II & III. RR,CVS.ppt

Unit 2
Disorders of the Respiratory system
For 3rd year Bsc nursing students
P.By DelelegnT
1

Chapter objective
• At the end of this chapter students will be
able to identify and manage different
respiratory disorders
2

Enabling objective
• Overview anatomy and physiology of the
respiratory system
• Perform nursing assessment for patients’ with
respiratory system p/ms
• Discuss upper respiratory tract disorders
• Discuss lower respiratory tract disorders
3

Anatomic and physiologic overview of the
respiratory system
• The respiratory system is composed of the
upper and lower respiratory tracts
• Nose, sinuses, pharynx, tonsils, larynx &
trachea
=> upper respiratory airways
• Lung with Bronchial & alveolar structures
=> lower respiratory airways
4

 Trachea->bronchi->Lobar bronchi->segmental bronchi-
>subsegmental bronchi->bronchioles-> terminal
bronchioles
=>Conducting airways=physiologic dead space
 Respiratory bronchioles
=> Gas exchange airways
 ->Alveolar duct-> alveolar sacs->alveoli
5

 There are three types of alveolar cells.
 Type I alveolar cells are epithelial cells that form
the alveolar walls
 Type II alveolar cells are metabolically active.
These cells secrete surfactant, a phospholipid
prevents alveolar collapse
 Type III alveolar cell are large phagocytic cells;
act as an important defense mechanism.
6

Function of respiratory system
O2 transport
Respiration - gas exchange b/n atm. air and the
b/d and b/n the b/d and cells of the body
Ventilation - movement of air in and out of
airways
7

Air Pressure Variances
 lung volume -> pressure -> O2 to lung
(inspiration)
Airway resistant
 Determined size/diameter of airways
 ed resistance -> greater than normal respiratory
effort needed
8

Compliance
• Measure of elasticity, expandability and
distensibility of lung & thoracic structure.
• compliance -> lung elasticity lost & thoracic
stays overdistended e.g. emphysema
• compliance -> lung & thoracic are stiff
9

• e.g. pneumothorax, hemothorax, pleural
effusion, pulmonary edema, atelectasis,
pulmonary fibrosis, and acute respiratory
distress syndrome (ARDS)
10

Nursing assessment of patients with
respiratory problems
Common s/s
• Dyspnea,
• Orthopnea,
• cough, sputum production,
• chest pain, wheezing,
• clubbing of the fingers,
• hemoptysis, and cyanosis
11

Examples of skin color changes: the bluish tint of cyanosis
(left) and the yellow hue of jaundice (right)
12

P/E
Upper respiratory system
Inspect nose (external & internal)
Palpate frontal & maxillary sinuses
14

P/E…
• Palpate pharynx & mouth
• Palpate trachea- position/deviation & mobility
Lower respiratory system
1. Thoracic inspection
• Color, symmetry
• Configuration – Barrel chest eg emphysema
- Fennel chest
- Pigeon chest
- Kyphoscoliosis
15

• Breathing patterns & respiration rates
 Rate & depth
 Eupnea – respiration with regular depth & rhythm
- 12-18 bpm
 Bradypnea- slow breathing <10 bpm
 Tachypnea- rapid, shallow breathing >24 bpm
 Hyperpnea- increase depth of respiration
 Hypeperventlation- increase in depth & rate
16

• Hypoventilation - shallow, irregular breathing
• Kussmaul's respiration – Hypeperventlation
associated with severe acidosis of diabetic or
renal origin
• Apnea – cessation of breathing
17

 Cheyne-Stokes- Regular cycle where the rate
and depth of breathing increase, then decrease
until apnea (usually about 20 seconds) occurs.
 Biot's respiration - Periods of normal breathing
(3-4 breaths) followed by a varying period of
apnea (usually 10 seconds to 1 minute)
18

Thoracic palpation
 Tenderness
 Mass
 Lesion
 Respiratory excursion
o ed with chronic fibrotic disease
o Asymmetry with pleurisy, rib fracture,
trauma & unilateral bronchial obstruction
 Vocal fremitus
19

Thoracic percussion
Purpose
 To determine whether the underlying tissues are
filled with air, fluid or solid
 To estimate size & location of certain structures
(diaphragm, heart & liver)
Diaphragmatic excursion
 8-10 cm for tall people, 5-7 average
20

• ed with pulmonary effusion &
emphysema
• Pregnancy & acites => positioned
diaphragm high in the thoracic
21

Percussion Notes
SOUND RELATIVE
INTENSITY
RELATIVE
pitch
Relative
duration
Location
example
Examples
Flatness Soft High Short Thigh Large pleural
effusion
Dullness Medium Medium Medium Liver Lobar
pneumonia
Resonance Loud Low Long Normal lung Simple chronic
bronchitis
Hyperreson
ance
Very loud Lower Longer None
normally
Emphysema,
pneumothorax
Tympany Loud High* * Gastric air
bubble
or puffed-out
cheek
Large
pneumothorax
22

Thoracic auscultation
 Breath sounds
 Vesicular, bronchovesicular & bronchial
 Adventitious
 Crackle or rales, wheez
 Voice sounds
 Bronchophony, egophony & whispered
pectoreloquy
23

Pharyngitis
• Inflammation of throat, includes palate, posterior wall of
larynx & tonsil
• Acute & chronic
Acute pharyngitis
• Acute inflammation or infection in the throat, usually
causing symptoms of a sore throat
25

Etiology – 30%-60% viral origin
e.g. Adenovirus, rhino virus, parainfluenza virus
Bacteria: - Group A Beta Hemolytic
Streptococcus /GABHS/
- Hemophilus influenza
- Niesseria gonorhea
26

Pathophysiology
• Virus/bacteria colonize throat->Tissue damage ->
inflammatory response in the pharynx -> vasodilatation ->
edema in the tonsillar pillars, uvula, and soft palate->
fever -> pain and redness
• A creamy exudates may be present in the tonsillar pillars
• usually subside promptly within 3 to 10 days after the
onset If viral origin
27

C/M
• Abrupt onset of sever sore throat
• Red pharyngyeal membrane & tonsils
• Fever
• Swellen, palpable lymph node
• Enlarged tonsil & edematous
28

Viral Vs Bacterial Pharyngitis
Viral pharyngitis
 Mild sore throat
 Low grade fever
 Slight hyperemia
 No exudates
 No lymph adenopathy
Bacterial pharyngitis
 Severe sore throat
 High grade fever
 Malaise/fatigue, tender, cervical
lymph adenopathy
 Exudative, hoarsness & cough
29

Dx: Throat culture – rule out the cause
WBC- elevated in bacterial origin
Mgt:
 Bacterial pharyngitis if not treated leads to severe
complications
Supprative complications
 Peritonsilar abscess
 Retropharyngeal abscess
Non supprative complications
 Acute glomerular nephritis
 Acute rheumatic fever
30

Mgts include:
• Administration of antibiotics for bacterial pharyngitis
• Ampicillin 500mg QID
• Amoxicillin 300mg TID
• Benzathine penicillin single IM dose
• Erythromycin for penicillin resistant
• Cephalosporin for penicillin and erythromycin resistant
• Administered for at least 10 days
31

2. liquid & soft diet depending on
 patients appetite &
 degree of discomfort during swallowing
 In severe case IV fluid is administered
Chronic pharyngitis
 Common in adults who:
 Works in polluted areas, use voice to excess
 Suffer from chronic cough, use alcohol & tobacco
32

Three types of chronic pharyngitis are recognized:
• Hypertrophic: Thickening and congestion of the
pharyngeal mucous membrane
• Atrophic: The membrane is thin, whitish, glistening, &
at times wrinkled
• Chronic granular (“clergyman’s sore throat”):
characterized by numerous swollen lymph follicles on
the pharyngeal wall
33

Clinical Manifestations
 A constant sense of irritation or fullness in the throat,
 Collected mucus expelled by and
 Difficulty of swallowing
Mgt
 Avoiding exposure to irritants
 Correcting any respiratory or cardiac condition responsible
for a chronic cough
 Nasal sprays /ephedrine sulfate/ for congestion
34

Nursing care
• Infection control
• Symptomatic relieve
• Prevention of complication
• Warm saline gargle or irrigation to relieve throat
discomfort
35

Tonsillitis & Adenoiditis
Tonsillitis – Inflammation of palatine tonsil
Adenoiditis – Inflammation of pharyngeal tonsil
Cause – Virus & bacteria
C/M - sore throat
- Fever
- Snoring
- Difficulty of swallowing
- Otalgia
36

Enlarged adenoid may cause
 Mouth breathing
 Earache
 Foul smelling breath
 Voice impairment and noisy respiration
 Complicated to acute otitis media
37

Dx
 C/M
 Throat culture
 WBC
Rx: Ampcillin
Amoxicillin
Benzantine penicillin 2.4 IU IM stat
38

Peritonsillar abscess
 A peritonsillar abscess is a collection of purulent
exudate between the tonsillar capsule and the
surrounding tissues, including the soft palate.
 Develop after untreated streptococcal pharynitis &
an acute tonsillar infection, which progresses to a
local cellulitis and abscess.
39

C/M
• Severe sore throat
• Difficulty in swallowing
• Thickening of the voice
• Marked swelling of the soft palate to the
extent of occluding from half of the mouth to
pharynx
• Tissue b/n tonsil becomes infected
40

Mgt
1. Antibiotics
2. Incision & drainage
3. Tonsillectomy
 Antibiotics – Extremely effective
- Early Dx & Rx resolves abscess
 Incision & drainage
 Incision is made & abscess will drained.
 Pus aspiration is performed to decompress abscess.
41

Tonsillectomy
 Surgical removal of the tonsil
 Usually performed by resolution of abscess & infection
to enhance recovery
Indications:
Recurrent tonsillitis with documented streptococcal
infection 4 times in a year
Hypertrophy of tonsils with distorted speech
42

