Disturbances in Oxygenation

Components involved in OXYGENATION

 Heart
 Lungs
 Red Blood Cells
 Blood Vessels
 Anatomy and Physiology Review
 Heart
 cone-shaped hollow
muscular organ
located in the
mediastinum
between the lungs
 Pumps about
60ml/beat or
5L/min
 Pericardium –
protective covering
of the heart
Anatomy and Physiology Review
 3 layers of cardiac muscle tissue:
 Epicardium– outermost layer
 Myocardium – middle layer
 Endocardium – innermost layer
 Anatomy and Physiology Review
 Chambers
 Right
atrium (0-5
mmHg)
 SVC, IVC, Coronary
sinus
 Right Ventricle
(25 mmHg)
 Left atrium
 Left ventricle
 Valves
 AV valves
 Semilunar valves
 Anatomy and Physiology Review
 Coronary arteries
 Left Coronary Artery
 Left anterior descending – LV, Ventricular septum,
chordae tendinae, papillary muscle, RV (lesser extent)
 Circumflex coronary artery – LA, lateral & posterior
surfaces of LV, portion of interventricular septum, SA
node, AV node
 Right Coronary Artery
 RA, RV, inferior portion of LV

Branching pattern of the

coronary arteries varies
considerably among individuals
Anatomy and Physiology Review
 Electrophysiologic Properties of the Heart
 Automaticity
 initiate an impulse spontaneously & repetitively
 Excitability (depolarization)
 respond to a stimulus
 Conductivity
 Transmit electrical impulses
 Contractility
 Contract

 Refractoriness
 Inability to respond until repolarization
The CONDUCTING SYSTEM OF THE HEART
Consists of the
 1. SA node- the pacemaker
 2. AV node- slowest conduction
 3. Bundle of His – branches into the Right
and the Left bundle branch
 4. Purkinje fibers- fastest conduction
Anatomy and Physiology Review
 Conduction
System of the
Heart
 SA node (60-100
times/min)
 AV node (40-60
beats/min)
 Bundle of His
 R & L bundle
branches
 Purkinje fibers
(20-40 beats/min)
Anatomy and Physiology Review
 Sequence of events
during cardiac cycle
Systole
(contraction) – emptying
Period of ventricular
contraction resulting to
ejection of blood into the
pulm. Artery and aorta

Diastole
(relaxation) – filling
Anatomy and Physiology Review
 Cardiac-muscle contraction
 Sarcoplasmic reticulum  release of Ca++ 
 diffuse to myofibril SARCOMERE (basic contractile unit of
the myocardial cell) 
 ACTIN & MYOSIN filaments links & overlaped 
 CONTRACTION ( sarcomere shortens)
 Anatomy and Physiology Review
Mechanical Properties of the Heart
 Cardiac Output
Cardiac Output = HR x SV
 HR
ANS – PNS and SNS, hormones (catecholamines),
CNS, Baroreceptors
 SV (stroke volume)
 Preload – volume of blood distending the ventricles at the
end of diastole just before contraction
 Afterload – resistance that the ventricles must overcome
to eject blood
 Contractility – force generated by the contracting
myocardium
 CONTROL OF STROKE VOLUME
1. PRELOAD – volume of the blood at the
end of the diastole
- The degree of STRETCH of the muscle
fiber
- FRANK STARLING LAW – the GREATER
the stretch of Cardiac Muscle the greater
the degree of SHORTENING (contraction)
- ↓ bld. Vol - ↓ preload
2. Afterload - amount of resistance to
ejection of blood from the ventricles
SYSTEMIC VASCULAR RESISTANCE
- resistance of the Left Vent. Ejection

PULMONARY VASCULAR RESISTANCE

- resistance of Right Vent. Ejection
Anatomy and Physiology Review
 Vascular System
Anatomy and Physiology Review
 Vascular System
Anatomy and Physiology Review
 Vascular System: FUNCTIONS
Provide conduits for blood to
travel from the heart to nourish
the various tissues of the body
Carries cellular waste to the
excretory organs
Allows lymphatic flow to drain
tissue fluid back into the
circulation
Returns blood to the heart for
recirculation
Anatomy and Physiology Review
 Vascular System
Assessment
Techniques
Assessment Techniques

