors
by the patient’s body surface area  Create a positive inotropic effect that increases the
 Patients with cardiogenic shock will have a CI (cardiac strength of the heart’s contraction and stroke volume
index) less than 2.2 L/min/m2  Dobutamine, Dopamine, Norepinephrine
 Normal CI: 2.5-4 L/min/m2 Norepinephrine
Causes of Cardiogenic Shock  It increases tissue perfusion by increasing blood pressure
 Acute MI and CO
 Pericardial tamponade Dobutamine
 Dysrhythmias  Increases contractility and cardiac output BUT can cause
 Myocarditis and endocarditis vasodilation
 Pulmonary edema Dopamine
 Valves and septal walls defects  Increases contractility, causes vasoconstriction increases
Pathophysiology blood pressure and MAP (<60 mmHg)
 Impaired contractility >>> reduction of cardiac
output >>> hypoperfusion (lack of blood and oxygen in Vasodilators
the heart and other organs) >>> Multiple Hypoxia  Nitropruside, nitroglycerine, phentolamine
Clinical Manifestations  Decrease preload and afterload
 Confusion, restlessness, mental lethargy  Improves CO
 Low systolic pressure and weak thread peripheral pulses  Decreases pulmonary congestion and left ventricular
 Oliguric phase pressure
 Decreased capillary refill, cool, pale, and clammy skin  Reduce myocardial oxygen consumption
 Dysrhythmias  Increase stroke volume
 Sinus tachycardia Digoxin (Lanoxin)
 Chest pain  Cardiac glycosides
 Dyspnea, tachypnea, cyanosis  Increase the contraction of the heart but decrease the HR
Diagnostic Test  Monitor the HR first before you give
 Elevated PAP, PCWP, and CVP pressure IV Fluids
 Chest x-ray pulmonary vascular congestion  Normal saline is used with extreme caution
 Elevated BUN, Crea Intra-Aortic Balloon Pump
Goals  A device placed to help improve coronary artery blood
 Reperfusion to the heart muscle flow and increase cardiac output
 Increase cardiac output  A catheter is inserted through a funeral artery up through
 Decrease fluid overload a section of the aorta. A balloon attached to the catheter
 Maintain oxygen status will inflate and deflate during systole (contraction) and
Nursing Interventions diastole (relaxation)
 Monitoring, assessing for signs of adequate tissue Pre-Operative Interventions
perfusion: mental status, blood pressure, heart rate,  Secure Consent
rhythm, urine output, skin color, and capillary refill, lung  NPO 6-8 hours post mid-night
sounds etc.  Stop taking any medicines
 Hemodynamic monitoring  Cardio Pulmonary Clearance – CBC, ECG, Chest x-ray
 Monitoring labs: high cardiac markers such as elevated and Echocardiogram
troponin, pulmonary edema on chest x-ray, During
echocardiogram, acid-base level  Under general anesthesia
 Monitor I and O, LOC and arrythmias  Monitor heart rate, blood pressure, and other vital signs
 Place patient in fowlers position  A small cut will be made through an artery in the upper
 Monitor blood pressure and MAP (greater than 60 mmHg) part of your inner thigh
 Auscultate lung field for abnormal sounds  A surgeon will advance the catheter to a part of the
 Reposition patient frequently to promote ventilation aorta in your chest region
 Monitor GCS and report changes immediately  The balloon will be programmed to inflate when your
Dependent heart relaxes. It will deflate when your heart contracts
 Administer oxygen as ordered  The end of the catheter will be secured
 Administer IV fluids Post Operative Care
 Administer medications as ordered  Stay on the pump for several days
 Diuretics, Vasopressors, Digoxin, Inotropic Drugs  The healthcare provider will monitor you and temporarily
turn the pump off to see the response
Diuretics  Evaluation of adequate timing oof balloon inflation and
 Furosemide deflation to assess the positioning of the intra-aortic
 To decrease pulmonary congestion balloon for kinking of the lungs
 To remove the pump, administer medicine to help you
relax, then remove the catheter and the attached balloon
and close up the incision on your leg

Mean Arterial Pressure (MAP)

 The pressure in your arteries during one cardiac cycle,
and it tells how well the vital organs are being perfused
 It is very important when calculating the cerebral
perfusion pressure
 Normal 70-100 mmHg