Tonsillar malignancy
Repeated attack of mastoditis
Tonsillitis as source of systemic disease
(rheumatic fever, acute glomerular nephritis)
Contraindications:
 Bleeding/coagulation disorder
 Uncontrolled systemic disease (DM,
Cardiac & renal disease)
43

Complications
1. Hemorrhage
2. Airway obstruction
3. Aspiration of blood & secretions to
respiratory tract
44

Laryngitis
 The larynx, or voice organ, is a cartilaginous
epithelium-lined structure that connects the pharynx
and the trachea.
 The major function of the larynx is vocalization
 Laryngitis is inflammation of the larynx.
Cause:
 Bacteria- group A streptococcus
 Viral- rhino virus, influenza & Para influenza viruses
 Voice abuse- overuse of voice or in singing or other
vocal activities.
45

C/M
• Severe cough
• Hoarseness
• Stride & dyspnea, if edema extends to
the vocal cord
46

Mgt
• Antibiotic if bacterial origin
• Voice rest
• Steam inhalation
• Absence of smoking
• Bed rest
• Parenteral steroids when edema causes
dyspnea & strider
47

Mgt…
• Majority of the cases recover with
conservative mgt
• However, if laryngitis tends to be more
severe may be complicated to
pneumonia
48

Lower respiratory tract infections
pneumonia
• Definition- an inflammatory process of the lung
parenchyma that is commonly caused by infectious
agents.
• Associated with marked increase in interstitial &
alveolar fluid
49

Classification of pneumonia
i. Depending on area where the infection
was acquired, pneumonia can be
 Community acquired pneumonia
 Hospital – acquired pneumonia
50

Classification cont’d
ii. Depending on the causative agent
 Bacterial (typical ) and atypical pneumonia
 Radiation pneumonia, which is caused after
radiation therapy
 Chemical pneumonitis, pneumonia after
ingestion of irritating gases, include aspiration
pneumonia
51

Classification cont’d
iii. Depending on the portion of lung
involved by pneumonia
– Lobar pneumonia - entire lobe
– Bronchopneumonia - alveoli adjacent to
bronchi
– Segmental or lobular pneumonia
– Interstitial pneumonia-Interstitial tissue
52

Etiology
For community acquired
1. Strep. pneumoniae
2. H. influenza
3. Mycoplasma pneumoniae
4. Chlamydia pneumoniae
 Viruses
 Influenza virus
 Cytomegalovirus
53

Etiology cont’d
• Fungi
– Histoplasmosis
– Aspergillus fumigates
For hospital acquired
• Gram negative bacilli
– Klebsiella, pseudomonas aeruginosa
– Escherichia coli.
– S. aurous
54

Etiology cont’d
• HIV associated
– Pneumocystis carinii
– M.tbc
– S. aurous
– H. Influenza
55

Predisposing factors for pneumonia include:-
• Preceding respiratory viral infections
• Alcoholism
• Cigarette smoking
• Underlying diseases such as Heart failure,
COPD
• Age extremes
• Immunosuppressive therapy and disorders
• Decreased consciousness, comma , seizure etc
• Surgery and aspiration of secretions
56

Pathophysiology
• Inflammation of alveoli
• Exudates formation interfere In movement of lung and
diffusion of O2 and Co2)
Additional air containing space are filled by WBC
(neutrophils)
• Mucosal edema and bronchial spasm result in occlusion
of bronchi or alveoli
• Arterial hypoxemia
57

Bacterial pneumonia
 The most common caused of bacterial
pneumonia is streptococcus pneumoniae
 It is Prevalent
 During the winter and spring when upper
respiratory infection are most frequent
 In all age group
 Occur as lobar or bronchopneumonia
58

• Atypical pneumonia syndrome
– Pneumonia associated with mycoplasm,
Chlamydia, PCP, viruses and fungus are
included in atypical pneumonia syndrome
59

Clinical manifestation
• For community acquired pneumonia(Typical &
atypical)
– typical CAP
– Sudden onset of fever, with single shaking chills
– Productive cough
– Difficulty of breathing (SOB)
60

– Respiratory grunting
– Pleuritic chest pain (stabbing type of chest pain
_ aggravated by breathing and coughing
– Use of accessory muscles for respiration
– Commonly caused by s. pneumonia but H.
influenza
61

Atypical pneumonia
 Symptom varies depending on the organism
 Mainly patients have hidden upper respiratory
tract infection (nasal congestion, sore throat)
 Gradual onset
 Dry cough
62

 SOB but predominantly extra pulmonary
symptoms i.e
Headache
Low grade fever
Pleuritic pain
Myalgia
Rash and pharngitis
63

 After few days mucoid or mucopurulent sputum
expectorated.
 Types of sputum depending on micro-organisms
Pneumococcal, staphylococcal and
streprotococeal infection result in rusty, blood
tinged sputum
Klebsiella result with green sputum
H. Influenza , with green sputum
64

Nasocominal /Hospital acquired
• It occurs after 48 hrs of admission or with
in 2 weeks after discharge from the hospital
65

Diagnostic evaluation
 History
 P/E
 Use of accessory muscle
 Chest retraction
 In pediatric age group
 Chest in drawing
 Tachypnea
 25 to 5 respiration /mint
66

–Sing of consolidation
• Dullness
• Tactile fremitus
• Egophony ( E changed to a sound)
• BBS, rales
67

Indication for admission
1. Age
2. Co -existing conditions
 Neoplastic disease
 CHF
 CVD
 Renal disease
 Liver disease
68

3. If abnormality in P/E
 Altered mental status
 Pulse >140/min
 R/R > 28/mi
 SB/P < 90/mmhg
 To < 350C and > 400C
69

– Hypoxemia (arterial PO2 < 60mm Hg) while
breathing room air or O2 saturation < 90 %
– Multilobar pneumonia
– Pneumonia caused by St. aureus or Gram
negative bacilli
– Failure of Outpatient treatment
– Inability to take oral medication or persistent
vomiting 70

Medical treatment
 For community acquired pneumonia treat as
outpatient other than admission indication, for
hospital acquired pneumonia admission is
needed.
 Rx for Bacterial pneumonia for strep
pneumonia
 Cry penicillin 3million IU every four hr.
 3rd generation cephalosporin
 Co-trimoxazole 960mg po bid
71

 For H. Influenza
 Amoxicillin 500 mg po tid
 Ampicillin 500 mg po qid
 Erythromycin 500 mg po qid
 For Atypical pneumonia
 Doxycycline 100 mg po bid for 03 weeks
clyndamycin
 Nasocominal
 Gentamycin 80mg IV bid for 14 dys
 Cloxacillin 500 mg IV bid for 10 days.
72

• In HIV
• PCP. Co-trimoxazol 4 tab po bid patient
improves with in 3-5 days then prophylaxis
2 tab po daily. Contnu with prophlaxsis
73

Complication
• Bacterial
– Shock, pleural effusion
– Lung abscess, empyema, otitismedia,
meningitis
• Atypical
– Hypotension, shock
– ARF, respiratory failure.
74

Acute Bronchitis /
trachiobronchitis
– Acute Bronchitis :- Is a common acute
inflammation of the mucous membrane lining the
inside of the bronchi
– Often follows infections of the upper respiratory
tracts and often occurs in person with chronic
lung disease.
75

• Causes
– Bacteria (common) Streptococcus pneumonia
» Hemophiles influenza
– Virus
– Chemical and smoke irritants also can cause
inflammation
76

Phathophysiology
• Colonization of bacteria to the bronchi
• Inflammation of bronchi
As inflammatory progress there is increased
blood flow to the bronchi
• Causing an increase in pulmonary secretions
• (so goblet cell produces mucus) 77

C/F
• Initially
– Dry, irritating cough
– Scanty amount of mucoid sputum
– Sternal soreness (middle of the neck, upper
chest pain)
• As the infection become severe, noisy (strider)
• Purulent sputum which is more profuse
78

• General symptom and sign of infection may
present.
– fever (low grade)
– Malaise
• Symptoms may continue for 3 to 4 weeks but
usually lasts with in 1 to 2 weeks (in viral
cases)
79

• P/E
– Rhonchi and
– Wheezes are heard on chest examination
• Inspection for sign of pneumonia is important,
b/c it can progress in to pneumonia.
80

• Cheek for sign of pneumonia
• Chest movement change
• Air entry change
• Percussion note change
• Pleuritic chest pain and rapid respirations rales
(crackles) or sign consolidation on P/E
81

Dx Evaluation
• Hx and P/E
• Chest x - ray to R/O pneumonia
• Management
• Rx
– At OPD
– Return if shortness of breath gets worse
(pneumonia or B. asthma)
82

– Co-trimoxazole 960 mg po bld for 7 days
– Amoxicillin 500 mg po TID for 7 days
– TTC and doxycycline are alternative
(mycoplasma pneumonia suspected case)
83

Analgesics
• Acetaminophen 500 mg of 2 tab po QID ibuprofen
400 mg po BID
• Hot remedies
• Nursing care
• Encourage removal of secretions by coughing
• Encourage up
• Discourage over exertion 84

Obstructive Airways Disease
85

Obstructive Airway Disease
Asthma
Explosion in
research
Revolution in
therapy
COPD
Little research
(? neglect)
Few advances in
therapy
86

Chronic Obstructive Disease
• Chronic bronchitis
• Emphysema
87

Bronchial Asthma
A chronic inflammatory disorder
characterised by hyperreactive airways
leading to episodic reversible
bronchoconstriction
88

Causes
• Exact cause is unknown. But the following are
predisposing factors:
1. Genetic predisposition or familial tendency
 History of allergy, rhinitis
E.g. seasonal allergens /pollen green/
non seasonal allergens / dusts, food moulds,
animal dander/
2. Drugs: NSAID & beta blockers
89

Predisposing factor…
3. Environmental and air pollution
4. Occupational factors
5. Infection
6. Exercise
7. Emotional stress
90