History (focus: obtaining

information about client’s risk
factors & symptoms of
cardiovascular disease)
 Demographic data – age, gender, ethnic origin
 Family history & genetic risk
 Personal history
 Diet history
 Socioeconomic status
Assessment Techniques
 History
 Modifiable

cigarette smoking
physical inactivity
Obesity
psychological variables
chronic diseases
 Non-modifiable risk factors
age, gender, ethnic background, family
history
Assessment Techniques

cigarette smoking –
major risk factor for the devp’t
of CAD & PVD
 Obesity – strong indicator of CVD
especially when abdominal
obesity is present
Assessment Techniques
 Physical assessment
 Major symptoms cardiovascular disease (CVD)
Pain or discomfort

Dyspnea (DOE, Orthopnea, Paroxysmal Nocturnal Dyspnea)

Fatigue
Palpitations
Weightgain – best indicator of fluid retention (edema)
Syncope – transient loss of consciousness ( cerebral
perfusion)
Extremity pain – due to ischemia & venous insufficiency
Assessment Techniques
 Physical assessment
 Skin color – pallor (anemia), cyanosis (late sign
of decreased perfusion)
  skin temperature – due to  blood flow
 Clubbing of fingers – chronic tissue hypoxia
 Edema
 BP changes
 Hypertension
 Postural
Hypotension
 Pulse pressure
(30-40mmHg)
Assessment Techniques
Precordium (area over the
heart)
Assessment involves:
 Inspection
 Apical impulse
 Palpation
 Percussion
 Auscultation
 Normalheart sounds
 Abnormal heart sounds
Assessment Techniques
 Normal Heart Sounds
S1 – closure of AV valves
 Low pitch, long; best heard at
the apex of the heart
 Palpate the carotid pulse while
listening
 Marks the beginning of
ventricular systole
S2 – closure of semilunar
valves
 Highpitch, short; best heard at
the base of the heart
Assessment Techniques
Abnormal Heart Sounds
 Paradoxical splitting
 Abnormal splitting of S2/ wider split heard on expiration
 Early closure of PV or a delay in AV closure
 MI, left bundle-branch block, aortic stenosis, aortic
regurgitation, right ventricular pacing
 Gallops
 S3 “Ventricular gallop”
 passive filling from atrium to a non-compliant
ventricle; vibration of the valves & supporting
structures
 S4 “atrial gallop”
 active filling phase
Assessment Techniques
Abnormal Heart Sounds
 Murmurs
 Reflectionof turbulence of
blood flow through the normal
or abnormal valves
 Pericardial friction rub
 Sign of inflammation, infection
or infiltration
Assessment Techniques
Laboratory Tests
 Serum markers of myocardial damage (cardiac
markers)
Troponin (T=<0.2ng/ml, I=<0.03ng/ml)
CreatineKinase (CK-MB)
Myoglobin (<90mcg/L)
 Serum lipids
 Cholesterol (122-200mg/dl), TGL (40-16035-
135mg/dl)
 HDL (45-50 55-60mg/dl), LDL (60-180mg/dl)
 HDL:LDL ratio (3:1)
Assessment Techniques
 Laboratory Tests
 Homocysteine (<12mmol/dL)
 its association w/ CVD is still controversial
 C-ReactiveProtein (<1.0mg/dl)
 Blood coagulation tests (evaluate the ability of the blood
to clot- thrombi)
 ABG
 Serum electrolytes (K+, Ca++, Na+, Magnesium)
 CBC
Assessment Techniques
 Radiographic
examinations
Chest
radiography
 Determine the size,
silhouette & position of
the heart
Angiography
(arteriography)
 Invasiveprocedure
involving fluoroscopy &
the use of contrast media
Assessment Techniques
 Cardiac catheterization
 Most definitive, most
invasive test used in the
diagnosis of heart
disease
 Right-sided heart
catheterization
 Left-sided heart
catheterization
Angiography in action: The beating heart and its
surrounding blood vessels can be watched and
recorded in extraordinary detail as a catheter injects
a contrast dye into a patient's coronary arteries
Assessment Techniques
 Coronary arteriography
 Technique is the same for left-sided heart
catheterization
 Complications: MI, Stroke, Arterial bleeding,
Thromboembolism, Lethal dysrhythmias, Death
 Intravascular ultrasonography (IVUS)
 Catheter with miniature transducer (soundwaves)
at the distal tip to visualize the coronary arteries
Assessment Techniques
 Electrocardiography (ECG)
 graphically measures &
records the electrical current
traveling through the
conduction system generated
by the heart
 measured by electrodes
placed on the skin &
connected to an amplifier &
strip chart recorder
 in a standard 12-lead ECG:
 fiveelectrodes attached to the
arms, legs, & chest
 measures electrical current from
12 different views or leads
Assessment Techniques
 Bipolar limb leads
 Lead I
 Lead II
 Lead III
 Unipolar augmented leads
 aVR
 aVL
 aVF
 Unipolar precordial leads
 V1
 V2
 V3
 V4
 V5
 V6
Assessment Techniques
 Bipolar limb leads
 Lead I
 Lead II
 Lead III
 Unipolar augmented leads
 aVR
 aVL
 aVF
 Unipolar precordial leads
 V1
 V2
 V3
 V4
 V5
 V6
Assessment Techniques
 Unipolar precordial leads
 V1
 V2
 V3
 V4
 V5
 V6
Assessment Techniques
Electrocardiographic Paper
 electrocardiogram (ECG) strip: each small block
measures 1 mm in height & width
 standard speed:25mm/sec
 1 small block = 0.04 sec 1 large block = 5 small blocks
 1 large block = 0.20 sec 5 large blocks = 1 sec
 15 large blocks = 3 sec 30 large blocks = 6 sec
Assessment Techniques
Assessment Techniques