Classification
• Allergic
• Non allergic
• Mixed asthma
91

pathopysiology
Allergic asthma
 Exposure to allergens
 Type I hypersensitivity reaction
 B-lymphocytes produce IgE
 Attach to mast cells
 Histamine secretion
o Muscle spasm
o Mucosal inflammation/edema
o Excessive mucus secretion
=>airway narrowing
92

Pathopysiology…
Non allergic asthma
Nerve endings of airways stimulated by:
 Infection
 Exercise parasympathetic nervous
 Cold air system activated & release Ach
 Emotion bronchoconstrictor
96

C/F
Common symptoms
 Cough
 Dyspnea
 Wheeze
 others like cyanosis, tachypnea, tachycardia
 Attack lasts 3 minute to several hours
97

P/E:
• Respiratory distress, tachypnea, tachycardia, audible
wheeze
• Dehydration
• Prolonged expiration, high pitched wheeze throughout
inspiration & most of expiration
• Cyanosis, confused & lathergy => respiratory failure
• More reliable symptoms are dyspnea at rest, cyanosis
& difficulty of speaking/use of accessory muscles
98

Diagnostic evaluation
1. Complete history
2. Chest x-ray: hyperinflation & flattened diaphragm
during attack
3. Arterial blood gas: hypoxemia during attack
4. P/E: wheezing & hyprerresonance on percussion
99

Management
Objective:
1. Prevent death from severe airway obstruction
2. Restore best level of activity & optimal lung function
3. Manage acute exacerbation
100

Drugs for treatment of asthma
Two categories
1. Drugs that inhibit smooth muscle contraction
2. Drugs that prevent or reverse inflammation
101

Mgt…
1. Drugs that inhibit smooth muscle contraction
A. Beta agonists
• Initial treatment
• Relax bronchial smooth muscle
• Increase ciliary movement
• Decrease secretion of chemical mediators
102

Mgt…
• Salbutamol every 20 minute 3 doses
• Adrenaline 0.2ml for children & 0.3 ml for adult once
or twice every 20-30 minutes
B. Metylxanthines
• Relax bronchial smooth muscles
• Increase ciliary movement
• Increase contraction of diaphram
103

Cont’d…
• E.g. Aminophylline 250 mg IV diluted in dextrose in
water slowly over 10 -15 minutes once.
• Theophylline po but not acute attack /slow onset/
104

Mgt…
• If the patient does not respond to single dose of
aminophylline IV, then the patient should be
admitted and managed as in-patient
Criteria for admission
• HR> 120bpm
• RR>30bpm
• Use of accessory muscles on respiration
105

Mgt…
• Cyanosis
• Unconscious
• Silent chest
• Paradoxical movement of chest and abdomen
• Pneumothorax, atelectasis…
• Unable to finish a sentence with single breath
• PaO2 < 60mmHg & Sa O2 <90%
• Pa Co2 > 42mmHg
106

Cont’d…
• Aminophylline 1mg/kg/hr in continious IV infusion
• Hydrocortisone 4mg/kg/4hrs IV
C. Anticholinergics
e.g. Atropin: broncho-dilator but limited due to side
effects.
107

2. Drugs that reverse inflammation
A. Glucocorticoides
e.g. Hydrocoritisone IV, Prednisolone po
B. Mast cell stabilizing agents
e.g. Cromolyn Na: a spray that decrease release of
histamine
108

Complications of asthma
• Pneumothorax
• Atelectasis due to obstruction
• Corpulmonale due to chronic hypoxemia and
pulmonary hypertension
• Respiratory failure
 Status asthmaticus
109

Status asthmaticus
• Severe life threatening asthma that does not respond
to usual treatment of asthma and lasts longer than
24 hrs.
Causes - viral infection
- ingestion of aspirin
- extreme anxiety
- increased environmental pollution
- abrupt discontinuation of drug therapy.
110

C/F
Similar to uncomplicated asthma but more
severe and prolonged
 Extreme anxiety
 Fear of sufocation or asphyxiation
 Severely increased work of breathing
 Diaphorosis
111

Mgt
• Initially treat with beta agonist drugs &
corticosteroids
• O2 therapy
• Iv fluid for hydration
• Antibiotics to prevent secondary infection
112

Chronic Obstructive Pulmonary
Disease
113

Why COPD is important?
• COPD is the only chronic disease that can show
upward trend in both mortality and morbidity
• It is expected to be the 3rd leading cause of death by
2020
114

Disease Trajectory of a Patients with
COPD
Symptoms
Exacerbations
Exacerbations
Exacerbations
Deterioration
End of Life
115

Other names of COPD
• Chronic Obstructive Lung Disease /COLD
• Chronic Obstructive Airway Disease /COAD
• Chronic Airflow Limitation /CAL
116

New Definition
• Chronic obstructive pulmonary disease (COPD)
is a preventable and treatable disease state
characterized by airflow limitation that is not
fully reversible.
• The airflow limitation is usually progressive and
is associated with an abnormal inflammatory
response of the lungs to noxious particles or
gases, primarily caused by cigarette smoking.
• Although COPD affects the lungs, it also
produces significant systemic consequences.
117

Definition…
• The inflammatory response in the larger airways is
chronic bronchitis, which is diagnosed clinically
when people cough up sputum
• In the alveoli, the inflammatory process causes
destruction of tissue of the lung, called emphysema
118

Definition…
• The natural course of COPD is characterized by
sudden worsening of symptoms called acute
exacerbations, most of which are caused by
infections or air pollution
119

Risk factors
• Cigarette smoking
• Air pollution
• Increasing age
• Infection and
• deficiency of a1 antitrypsin
120

Pathophysiology of COPD
• Increased mucus production and reduced mucociliary
clearance - cough and sputum production
• Loss of elastic recoil - airway collapse
• Increase smooth muscle tone
• Pulmonary hyperinflation
• Gas exchange abnormalities - hypoxemia and/or
hypercapnia
121

Key Indicators for COPD Diagnosis
Chronic cough Present intermittently or every day
often present throughout the day;
seldom only nocturnal
Chronic sputum production Present for many years, worst in
winters. Initially mucoid – becomes
purulent with exacerbation
Dyspnoea that is Progressive (worsens over time)
Persistent (present every day)
Worse on exercise
Worse during respiratory infections
Acute bronchitis Repeated episodes
History of exposure to risk
factors
Tobacco smoke ,occupational dusts
and chemical smoke from home
cooking and heating fuel
122

Physical signs
• Large barrel shaped chest
(hyperinflation)
• Prominent accessory
respiratory muscles in neck
and use of accessory
muscle in respiration
• Low, flat diaphragm
• Diminished breath sound
123

Chronic Bronchitis
 Chronic inflammation of the bronchi or bronchioles
caused by chronic exposure to irritants, especially
tobacco smoke
 Also defined as the presence of chronic productive
cough on most days for 3 months of at least 2
successive years
124

Pathophysiology
 Pathophysiologic changes in the lung consists:
 Hyperplasia of mucus secreting glands in the
trachea and bronchi
 Increase in number of goblet cells
 Disappearance of cilia
 Chronic inflammatory changes and narrowing
of small airways
125

Cont’d…
 Greater resistance to airflow increases work of
breathing
 Hypoxemia and hypercapnia develop more
frequently in chronic bronchitis than empysema
 Altered function of alveolar macrophages leading to
increased bronchial infection
126

C/F
• Frequent productive cough
• Frequent respiratory infection
• Dyspnea on exertion
• Hypoxemia and bluish color of skin from cyanosis
and polycythemia/bone marrow produce large
amount of RBC/
127

Normal vs. Chronic Bronchitis
128

Emphysema
• Abnormal permanent enlargement of air
spaces distal to the terminal bronchiole,
accompanied by destruction of their wall
without obvious fibrosis.
129

Classification
1. Panlobular (panacinar)- destruction of the entire
alveolus uniformly
2. Centrilobular (centriacinar)
 opening occurs in the bronchioles and
 allow space to develop as tissue wall break down
 seen in long stand smokers
3. Paraseptal or distal acinar confined only in the
alveolar ducts and alveolar sacs.
- Forms bullae and often affects the upper half of
the lungs
130

Loss of surface area (emphysema)
134

Pathophysiology
• Structural changes are
1. Hyper inflation of alveoli
2. Destruction of alveolar wall
3. Destruction of alveolar capillary wall
4. Narrowed tortuous
5. Loss of lung elasticity
135

C/F
• Dyspnea - progressive
• Minimal coughing with no/small amount of sputum
• Hypoxemia
• Marked increase in AP diameter
136

As disease advances….
Pa O2 leads to:
• Dyspnoea and increased respiratory rate
• Pulmonary vasoconstriction (and pulmonary
hypertension)
137

Mgt of COPD
Management strategies are
 Smoking cessation
 Vaccination
 Drug therapy with inhalers
 Rehabilitation
 Some patients may require Long Term Oxygen
Therapy/ LTOT
 Lung transplantation
138

COPD classification based on spirometry
Severity Post
bronchodilator
FEV1/FVC
Post bronchodilator
FEV1% predicted
At risk >0.7 >80
Mild COPD <0.7 >80
Moderate COPD <0.7 50-80
Severe COPD <0.7 30-50
Very severe
COPD
<0.7 <30
139

Pharmacotherapy for Stable COPD
Bronchodilators
• Short-acting b2-agonist
– Salbutamol
• Long-acting b2-agonist -
Salmeterol and Formoterol
• Anticholinergics –
Ipratropium, Tiiotropium
• Methylxanthines -
Theophylline
Steroids
• Oral – Prednisolone
• Inhaled - Fluticasone,
Budesonide
140

Post-bronchodilator
FEV1
(% predicted)
Management based on GOLD
141

How Do Bronchodilators Work?
• Reverse the increased
bronchomotor tone
• Relax the smooth muscle
• Reduce the hyperinflation
• Improve breathlessness
142

definition
• A localized area of destruction of lung
parenchyma in which infection by pyogenic
organisms results in tissue necrosis &
suppuration .

• Necrosis with multiple micro abscesses
form a larger cavitary lesion (less than
2cm in diam)

Lung Abscess - Classification
• May be primary or secondary
• Primary = abscess in previously healthy
patient or in a patient at risk for aspiration
• Secondary = associated bronchogenic
neoplasm or immunocompromised patient.

Etiology
• Aspiration of Oropharyngeal flora
 Dental/Periodontal sepsis
 Paranasal sinus infection
 Depressed conscious level
 Disturbances of swallowing
 Delayed gastric emptying

Etiology
• Necrotizing pneumonia
 Staph aureus
 Klebsiella pneumoniae
 Pseudomonas aeruginosa

Etiology
• Hematogenous spread from a distal site
 UTI
 Abdominal sepsis
 Pelvic sepsis
 Infective endocarditis
 Infected IV cannulae
 Septic thrombophlebitis

Etiology
• Pre existing lung disease
 Bronchiectasis/abnormal permanent
dilation of bronchial tubes/
 Cystic fibrosis
 Bronchial obstruction : tumor, foreign
body, congenital abnormality

Pathology
• Most often as a complication of aspiration pneumonia
• Oral anaerobes
• “Typical patient” is predisposed to aspiration due to
compromised consciousness ( alcoholism, drug abuse, general
anesthesia) or dysphagia
• Periodontal disease, especially gingivitis, with concentrations of
bacteria in the gingival crevice as high as 1011/mL

… pathology
1. Inoculum from gingival crevice reach lower airways -
while the patient is in the recumbent position.
2. Pneumonitis arises first but progresses to tissue
necrosis after 7-14 days.
3. Necrosis results in lung abscess and/or
 An empyema/collection of pus in natural cavity/
- can be due to a bronchopleural fistula or direct
extension of infection into the pleural space

… pathology
• Lung abscesses begin as areas of pneumonia on
which small zones of necrosis ( microabscesses )
develop within consolidated lung.
• Some of these areas coalesce to form single /
sometimes multiple areas of suppuration and when
they reach a size of 1 -2 cm dia – abscess.
• If the natural history of this pathological process is
interupted at an early stage by an appropriate
antimicrobial , then healing may be complete with no
residual radiographic evidence of damage.

… pathology
• If treatment is delayed / inadequate , the
inflammatory process may progress , entering a
chronic phase.
• Abscesses arising as a result of aspiration usually occur
close to visceral pleural surface in dependent parts of
lungs.
• ¾ ths of lung abscesses occur in posterior segment of
right upper lobe or apical segment of either lower
lobes,
• Those d/t haematogenous spread can occur in any
part of lungs

Clinical Features - Symptoms
• The presenting features of lung abscess vary
considerably .
1. Symptoms progress over weeks to months
2. Fever, cough, and sputum production
3. Night sweats, weight loss & anemia
4. Hemoptysis, pleurisy

Clinical Features - Signs
• Digital clubbing – develop within a few weeks
if treatment is inadequate.
• Dullness to percussion
• Diminished breath sounds if abscess is too
large and situated near the surface of lung.

diagnosis
1. CXR, CT scan
2. Gram stain: both +ve &-ve, mixed
3. AFB & Anaerobic culture
4. Transtracheal aspirates (TTA), transthoracic needle
aspirates (TTNA), pleural fluid, or blood cultures
allow uncontaminated specimens
5. Bronchoscopy

Differential diagnosis
• Cavitating lung cancer
• Localized empyema
• Infected congenital pulmonary lesions
• Pulmonary haematoma
• Hiatus hernia

Treatment – antibiotic therapy
1. Ampi / Amoxicillin x orally
2. Cry.penicillin & clindamycin +/-
metronidazole IV – in hospitalised pts.
3. Can change – according to sensitivity

Duration of treatment
• Some advocate 4-6 weeks
• Most treat until radiographic abnormalities
resolve , generally requiring months of
treatment

Surgical intervention
1. Surgery rarely required
2. Indications: failure of medical management,
suspected neoplasm, or hemorrhage.
3. Predictors of poor response to antibiotic therapy
alone: abscesses associated-with an obstructed
bronchus, large abscess (>6 cm in diameter),
relatively resistant organisms, such as P.
aeruginosa.
4. The usual procedure in such cases is a
lobectomy or pneumonectomy

Treatment cont’d…
1. Alternative for patients who are considered
poor operative risks is percutaneous
drainage.
2. Bronchoscopy- may be done as a diagnostic
procedure, especially to detect an
underlying lesion, but is of relatively little
use to facilitate drainage

Delayed response to treatment
Consider:
1. Wrong microbial diagnosis
2. Obstruction with a foreign body or neoplasm
3. Large cavity size (>6 cm) which may require
unusually prolonged therapy or empyema
which necessitates drainage
4. Non-infectious causes - pulmonary infarcts

complications
1. Empyema
2. Bronchopleural –fistula
3. Pneumothorax
4. Metastatic cerebral abscess
5. Sepsis
6. Fibrosis, bronchiectasis,amyloidosis

Unit Three
Disorders of the Cardio-Vascular
System

A. Cardiac disorders
1. congestive heart failure (CHF)
• Heart failure - is the inability of the heart to pump
sufficient amount of blood to meet the needs of the
tissues for oxygen and nutrients

• CHF - a fluid overload condition (congestion)
• May or may not be caused by HF;
• An acute presentation of HF with increased
amount of fluid in the blood vessels
• Not diagnosed;
• Diagnosed for example, as CHF precipitated
by HTN 2o to myocardial infraction

CHF…
• Heart failure can be;
• Systolic heart failure: reduced cardiac
contractility or,
• Diastolic heart failure: impaired cardiac
relaxation and abnormal ventricular filling

Causes
A. Intrinsic cause (underlying); like
1. Myocardial cause
• Acute myocardial infraction/AMI
• Dilated cardiomyopathy
• Restrictive cardiomyopathy
• Myocarditis

Causes…
2. Valvular causes
• Congenital valular heart disease
• Rheumatic fever
• Infective endocarditis
3. Pericardial cause
• Pericarditis/constrictive pericarditis
• Pericardial tamponade /fluid in the
pericardium/

B. Precipitating causes
HEART FAILES
H- Hypertension (systemic)
E- Endocarditis (infections)
A- Anemia
R- Rheumatic fever and myocarditis
T- Thyrotoxicosis and pregnancy
F- Fever (infections)
A- Arrhythmia
I- infarction (myocardial)
L- Lung infection
E- Embolism (pulmonary)
S- Stress (emotional, physical, environment, dietary, fluid excess)

Pathophysiology
• CO => tissue perfusion => stress to the
tissue/hypoxia => stimulate sympathetic nervous
system => release epinephrine(E) & nor epinephrine
(NE) =>
• E is peripheral vasoconstrictor => b/d flow to
vital organ
• NE increase HR/increase cardiac contractility/

P. physiology…
• CO => BP => b/d flow to kidney => rennin
release => Ang I => Ang II
• Aldostrone release => Na & H2O retention
• Potent vasoconstriction => BP( vascular vol.)

Body compensation mechanisms for HCF
Two mechanisms
1. Systemic compensation
A. Sympathetic Nervous System /SNS
B. Rennin – Angiotensin – Aldosterone - System
/RAAS
C. Anaerobic respiration
2. Cardiac compensatory mechanism
• Dilation => Cardiomegally
• Hypertrophy

C/F
• Based on C/F CHF can be classified in to 3
o Right sided heart failure/RHF
o Left sided heart failure/LHF or
o Both
LHF- Peripheral hypoxia
- Cyanosis
- Dyspnea: progressive
- Orthopnea
- Cough
- Paroxysmal nocturnal dyspnea/PND
- Tachycardia
- Tachypnea
175

RHF
• Hepathomegally
• Splenomegally
• Ascietes
• Leg edema
• Distended neck vein
• Increased jugular venous pressure
176

Heart Failure Symptom Classification
Grade Symptoms
I No symptom limitation with ordinary physical
activity
II Ordinary physical activity somewhat limited by
dyspnea (i.e., long distance walking, climbing 2
flights of stairs)
III Exercise limited by dyspnea at mild workloads
(i.e., short distance walking, climbing one flight
of stairs)
IV Dyspnea at rest or with very little exertion
177

Dx
• Hx
• P/E
• Chest x-ray: size & shape of heart
• Echocardiography:
 valvular abnormalities,
 ventricular dysfunction,
 cardiac temponade,
 pericardial constriction, and
 pulmonary embolus
• Electrocardiogram (ECG): cardiac rhythm &
conduction
178

Management
• Identify and treat the underlying cause
• Treat the precipitating factors
• Control the congestive state
179

Pharmacologic Rx
A. Drugs with positive inotropic effect
B. Drugs without positive inotropic effect
180

A. Drugs with positive inotropic effect
Force of contraction of the heart muscle => CO
Includes:
1. Cardiac glycosides
e.g. digoxin
Action – increase force of myocardial contraction
- increase cardiac output
Side effect: bradycardia, heart block, arrhythmia
GI disturbance
Rx of toxicity: mild decrease dose of digoxin
severe discontinue digoxin
181

2. Beta - adrenergic stimulants
e.g. dobutamine, dopamine
• Increase in myocardial contractility by beta
stimulants increase the cardiac out put
3. Methylxanthines,
e.g. Aminophylline
• Has a bronchodilating effect and a modest effect
on renal blood flow.
• Indication patients with acute left ventricular
failure associated with pulmonary edema
182

B. Drugs without positive inotropic effect
Includes:
1. Diuretics
e.g. hydrochlorothiazide - for mild CHF
furosemide – for severe CHF
Action: fluid volume by decreasing fluid & salt
retention.
so decrease edema and its symptom.
183

2. Vasodilators
e.g. hydralazine, sodium nitroprusside
Action: Dilation of systemic vessels
Preload by venous dilation
After load by arterial dilation
i.e. work load on heart
184