 P wave – represents atrial depolarization

Assessment Techniques

 PR segment – represents the time required for the impulse to

travel through the AV node, where it is delayed, and through
the Bundle of His, Bundle branches, & Purkinje fiber network,
just before ventricular depolarization
Assessment Techniques

 PR interval – represents the time required for atrial

depolarization as well as impulse travel through the conduction
system and Purkinje fiber network, inclusive of the P wave and
PR segment. It is measured from the beginning of the P wave
to the end of the PR segment (0.12-0.20 sec)
Assessment Techniques

 QRS complex – represents ventricular depolarization and is

measured from the beginning of the Q (or R) wave to the end
of the S wave (0.04 - 0.10 sec)
Assessment Techniques

 ST segment – represents early ventricular repolarization

Assessment Techniques

 T wave – represents ventricular repolarization

 U wave – represents late ventricular repolarization
Assessment Techniques

 QT interval – represents the total time required for ventricular

depolarization and repolarization and is measured from the
beginning of the QRS complex to the end of the T wave
Assessment Techniques
Assessment Techniques
Characteristics of the Normal rhythm:
 HR is 60-100 bpm
 P waves are found BEFORE the QRS
complex
 PR interval is 0.12 to 0.20 seconds duration
 QRS complex is 0.04 to 0.10 seconds
duration
 conduction is forward and cyclical
 The rhythm is regular with no delay
Assessment Techniques
 Various forms of ECG
 Resting ECG
 Ambulatory ECG (Holter
monitoring) – 24 hrs.
 Exercise ECG (Stress test)
Assessment Techniques
 Echocardiography
 usesultrasound waves to assess cardiac
structure & mobility, particularly at the valves
Assessment Techniques
 Hemodynamic Monitoring
 Useto assess the volume & pressure of blood in
the heart & vascular system by means of a
surgically inserted catheter
Methods:
 Direct BP monitoring
 Artery used: radial, brachial, femoral
 Catheter tip contains sensor that measures & transmits
the fluid pressure to a transducer
 CVP monitoring
 Pulmonary artery pressure monitoring
Assessment Techniques
 CVP monitoring
 Pressureproduced by venous blood in the RA
 NV: 2-7 mmHg or 4-10cm H2O
Assessment Techniques
 Pulmonary artery pressure monitoring
Disturbances in O2 Transport Mechanism
 Infectious Disorders
 Pericarditis, Myocarditis, Endocarditis, RHD
 Coronary Artery Disease
 Atherosclerosis
 Anginapectoris
 Myocardial infarction

 Congestive Heart Failure

 Pulmonary edema
 Arrythmias
Pericarditis
 Inflammation of the pericardium
Associated w/ the following:
 Malignant neoplasms
 Idiopathic cause
 Infective organisms (bacteria, viruses, fungi)
 Post-MI syndrome (Dressler’s syndrome)
 pericarditis,
fever, pericardial & pleural effusion 1-12
weeks after MI)
 Postpericardiotomy syndrome
 Systemic connective tissue disease
 Renal failure
Pericarditis
Chronic pericardial inflammation causes fibrous
thickening of the pericardium
 “Chronic Constrictive Pericarditis”

rigid pericardium

inadequate
ventricular
filling

Heart Failure
Pericarditis
 Assessment:
 PAIN radiating to the neck, shoulder & back
 aggravated by inspiration, coughing & swallowing
 worst in supine position (relieved by sitting up & leaning
forward)
 Pericardialfriction rub (scratchy high pitch sound)
 If w/ chronic constrictive pericarditis: Signs of RSHF
 Echocardiography, CT scan – reveals thickening of
pericardium
 WBC count
 ECG changes: ST-T spiking (w/ the onset of inflammation w/c
returns to baseline w/ treatment)
 Atrial fibrillation is also common
Pericarditis
 Interventions:
 NSAIDs for PAIN
 Corticosteroids
 Antibiotics
 Pericardial drainage
 Radiation or chemotherapy if caused by malignancy
 Hemodialysis (uremic pericarditis)
 Assist to assume position of comfort
 Pericardiectomy (chronic constrictive pericarditis)
 Monitor for complications: pericardial effusion
Pericarditis
Monitor for complications:
 pericardial effusion  cardiac tamponade
Findings:
 Jugular distention
 Paradoxical pulse
(systolic BP 10mmHg
or more on expiration
than on inspiration)
 cardiac output
 Muffled heart
sounds
 Circulatory collapse
 emergency care: pericardiocentesis
Myocarditis
Causes:
 Viral, bacterial, fungal & parasitic infection
 Chronic alcohol & cocaine abuse
 Radiation therapy
 Autoimmune disorders
 Bulimic patients taking ipecac syrup to
facilitate purging (myocardial damage)
 Due to inflammation  abnormal
function
 cardiac output, impaired blood
circulation, predispose client to CHF
 Due to ischemia: tachycardia,
dysrhythmias
 Cardiomyopathy
Myocarditis
 Assessment:
 PAIN, Fever, Tachycardia,
Dysrhythmias, Dyspnea,
Malaise, Fatigue, Anorexia,
Pale or cyanotic skin, signs of
RSHF
 WBC count, elevated CRP,
elevated cardiac isoenzymes,
abnormal ECG
 Abnormal chest radiography,
echocardiography
Myocarditis
 Intervention:
 Treatment of underlying cause (antibiotic)
 Promote bed rest, Na+-restricted diet, cardiotonic
drugs (digitalis) are prescribed
 Monitor cardiopulmonary status and complications
(CHF, dysrhythmias)
 VS
 Daily weight
 I&O
 Heart & lung sounds
 Pulse oximetry measurements
 Cardiac monitoring
 Dependent edema
Rheumatic Fever
A systemic inflammatory disease that usually
develops after an URTI
 group A ß-hemolytic streptococci
 Rheumatic carditis (Rheumatic endocarditis)
Rheumatic Carditis/ Endocarditis
Antibodies are formed to destroy the group A ß-
hemolytic strep microorganism