3. Angiotensin converting enzyme inhibitors e.g.
captopril, enalapril
Action: peripheral resistance / decrease after load
H2O and salt retention / decrease preload
185

Nsg mgt
• Input & output monitoring
• Monitoring Weight gain
• Auscultating lung sounds at least daily to
detect an increase or decrease in
pulmonary crackles
• Determining the degree of JVD
• Identifying and evaluating the severity of
dependent edema
186

• Monitoring PR & BP
• Examining skin turgor and mucous membranes for
signs of dehydration
• Assessing symptoms of fluid overload (eg. orthopnea,
paroxysmal nocturnal dyspnea, and dyspnea on
exertion)
• Monitoring and managing potential complications like
digitalis toxicity and hypokalemia
• Digoxin immune FAB (Digibind) quickly decreases the
amount of available digoxin
187

Long -term Mgt of chronic heart failure:
Modify cardiovascular risk factors
Nonmodifiable risk factors like:
o Family history of coronary artery disease
o Increasing age
o Gender (men and postmenopausal women)
o Race (Africa American)
188

…Modifiable risk factors:
o Hyperlipidemia
o Hypertension
o Cigarette smoking
o Elevated blood glucose level (i.e., DM)
o Obesity
o Physical inactivity
o Use of oral contraceptives
189

2. Rheumatic fever/RF
 An inflammatory disease affecting
 Joints
 CNS
 Heart
 Skin
 Subcutaneous tissues
 The only severe complication occurs in the heart
 Rheumatic heart disease/RHD is the
complication of RF
190

Pathophysiology
Onset follows throat infection (pharyngitis &
tonsilitis) by group A streptococci
The mechanism is elusive, but the followings
are proposed ones:
1. Dysfunction of the immune Response
2. Antigenic Mimicry
191

• Molecular similarity between some streptococcal
antigens and of human myocardial cells
• Streptococci => Ag-Ab reaction /autoimmune
complex/ in valves and myocardium
• Contracture of valves => two way b/d flow =>
heart disease
192

C/F
Joint pain after throat infection
Fever
Major sign
1. Migratory poly arthritis:
 Involves many joints at a time
 The larger joints are mainly affected
2. Carditis:
 Mitral & aortic valves affected more
 Murmur, Tachycardia, Palpitation ,
Cardiomegally
 CHF, Pericarditis & Valvulitis
193

3. Sydenham's Chorea:
 characteristic movement disorder
 Sydenham’s chorea consists of rapid
purposeless movements of the face and
upper extremities
4. Erythma marginatum
 macular, well demarcated rash
5. Subcutaneous nodules
 Non tender swelling on the extensor surfaces
of wrists, elbows, and knees
194

Minor signs
Arthralgia
Non specific tests indicated inflammation
o ESR
o C- reactive protein
o Leucocytosis
Anemia
Prolonged PR & QT intervals
positive throat culture
o ASO titer (Antistreptolysin “O” titer)
195

Dx
2 major criteria
1 major & 2 minor criteria
Rx
Antibiotics: penicillin / benzyl penicillin or
erythromycin
To eradicate the residual bacteria
Aspirin for inflammation, fever & pain
o 1st Rx pharyngitis & tonsilitis
o 2nd Rx RF before heart is damaged
o 3rd if heart damaged difficult to Rx
196

3. Infective endocarditis
Infective endocarditis is an infection of the valves
and endothelial surface of the heart
Caused by micro organisms leading to:
1. thickening of the leaflets result is leakage,
valvular regurgitation
2. Adhesion of inflamed margins of the valve
leaflets, valvular stenosis
197

Intracardiac effects are:
severe valvular insufficiency, which may lead to
o Intractable congestive heart failure &
o Myocardial abscesses
198

Classification based on type of valve affected
1. Native valve endocarditis (NVE):
2. Prosthetic valve endocarditis: when develops
on prosthetic/’artificial’ valve
3. Endocarditis in intravenous drug abuser
(IVDA)
199

Based on clinical course of IE has been classified as
Acute IE: frequently involves healthy valves.
It is a rapidly progressive illness with destruction of
valvular structures
Subacute IE: affects only previously damaged valves
Insidious even untreated
200

Etiologic agents
• Bacteria: strepto,pneumono, entro &
staphylo cocci
• Fungus
• Rickettsiae
201

Risks factors
• In a person who have Hx of valvular disease
• Person with rheumatic heart disease
• Mitral valve prolapse
• Individuals with prosthetic valve surgery
202

Pathophysiology
IE development of commonly shares:
1. Bacteremia (nosocomial or spontaneous)
that delivers the organisms to the valve's
surface
2. Adherence of the organisms to valvular
structures
3. Eventual invasion of the valvular leaflets and
formation of vegetations
203

C/F
Non specific sx
Fever, fatigue, anorexia, back pain, and weight loss
Cardiac manifestations
 Murmur due to vegetations
 Cardiomegally
 evidence of CHF
 Transient ischemia
204

Emboli manifestations
• Lung – recurrent pneumonia
• Kidney – hematuria, renal failure
• Spleen – left upper quadrant pain
• Heart- myocardial infraction
• Brain – cerebrovascular accident/shock
205

Dx
1. Blood Culture :
gold standard test for the Dx of IE is the
documentation of a continuous bacteremia (>30
min in duration) through blood culture
Dx SBE draw 3-5 sets of blood cultures , at 3
different sites , over 24 hours.
For acute IE, 3 sets may be drawn over 30 minutes
206

2. Echocardiography
 The diagnosis of IE can never be excluded
by a negative echocardiogram.
3. Other Tests:
ECG: increasing P-R interval.
Rheumatoid factor: becomes positive for
most of suacute cases
207

Major Criteria
1. Positive blood culture:
2. Positive echocardiogram:
• Definitive vegetation
• Abscess
• New partial dehiscence of prosthetic
valve
• New valvular regurgitation
208

Minor Criteria
• Predisposition: predisposing heart condition or IV drug
abuse
• Fever >38 oC
• Embolic phenomena:
• Immunologic phenomena:
glomerulonephritis, Osler's nodes,
Roth's spots, rheumatoid factor
• Microbiologic evidence: positive blood
culture but not meeting major criterion.
• Echocardiogram: consistent with IE but
not meeting major criterion
209

Definitive Diagnosis can be made by:
 Two major criteria or
 One major and three minor criteria or
 Five minor criteria allows a clinical
diagnosis of definite endocarditis.
210

Mgt
NVE of sub acute nature:
• Crystalline penicillin 3-4 million IU IV every 4
hrs for 4- 6 wks plus
• Gentamicin 1mg/kg ( 80 mg ) IV TID for 2 wks
Prosthetic Valve endocarditis:
• Vancomycin 1gm IV BID for 6 wks Plus
• Gentamicin 1mg/kg ( 80 mg ) IV TID for 2 wks
plus
• Refampicin 300 mg PO /TID for 6 weeks
211

Acute IE where S.aureus is suspected:
• Naficillin 1.5-2gm IV every 4 hrs OR
Vancomycin 1gm IV BID for 6 wks Plus
• Gentamicin 1mg/kg (80 mg) IV TID for 2 wks
212

• Diet: Na-restriction if CHF
• Activity: limit activity level if stroke & CHF
213

 Surgical valve replacement
Indication for Surgery:
• Fungal endocarditis
• Mobile vegetation > 10mm in size
• Evidence of myocardial abscess
• Recurrent embolization despite adequate
antibiotics
• Poor response to antibiotics
• Prosthetic valve dysfunction associated with CHF
214

4. Pericarditis
• Definition :- Inflammation of the pericardium,
the membranous sac enveloping the heart
• Pericardial inflammation
• Accumulation of exudates (in pericardial cavity)
• Reduced cardiac output & edema due to
congestion
215

Cause
1. idiopathic
2. Infection
Bacterial
Viral
 Coxsackia
 Influenza
Mycotic funfal
216

3. Connective tissue disorder
 Rheumatoid arthritis
 Polyarthrits
4. Hypersensitivity
 Immune rxn
 Drug rxn
217

5. Disease of the adjacent structure
 Myocardial infarction
 Dissecting aneurysm
 Pleural and pulmonary disease (pneumonia)
6. Neoplastic disorder
To metastasis from lung cancer
 To metastasis from breast cancer
 Leukemia (abnormal 4es in WBC
218

7. Trauma
Chest injury
Cardiac surgery
indwelling cardiac catheterization
Pacemaker implantation
8. Tuberculosis
219

C/F
1. Pain
Beneath the clavicle, to left sternum
Neck, epigastric area
Scapular, arm, back
Pain is Aggravated by
Inspiration , turn in bed, twisting the body
During swallowing, coughing
220

2. Friction rub: due to loss of their lubricating fluid
Relieved by
 Sitting up position
3. Dyspnea
 Pt may appear extremely ill
 Pt may have fever and a friction rub
only while pt- is severely ill
221

Dx
• Clinically
– Hx
– P/E
• ECG To confirm the diagnosis
• Echo
222

Mgt
Objective
1. To determine the cause
2. To administer therapy for the specific cause
3. To be alert for cardiac tamponade (compression
of the heart)
223

• Bredrest (when cardiac out put is impaired
• Analgestics
• Corticosteroid
• Be alert to the possibility of cardiac tamponade
• Antimicrobial agent depending on the cause
224

225
– Rheumatic fever
– Tuberculosis
– Fungal
• Penicillin
• Anti TB
• Amphotercin B

Complication
o Pericardial effusion - cardiac tamponade
Nursing care
Relief the pain, bed rest or chair rest
Recording the medication taken
 Antibiotic
 Corticosteroid
 Analgestics
Assess pt condition if there is a
pericardocentesis procedure
226