Antibodies “mistakenly” cross-react against the

proteins in the connective tissue of the heart,
joints, skin & nervous system

PanCARDITIS (all layers)

due to inflammation, WBC migrate to endocardium
causing accumulation of inflammatory debris
“vegetations” around the valve leaflets
Rheumatic Carditis/ Endocarditis
Rheumatic Carditis/ Endocarditis
Assessment:
 Major/ Classic symptoms

Carditis
Polyarthritis
Chorea (Sydenham’s chorea, St. Vitu’s dance)
Subcutaneousnodules
Erythema marginatum
Rheumatic Carditis/ Endocarditis
Assessment:
Major/ Classic symptoms
 Carditis
 Characterized by
formation of Aschoff’s
bodies
 Murmur (valve
damage)
 pericardial friction rub
(pericarditis)
 CHF
Rheumatic Carditis/ Endocarditis
Assessment:
Major/ Classic symptoms
 Polyarthritis
 Swelling of several joints (knees, ankle,
hips, shoulders) that is warm, red and
painful
 Chorea (Sydenham’s chorea, St.
Vitu’s dance)
 Involuntary grimacing & inability to use
skeletal muscles in a coordinated
manner
 Involvement of CNS
Rheumatic Carditis/ Endocarditis
Assessment:
Major/ Classic symptoms
 Subcutaneous nodules
 Sometimes marble-sized
nodules appear around the
joints
 Erythema marginatum
 Red, spotty rashes on the
trunk that disappears rapidly
leaving irregular circles on
the skin
Rheumatic Carditis/ Endocarditis
Assessment:
 Minor symptoms
 Reliable history of RF or evidence of pre-existing
rheumatic heart disease
 Arthralgia- pain in one or more joints without
evidence of inflammation, tenderness, or limited
movement
 Fever (38.9 - 40°C or 101 - 104°F)
 Diagnostic tests:  in ESR and ASO titer, (+) C-
reactive protein
 ECG changes: prolonged P-R interval
Rheumatic Carditis/ Endocarditis
 Diagnosed clinically
through the use of the
JONES criteria
 presence of 2 major
manifestation or
 1 major + 2 minors
with supporting evidence
of a recent streptococcal
infection
Rheumatic Carditis/ Endocarditis
 Management/ Intervention:
PREVENTION - ideal management
 RHD is prevented through early
identification &
adequate treatment of streptococcal
infection

A nurse should be familiar with the signs &
symptoms of streptococcal pharyngitis
Signs & symptoms of streptococcal pharyngitis:
 Fever (38.9 - 40°C or 101 - 104°F)
 Chills
 Sore throat (sudden onset)
 diffuse redness of throat with exudates on
oropharynx
Signs & symptoms of streptococcal pharyngitis:
 Enlarge & tender lymph nodes
 Abdominal pain ( common in children)
 Acute sinusitis & acute otitis media
Rheumatic Carditis/ Endocarditis
 Management/ Intervention:
 Antibiotic: DOC – penicillin
 Aspirin (control blood clot formation around the
valves)
 Steroids (suppresses inflammation)
 Fever (antipyretics, hydration)
 Antibiotic prophylaxis to prevent recurrence
 Provide bed rest; provide diversional activities that
require minimal activity (reading, putting puzzles
together)
 Assess for progression or improvement of heart
involvement
Disturbances in O2 Transport Mechanism
 Infectious Disorders
 Pericarditis, Myocarditis, Endocarditis, RHD
 Coronary Artery Disease
Atherosclerosis
Anginapectoris
Myocardial infarction
 Congestive Heart Failure
 Pulmonary edema
 Arrythmias
Coronary Artery Disease
Coronary Artery Disease
 Arteriosclerosis
 Thickening or hardening
of the arterial wall
 Atherosclerosis
A type of arteriosclerosis
caused by formation of
PLAQUE (chiefly
composed of cholesterol)
 Leading contributor to
coronary artery and
cerebrovascular disease
Coronary Artery Disease
 Pathophysiology
(atherosclerosis): UNKNOWN
 Vascular damage (cause
inflammation)