Conduction system of heart
• Cardiac conduction cells:
• generate and coordinate the transmission of electrical
impulses to the myocardial cells
• Atrioventricular contraction; optimizing cardiac output
• 3 physiologic characteristics of the cardiac conduction
cells:
• Automaticity/initiate an electrical impulse,
• Excitability/respond to an electrical impulse
• Conductivity/transmit an electrical impulse
227

Sinoatrial (SA) node
• primary pacemaker of the heart
• has an inherent firing rate of 60 to 100 impulses per
minute/normal resting heart/
• Conduct impulse along the myocardial cells causing the
electrical stimulation/depolarization and subsequent
contraction/atrial systole
• then conduct to the atrioventricular (AV) node
229

AV node
• Coordinates the incoming electrical impulses from the
atria and relays to the ventricles
• This impulse is then conducted through a bundle of
specialized conduction cells (bundle of His) that travel in
the septum separating the left and right ventricles
• Has an inherent firing rate of 40 to 60 impulses/min.
230

Bundle of His
• divides into the right & left bundle branch
• left bundle branch bifurcates into the left anterior and left
posterior bundle branches
• Impulses travel through the bundle branches to reach the
terminal point in the conduction system, called the Purkinje
fibers
• myocardial cells are stimulated/ventricular contraction
231

• The heart rate is determined by the myocardial cells
with the fastest inherent firing rate
• Under normal circumstances, the SA node has the
highest inherent rate, the AV node has the second
highest inherent rate (40 to 60 impulses per minute),
and the ventricular pacemaker sites have the lowest
inherent rate (30 to 40 impulses/ min)
232

• If the SA node malfunctions, the AV node takes
over the pacemaker function of the heart at its
inherently lower rate.
• If both the SA and the AV nodes fail in their
pacemaker function, a pacemaker site in the
ventricle will fire at an inherent bradycardic rate of
30 to 40 impulses per minute.
233

Dysrhythmias/arrhythmia
• disorder of the formation or conduction (or both)
of the electrical impulse within the heart
• Altering the heart rate, heart rhythm, or both and
potentially causing altered blood flow
234

• P wave represents atrial muscle depolarization
• It is normally 2.5 mm or less in height and 0.11 second or less in duration
• PR interval is measured from the beginning of the P wave to the
beginning of the QRS complex and represents the time needed for sinus
node stimulation, atrial depolarization, and conduction through the AV
node before ventricular depolarization.
• Normally ranges from 0.12 to 0.20 seconds in duration
235

• QRS complex represents ventricular muscle depolarization
• Not all QRS complexes have all three waveforms.
• The first negative deflection after the P wave is the Q wave, which
is normally less than 0.04 second in duration and less than 25% of
the R wave amplitude; the first positive deflection after the P wave
is the R wave; and the S wave is the first negative deflection after
the R wave.
236

• When a wave is less than 5 mm in height,
small letters (q, r, s) are used; when a wave is
taller than 5 mm, capital letters
• (Q, R, S) are used.
• The QRS complex is normally less than 0.12
second in duration

• T wave represents ventricular muscle
repolarization (resting state)
• It follows the QRS complex and is usually the
same direction as the QRS complex
238

• U wave-represent repolarization of the
Purkinje fibers
• Also seen in patients with hypokalemia,
hypertension, or heart disease
• Follows the T wave and is usually smaller than
the P wave
239

• ST segment - early ventricular
repolarization, from the end of the QRS
complex to the beginning of the T wave
240

• QT interval-the total time for ventricular depolarization
and repolarization
• measured from the beginning of the QRS complex to
the end of the T wave.
• The QT interval is usually 0.32 to 0.40 seconds in
duration if the heart rate is 65 to 95 beats per minute
241

• TP interval is measured from the end
of the T wave to the beginning of the
next P wave
242

• PP interval is measured from the beginning of one
P wave to the beginning of the next.
• used to determine atrial rhythm and atrial rate.
• The RR interval is measured from one QRS complex
to the next QRS complex
• Used to determine ventricular rate and rhythm
243

Normal Sinus Rhythm
• Normal sinus rhythm occurs when the
electrical impulse starts at a regular rate and
rhythm in the sinus node and travels through
the normal conduction pathway.
• The following are the ECG criteria for normal
sinus rhythm :
245

• Ventricular and atrial rate: 60 to 100 in the adult
• Ventricular and atrial rhythm: Regular
• QRS shape and duration: Usually normal,
• P wave: Normal and consistent shape; always in front
of the QRS
• PR interval: Consistent interval between 0.12 and
0.20 seconds
• P: QRS ratio: 1:1
246

Types of Dysrhythmias
• Dysrhythmia can be originated from
• sinus node,
• atria,
• atrioventricular node / junctional, &
• ventricle
247

A.Sinus dysrhythmia
1. Sinus Bradycardia
• When SA node generate slower-than-normal rate
Causes
• lower metabolic needs (sleep, athletic training,
hypothermia, hypothyroidism),
• Vagal stimulation, medications
• Increased intracranial pressure,
• Myocardial infarction (MI),
248

Characteristics:
• Similar to normal sinus rhythm except rate (<60 bpm)
Mgt: prevent Vagal stimulation. withhold medication
• That can cause bradycardia
• Atropine, 0.5 to 1.0 mg rapid IV bolus, is the medication of
choice in treating sinus bradycardia
249

2. Sinus Tachycardia
• when SA node generate faster-than-normal rate
Cause
• acute blood loss, anemia, shock, congestive heart
failure, pain, fever, exercise, anxiety
• All aspects of sinus tachycardia are the same as those
of normal sinus rhythm, except for the rate(100-
180bpm)
250

Mgt
• Avoid the cause
• Ca channel blockers & beta blockers
e.g. propranolol drug of choice to decrease HR
251

…B. ATRIAL DYSRHYTHMIAS
1. Atrial Flutter
• Atrial flutter occurs in the atrium and creates impulses at
an atrial rate between 250 and 400 times per minute
• Because the atrial rate is faster than the AV node can
conduct, not all atrial impulses are conducted into the
ventricle, causing a therapeutic block at the AV node.
252

Characteristics:
• Ventricular and atrial rate: Atrial rate ranges
between 250 and 400; ventricular rate usually
ranges between 75 and 150
• Ventricular and atrial rhythm: The atrial rhythm is
regular; the ventricular rhythm is usually regular
but may be irregular because of a change in the AV
conduction.
253

• QRS shape and duration: Usually normal, abnormal
or may be absent
• P wave: Saw-toothed shape.
• These waves are referred to as F waves.
• PR interval: Multiple F waves may make it difficult to
determine the PR interval.
• P: QRS ratio: 2:1, 3:1, or 4:1
254

2.Atrial Fibrillation
• Causes a rapid, disorganized, and uncoordinated
twitching of atrial musculature
• It is the most common dysrhythmia that causes
patients to seek medical attention.
• It may start and stop suddenly.
• Atrial fibrillation may occur for a very short time
(paroxysmal), or it may be chronic.
255

• Causes: advanced age, valvular heart disease, coronary
artery disease, hypertension, CHF, cardiomyopathy,
hyperthyroidism, pulmonary disease, moderate to heavy
ingestion of alcohol (“holiday heart” syndrome)
• Sometimes it occurs in people without any underlying
Pathophysiology (termed lone atrial fibrillation).
256

Characteristics
• Rate: Atrial rate is 300 to 600.
Ventricular rate is usually 120 to 200
• Rhythm: Highly irregular
• QRS shape and duration: Usually normal, but may be abnormal
• P wave: No visible P waves; irregular undulating waves are seen
and are referred to as fibrillatory or f waves
• PR interval: Cannot be measured
• P: QRS ratio: many:1
257

Rx
• Direct toward decreasing the atrial irritability
& decreasing rate ventricular response
• Decrease risk of embolism
• Drugs: Digoxin
Anticoagulant
258

JUNCTIONAL DYSRHYTHMIAS
1. Junctional Rhythm
• Occurs when the AV node, instead of the sinus node, becomes
the pacemaker of the heart.
• When the sinus node slows or when the impulse cannot be
conducted through the AV node (eg, because of complete
heart block), the AV node automatically discharges an impulse
259

Characteristics:
• Rate: Ventricular rate 40 to 60;
Atrial rate 40 to 60
• Rhythm: Regular
• QRS shape and duration: Usually normal, but may be
abnormal
• P wave: May be absent, after the QRS complex, or
before the QRS; may be inverted
260

• PR interval: If P wave is in front of the QRS, PR
interval is less than 0.12 second.
• P: QRS ratio: 1:1 or 0:1
• Junctional rhythm may produce signs and
symptoms of reduced cardiac output.
• Treatment is the same as for sinus bradycardia
261

VENTRICULAR DYSRHYTHMIAS
1.Ventricular Tachycardia (VT)
• Due to myocardial irritability
• Associated with coronary artery disease
• Need medical emergency
 VT has the following characteristics:
• Rate: Ventricular rate is 100 to 200 beats per minute;
• Rhythm: Usually regular
• QRS shape and duration: Duration is 0.12 seconds or more;
bizarre, abnormal shape
262

• P wave: Very difficult to detect, buried in QRS
complex
• PR interval: Very irregular, if P waves seen.
• P: QRS ratio: Difficult to determine, but if P waves
are apparent, there are usually more QRS
complexes than P waves.
263

Rx:
• Cardioversion - apply an electrical current to
terminate dysrhythmia
264

2.Ventricular Fibrillation
• A rapid but disorganized ventricular rhythm that
causes ineffective quivering of the ventricles.
• There is no atrial activity seen on the ECG
• No audible heart beat
• No palpable pulse =>cardiac arrest or death may occur
265

Characteristics:
• Ventricular rate: Greater than 300 per minute
• Ventricular rhythm: Extremely irregular, without
specific pattern
• QRS shape and duration: Irregular, undulating
waves without recognizable QRS complexes

Rx:
• Defibrillation - depolarize all myocardium at once
- allow SA node to restore as apace maker
267

Conduction abnormalities
1. First-Degree Atrioventricular Block
• Occurs when all the atrial impulses are conducted
through the AV node into the ventricles at a rate
slower than normal.
characteristics:
• Ventricular and atrial rate: Depends on the underlying
rhythm

• Ventricular and atrial rhythm: Depends on the underlying
rhythm
• QRS shape and duration: Usually normal, but may be abnormal
• P wave: In front of the QRS complex; shows sinus rhythm,
regular shape
• PR interval: Greater than 0.20 seconds; PR interval
measurement is constant.
• P: QRS ratio: 11

2. Second-Degree Atrioventricular Block
a. Type I
• Occurs when all but one of the atrial impulses are conducted
through the AV node into the ventricles.
• Each atrial impulse takes a longer time for conduction than the
one before, until one impulse is fully blocked.

Characteristics:
• Ventricular and atrial rate: Depends on the underlying rhythm
• Ventricular and atrial rhythm: The PP interval is regular if the
• patient has an underlying normal sinus rhythm; the RR interval
characteristically reflects a pattern of change. Starting from
the RR that is the longest, the RR interval gradually shortens
until there is another long RR interval.
• QRS shape and duration: Usually normal, but may be
abnormal

• P wave: In front of the QRS complex; shape depends on
underlying rhythm
• PR interval: PR interval becomes longer with each succeeding
• ECG complex until there is a P wave not followed by a
• QRS. The changes in the PR interval are repeated between
each “dropped” QRS, creating a pattern in the irregular PR
interval measurements.
• P: QRS ratio: 32, 43, 54, and so forth

b. Type II.
• Occurs when only some of the atrial impulses are conducted
through the AV node into the ventricles.
Characteristics:
• Ventricular and atrial rate: Depends on the underlying rhythm
• Ventricular and atrial rhythm: The PP interval is regular if the
patient has an underlying normal sinus rhythm.

• QRS shape and duration: Usually abnormal, but
may be normal
• P wave: In front of the QRS complex; shape depends
on underlying rhythm.
• PR interval: PR interval is constant for those P
waves just before QRS complexes.
• P: QRS ratio: 21, 31, 41, 51, and so forth

2. Third-Degree Atrioventricular Block
• Occurs when no atrial impulse is conducted through the AV node into
the ventricles.
• In third-degree heart block, two impulses stimulate the heart:
• One stimulates the ventricles (eg, junctional or ventricular
escape rhythm), represented by the QRS complex, and
• One stimulates the atria (eg, sinus rhythm, atrial fibrillation),
represented by the P wave.

• P waves may be seen, but the atrial electrical activity is not
conducted down into the ventricles to cause the QRS
complex, the ventricular electrical activity.
• This is called AV dissociation. Complete block (third-degree
AV block) has the following

Characteristics:
• Ventricular and atrial rate: Depends on the escape and
underlying atrial rhythm
• Ventricular and atrial rhythm: The PP interval is
regular and the RR interval is regular; however, the PP
interval is not equal to the RR interval.
• QRS shape and duration: Depends on the escape
rhythm; in junctional escape

• QRS shape and duration are usually normal,
• and in ventricular escape, QRS shape and duration
are usually abnormal.
• P wave: Depends on underlying rhythm
• PR interval: Very irregular
• P: QRS ratio: More P waves than QRS complexes

Coronary vascular Disease
Angina pectoris
• A clinical syndrome usually characterized by
episodes or paroxysms of pain or pressure in the
anterior chest
Occurs when myocardial oxygen demand exceeds the
supply
Cause
• Insufficient coronary blood flow due to atherosclerosis
Risk factors for atherosclerosis
- Alcohol - Obesity
- Cigarette - Physical inactivity
- oral contraceptive pills
280

Precipitating factors
• Physical exertion – increase myocardial O2 demand
• Exposure to cold – increase BP, increase O2 demand
• Eating heavy meal – increase b/d flow to mesenteric area
• Stress or emotion - increase BP, increase myocardial workload
281

Canadian Cardiovascular Society
Classification of Angina
CLASS ACTIVITY EVOKING ANGINA LIMITS TO ACTIVITY
I Prolonged exertion None
II Walking >2 blocks Slight
III Walking <2 blocks Marked
IV Minimal or rest Severe
282

Types
• Stable angina: predictable and consistent pain that occurs on
exertion and is relieved by rest
• Unstable angina: symptoms occur more frequently and last
longer than stable angina. The threshold for pain is lower, and
pain may occur at rest.
• Intractable or refractory angina: severe incapacitating chest
pain
• Variant angina: pain at rest with reversible ST-segment
elevation; thought to be caused by coronary artery vasospasm
• Silent ischemia: objective evidence of ischemia by ECG, but
patient reports no symptoms
283

C/M
• Pain – ischemic death or myocardial deaths
• Varying in severity from
• a feeling of indigestion to a choking or heavy
sensation in the upper chest
• ranges from discomfort to agonizing pain
• accompanied by severe apprehension and
a feeling of impending death

Cont…
• Commonly in the chest behind upper or
middle 3rd of the sternum
• Poorly localized; radiate to neck, jaw,
shoulder and inner aspect of upper
extremities

Cont…
• Pain is accompany by tightness, choking,
weakness and numbness in the arms, wrist and
hands and also shortness of breath, pallor,
diaphoresis, dizziness or lightheadedness, and
nausea and vomiting.

Dx
• Hx or c/m of ischemia
• Exercise-stress test, then ECG, echocardiogram
• Blood laboratory evaluation
 Increase C-reactive protein - a marker for inflammation
 Increase Homocysteine - toxic to endothelium

Medical Management
• Objective – to decrease oxygen demand of the
myocardium and to increase oxygen supply
• Especially supply is increased by pharmacologic
therapies and demand will be decreased by
decreasing risk factors

1. Pharmacologic
a. Nitroglycerine dilate vein & arteries,
decrease b/d return
b. Beta adrenergic blockers e.g. propranolol
decrease [HR, BP& myocardial contractility];
decrease O2 demand

Cont…
c. Ca channel blockers e.g. Nifedipine
• increase O2 supply by relaxing smooth muscles of
coronary artery and by decreasing systemic arterial
pressure
290

Problem Magnitude
• Hypertension(HTN) is the most
common primary diagnosis in
America.
• 35 million office visits are as the
primary diagnosis of HTN.
• 50 million or more Americans have
high BP.
• 7.1 million deaths per year may be
attributable to hypertension.

Definition
• A systolic blood pressure ( SBP) >139
mmHg and/or A diastolic (DBP) >89
mmHg.
• Based on the average of two or more
properly measured, seated BP readings.
• At least two measurements should be
made and the average recorded.
• On each of two or more office visits.

….Accurate Blood Pressure Measurement
• The equipment should be regularly inspected and validated.
• The operator should be trained and regularly retrained.
• The patient must be properly prepared and positioned and
seated quietly for at least 5 minutes in a chair.
• Caffeine, exercise, and smoking should be avoided for at
least 30 minutes before BP measurement.
• An appropriately sized cuff should be used.

Recommended for Follow-up Based on Initial
BP Measurements for Adults
INITIAL BLOOD PRESSURE (mm Hg)*
Systolic Diastolic FOLLOW UP RECOMMENDED†
<130 <85 Recheck in 2 years
130–139 85–89 Recheck in 1 year
140–159 90–99 Confirm within 2 months
160–179 100–109 Evaluate or refer to source of
care with in 1 month
>180 >110 Evaluate or refer immediately

Classification of BP for Adults Age 18
and Older
CATEGORY SYSTOLIC (mm Hg) DIASTOLIC
(mm Hg)
Normotensive Optimal <120 <80
Normal <130 <85
High-normal 130–139 85–89
Hypertension‡
Stage 1 140–159 90–99
Stage 2 160–179 100–109
Stage 3 ≥180 ≥110

Prehypertension
• SBP >120 mmHg and <139mmHg and/or
• DBP >80 mmHg and <89 mmHg.
• Prehypertension is not a disease category
rather a designation for individuals at high risk
of developing HTN.

Pre-HTN
• Individuals who are prehypertensive are not
candidates for drug therapy but Should be firmly and
unambiguously advised to practice lifestyle
modification
• Those with pre-HTN, who also have diabetes or
kidney disease, drug therapy is indicated if a trial of
lifestyle modification fails to reduce their BP to
130/80 mmHg or less.

Isolated Systolic Hypertension
• Not distinguished as a separate entity as far as
management is concerned.
• SBP should be primarily considered during
treatment and not just diastolic BP.
• Systolic BP is more important cardiovascular
risk factor after age 50.
• Diastolic BP is more important before age 50.

Hypertensive Crises
• Hypertensive Urgencies: No progressive
target-organ dysfunction. (accelerated
Hypertension)
• Hypertensive Emergencies: Progressive end-
organ dysfunction. (malignant Hypertension)

Hypertensive Urgencies
• Severe elevated BP in the upper range of
stage II hypertension.
• Without progressive end-organ dysfunction.
• Examples: Highly elevated BP without severe
headache, shortness of breath or chest pain.
• Usually due to under-controlled HTN.

Hypertensive Emergencies
• Severely elevated BP (>180/120mmHg).
• With progressive target organ dysfunction.
• Require emergent lowering of BP.
• Examples: Severely elevated BP with:
 Hypertensive encephalopathy
 Acute left ventricular failure with pulmonary edema
 Acute MI or unstable angina pectoris
 Dissecting aortic aneurysm

…Types of Hypertension
• Primary HTN:
also known as essential
HTN.
• accounts for 95%
cases of HTN.
• no universally
established cause
known.
• Secondary HTN:
less common cause
of HTN (5%).
• secondary to
other potentially
rectifiable causes.

Complications of Prolonged Uncontrolled HTN
• Changes in the vessel wall leading to vessel trauma
and arteriosclerosis throughout the vasculature
• Complications arise due to the “target organ”
dysfunction and ultimately failure.
• Damage to the blood vessels can be seen on
fundoscopy.