 Fatty streak development (intimal

layer)

 Plaque (partial or complete occlusion

of blood flow)

 Complications
 Calcifications
 Ulceration
 Thrombosis
Coronary Artery Disease
 Assessment:
 BP (hypertension)
 Elevated cholesterol &
triglycerides
 Elevated homocysteine (risk if
level > 15mmol/L)
 Blocks the production of nitric
oxide on the endothelium
making cell wall less elastic &
permitting plaque to build up
 Diet: B-complex vitamin rich diet
(folic acid) - homocysteine
 Presence of abdominal obesity
 Elevated FBS
Coronary Artery Disease
 Interventions:
 Cholesterol
screening
 Diet

Smoking
cessation
 Exercise
 Drug therapy
 HMG-CoA
reductase
inhibitors “Statins”
In combination with other substances,
LDLs can lead to plaque formation,
greatly increasing the chances
for myocardial infarction and stroke.
HDLs work to remove harmful LDLs
from the blood, thereby preventing
fatty buildup and formation
of plaque in arterial walls.
Coronary Artery Disease
 The American Heart Association (AHA) now
suggest the term ACUTE CORONARY
SYNDROME to describe any group of clinical
symptoms compatible with acute myocardial
ischemia
O 2
 Ischemia – insufficient blood supply
 Atherosclerosis  ischemia ANGINA PECTORIS

Myocardial Infarction
Coronary Artery Disease
 Angina Pectoris
 “Chest pain” of
cardiac origin
 Most common
clinical manifestation
of myocardial
ischemia
 Myocardial ischemia
causes chemical and
mechanical
stimulation of
sensory afferent
nerve endings in the
coronary vessels and
myocardium
Types of Angina: CAUSE SYMPTOMS

Stable -75% coronary occlusion -Chest pain (15mins or

that accompanies less) and may radiate
exertion -Similar pain severity,
-Elevated HR or BP frequency & duration
-Eating a large meal with each episode
Unstable -Progressive worsening - Chest pain of
of stable angina with increased frequency,
>90% coronary severity & duration
occlusion poorly relieved by rest
or oral nitrates
Variant -Arterial
spasm in -chest pain that occurs
(Prinzmetal’s) normal or diseased at rest (usually bet. 12
coronary artery & 8am), sporadic over
3-6 mos & diminishes
over time (ECG: ST –
elevation)
Coronary Artery Disease
 What is the most serious acute coronary
syndrome??? Subendocardial MI

Transmural MI
Myocardial Infarction
 Etiology & Genetic Risk:
 PRIMARY FACTOR: Atherosclerosis
 Nonmodifiable risk factors
 Modifiable risk factors
 Elevated serum cholesterol levels
 CIGARETTE SMOKING!!!
 Hypertension
 Impaired glucose tolerance
 Obesity
 Physical inactivity
 Stress
Myocardial Infarction
 Physical assessment/ Clinical Manifestations:
Myocardial Infarction
Interventions:
 Pain management: MONA
 Morphine
 2- to 10-mg IV q 5-15 minutes
 AE: respiratory depression, hypotension, bradycardia,
severe vomiting
 Antidote: Naloxone (Narcan) 0.2 – 0.8 mg IV
 Oxygen: 2-4L/min by nasal cannula
 Nitroglycerin
 Aspirin
 Positioning – semifowler’s
 Provide a quiet & calm environment
 Medications
 Nitrates
 Nitroglycerine,
Isosorbide dinitrate (Isordil),
Isosorbide mononitrate (Imdur)
 Beta Blockers
 Calcium Channel Blockers
 Thrombolytics/ Fibrinolytics
Coronary Artery Disease
Coronary Artery Disease
Disturbances in O2 Transport Mechanism
 Infectious Disorders
 Pericarditis,Myocarditis, Endocarditis, RHD
 Coronary Artery Disease
 Atherosclerosis
 Angina pectoris
 Myocardial infarction