Target Organs
• CVS (Heart and Blood Vessels)
• The kidneys
• Nervous system
• The Eyes

Effects On CVS
• Ventricular hypertrophy, dysfunction and failure.
• Arrhithymias
• Coronary artery disease, Acute MI
• Arterial aneurysm, dissection, and rupture.

Effects on The Kidneys
• Glomerular sclerosis/hardning/ leading to impaired
kidney function and finally end stage kidney disease.
• Ischemic kidney disease especially when renal artery
stenosis is the cause of HTN

Nervous System
• Stroke, intracerebral and subaracnoid hemorrhage.
• Cerebral atrophy and dementia

The Eyes
• Retinopathy, retinal hemorrhages and impaired
vision.
• Vitreous hemorrhage, retinal detachment
• Neuropathy of the nerves leading to extraoccular
muscle paralysis and dysfunction

Goals of Treatment
• Treating SBP and DBP to targets that are <140/90 mmHg
• Patients with diabetes or renal disease, the BP goal is <130/80
mmHg
• The primary focus should be on attaining the SBP goal.
• To reduce cardiovascular and renal morbidity and mortality

Benefits of Treatment
• Reductions in stroke incidence, averaging
35–40 percent
• Reductions in MI, averaging 20–25 percent
• Reductions in HF, averaging >50 percent.

Lifestyle Changes Beneficial in Reducing Weight
• Decrease time in sedentary behaviors such as
watching television, playing video games, or
spending time online.
• Increase physical activity such as walking,
biking/riding bicycle/, aerobic dancing, tennis,
soccer, basketball, etc.
• Decrease portion sizes for meals and snacks.
• Reduce portion sizes or frequency of consumption
of calorie containing beverages.

ANEURYSM
o Localized sac or dilation formed in the wall of arteries
1. AORTIC ANEURYSM
 Classified by its shape or form
 Most common forms are saccular/sac/ or fusiform
 A saccular aneurysm projects from one side of the
vessel only
 A fusiform aneurysm entire arterial segment
becomes dilated
 It’s serious because it can rupture leading to
hemorrhage and death

Characteristics of arterial aneurysm
 False aneurysm
 True aneurysm
 Fusiform aneurysm
 Saccular aneurysm
 Dissecting aneurysm

Causes of aneurysm formation
• Congenital
• Mechanical
• Traumatic
• Inflammatory (noninfectious)
• Infectious
• Pregnancy-related degenerative
• Graft aneurysms

A. THORACIC AORTIC ANEURYSM
• 85% of cases caused by atherosclerosis.
• Common in men between the ages 40 and 70 years.
• The most common site for a dissecting aneurysm.
• About 1/3 of patients die from ruptured aneurysm.
 Pain- common
 dyspnea
 cough
 hoarseness
 stridor
 Complete loss of the voice (aphonia)
 dysphagia

Diagnostic Findings
• C/F - Superficial veins become dilated, edematous areas
on the chest wall, cyanosis
• Chest x-ray
• CT
Medical Management
 Mostly treated by surgical repair/vascular graft
 Controlling blood pressure and correcting risk factors

B. ABDOMINAL AORTIC ANEURYSM
• The most common cause is atherosclerosis
• Affects men 4 times more than women and is
most prevalent in elderly patients
• Occur below the renal arteries
• If untreated, eventual outcome may be
rupture and death.

• About 2/5 of patients are symptomatic
• Patients can feel their heart beating in their abdomen
when lying down, or
• They may say we feel an abdominal mass
• Vascular obstruction, if associated with thrombus

Diagnostic Findings
• A pulsatile mass in the middle & upper
abdomen
• Duplex ultrasonography or CT is used to
determine it’s size, length, and location
Management
• Surgery - for abdominal aneurysms wider
than 5 cm or those that are enlarging

Venous Disorders
a. Venous thrombosis/phlebothrombosis
b. Thrombophlebitis
c. Varicose vein
a. Venous thrombosis/phlebothrombosis
Cause: Unknown
Risk factors:
• Stasis of blood (venous stasis),
• Vessel wall injury, &
• Altered blood coagulation
At least two of the factors seem to be necessary for thrombosis to occur.
b. Thrombophlebitis:
• Formation of a thrombus frequently accompanies
thrombophlebitis, an inflammation of the vein walls

In Deep Vein Thrombosis
• The entire extremity becomes massively swollen, tense,
painful, & cool to the touch
• Edema and swelling of the extremity because of inhibited
outflow of venous blood
• Tenderness, upon gently palpation due to inflammation
• Homans’ sign (pain in the calf after the foot is sharply
dorsiflexed)
In Superficial Veins
• Pain or tenderness, redness, and warmth in the involved
area
• Risk of emboli is very low because most of them dissolve
spontaneously

Prevention
 It’s preventable, if risks are identified and preventive
measures are instituted early
Measures include:
• application of elastic compression stockings or use of
intermittent pneumatic compression devices
• Special body positioning and exercise.
• Administration of subcutaneous unfractionated or low
molecular weight heparin

Medical Management
1. Anticoagulation Therapy
a. Unfractionated Heparin:
• S/C or intermittent/continuous IV infusion for 5 to 7 days
• Warfarin (po) are administered with heparin therapy
b. Low-Molecular-Weight Heparin (LMWH):
• has longer half-life, and given in one or two S/C
injections/day
• Associated with fewer bleeding complications than
unfractionated heparin
2. Thrombolytic Therapy:
• Lyses and dissolve thrombus in 50% of patients.
• Given within the first 3 days after acute thrombosis.
• Beyond 5 days after onset, it’s significantly less effective

Surgical management
• A thrombectomy (surgical removal of the thrombosis)
• If :
 medical mgt is contraindicated
 danger of pulmonary embolism is extreme, or
 venous drainage is severely compromised

VARICOSE VEINS
• Varicose veins (varicosities):- abnormally dilated,
tortuous/twisting/, superficial veins
• Most commonly occurs in the lower extremities
• Most common in people whose occupations require
prolonged standing
• Leg veins dilate during pregnancy because of increased
pressure by the gravid uterus, and increased blood volume

Pathophysiology
• Hereditary weakness of the vein wall may contribute to
the development of varicosities
• Varicose veins may be primary (without involvement of
deep veins) or secondary (resulting from obstruction of
deep veins)
• A reflux/backward flow/ of venous blood in the veins
results in venous stasis.

• Dull ache, muscle cramps, and increased muscle fatigue in
the lower legs
• Ankle edema and a feeling of heaviness of the legs
• Signs and symptoms of chronic venous insufficiency:
edema, pain, pigmentation, and ulcerations due to deep
venous obstruction.
• Increased susceptibility to injury and infection

. Assessment and Diagnostic Findings
• Duplex scan-documents the anatomic site of reflux and provides
a quantitative measure of the severity of valvular reflux
• Air plethysmography measures the changes in venous blood
volume
• Venography is visualizing anatomy of veins by injecting an x-ray
contrast agent through X-ray studies

Prevention
• Avoid activities that cause venous stasis
• Changing position frequently, elevating the legs
• Encourage walking; 1 or 2 miles each day if not
contraindicated
• Swimming

Medical Management
SCLEROTHERAPY
• In sclerotherapy, a chemical is injected into the vein, irritating
the venous endothelium and producing localized phlebitis
and fibrosis.
Surgically;
• After the vein is ligated, an incision is made and a metal or plastic
wire is passed the full length of the vein to the point of ligation.
• The wire is then withdrawn, pulling the vein as it is removed.

Myocardial infarction
A. General information:
1. The death of myocardial cells from inadequate
oxygenation, often caused by a sudden complete blockage of
a coronary artery; characterized by localized formation of
necrosis (tissue destruction) with subsequent healing by scar
formation and fibrosis.
2. Risk factors:
- atherosclerotic CAD - DM
- thrombus formation - hypertension

Cont…
B. Assessment findings:
1. Pain same as in angina, crushing, viselike with sudden
onset; UNRELIEVED by rest or nitrates
2. nausea/vomiting, dyspnea
3. skin: cool, clammy, ashen
4. elevated temperature
5. initial increase in BP and pulse, with gradual drop in BP
6. Restlessness

Cont…assessment finding
7. Occasional findings: rales or crackles; presence of S4; pericardial
friction rub; split S1, S2
8. Diagnostic tests:
a. elevated WBC, cardiac enzymes (troponin, CPK-MB, LDH,
SGOT)
b. ECG changes (specific changes dependent on location of
myocardial damage and phase of the MI; inverted T wave and
ST segment changes seen with myocardial ischemia
c. increase ESR, elevation serum cholesterol

Cont’d….
C. Nursing interventions:
1. establish a patent IV line
2. provide pain relief; morphine sulfate IV (poor
peripheral perfusion, false + for enzymes)
3. Administer O2 as ordered to relieve dyspnea and
prevent arrhythmias
4. Provide bed rest with semi fowler’s position
5. Monitor ECG and hemodynamic procedures
6. Administer anti-arrhythmias as ordered.

Cont….
7. Monitor I & O, report if UO <30 ml/hr
8. Maintain full liquid diet with gradual increase to soft, low
salt
9. Maintain quiet environment
10. Administer stool softeners as ordered
11. Relieve anxiety
12. Administer anticoagulants, thrombolytics (streptokinase)
as ordered and monitor for S/E

Cont…
13. Provide client teaching and discharge instruction
concerning
- effects of MI, healing process and treatment regimen
- Medication regimen: name, purpose, schedule, dosage, S/E
- Risk factors with necessary lifestyle modification
- Dietary restrictions: low salt, low cholesterol, avoidance of
caffeine
- Resumption of sexual activity as ordered (usually 4-6weeks)

- Need to report the ff. symptoms:
* increased persistent chest pain
* pain, dyspnea, weakness, fatigue
* persistence palpitations, light headedness
- Enrollment of client in a cardiac rehabilitation program

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