CongestiveHeart Failure
Pulmonary edema
 Arrythmias
Heart Failure
 “Pump failure”, inadequacy of the heart to
pump blood throughout the body
 Congestive Heart Failure
 accumulationof blood & fluid in organs & tissues
due to impaired circulation
 Types:
 Left-sidedheart failure
 Right-sided heart failure

 Causes:
 Damage to muscular wall (M.I.), Cardiomyopathy,
Hypertension, CAD, Valvular defects, Infections
Heart Failure
Left = Lungs
Heart Failure
 Diagnostic Findings:
 Chest x-rays: reveals cardiomegaly
(hypertrophy)
 Pleural effusions develops
 ECG: abnormal findings
(ventricular hypertrophy,
dysrhythmias)
 Echocardiography – reveals cardiac
valvular changes, pericardial
effusions, chamber enlargement,
ventricular hypertrophy
 Multigraded angiographic (MUGA)
scans – information about ejection
fraction
Heart Failure
Medical Management:
 Low-sodium diet, fluid restriction
 Inotropic agents:
 Digitalis: Digoxin (Lanoxin)
  contractility,  HR,  conduction (AV node)
 (-) sympa. activity, (+) parasympa. Activity
 Watch out for DIGITALIS toxicity: loss of
apetite, N&V, rapid, slow, irregular heart rate,
disturbance in color vision
 Dopamine (Intropin), Dobutamine (Dobutrex)
 Diuretics: Furosemide (Lasix), Chlorothiazide (Diuril)
 Vasodilators (Nitroglycerin), ACE inhibitors (pril)
Heart Failure
 Cardiac Resynchronization Therapy (CRT)
 New technique that restores synchrony in the
contractions of the R & L ventricles
 Used primarily for clients with heart failure caused
by dilated cardiomyopathy
Heart Failure
 Intra-Aortic Balloon Pump (IABP)
 Act as a temporary, secondary mechanical
circulatory pump to supplement the ineffective
contraction of the left ventricle especially
following cardiogenic shock

 COUNTERPULSATION: IABP is connected to a

machine that inflates the balloon portion during
ventricular diastole & deflates during systole

 Intended for only a few days’ use

Heart Failure
 Intra-Aortic Balloon Pump (IABP)
Heart Failure
 Surgical Management:
 Done when medical treatment alone is unsuccesful
 Insertion of Ventricular Assist Device (VAD)
 Used for weeks to months to 1 year
 Cardiomyoplasty
 Chest muscle
(latissimus dorsi)
is grafted to the
aorta & wrapped
around the heart
 Artificial Heart
Cardiomyoplasty technique: the left latissimus dorsi muscle
(LDM) is transposed into the chest through a window created by
resecting the anterior segment of the 2nd rib (5 cm). The LDM is
then wrapped around both ventricles. Sensing and pacing
electrodes are connected to an implantable cardiomyostimulator.
Heart Failure
 Surgical Management: Artificial Heart
  Heart transplantation is the treatment
of choice for clients with severe dilated
cardiomyopathy (DCM)
Heart Failure
 Nursing Management:
- Most clients manage chronic heart failure at home
- Many medications, lifestyle changes & diet restrictions are involved to
control heart failure
 Administer prescribed medications & monitor for
therapeutic & adverse effects
 Promote heart’s ability to eject as much as blood
as possible
 Monitor for signs of excess fluid volume,
electrolyte imbalances
 Promote oxygenation, balance activity according to
client’s tolerance
 Support family members
Pulmonary Edema
 Fluid accumulation in
the lungs
 Usually a complication
of LSHF
 Causes:
 Cardiogenic– LSHF
 Noncardiogenic
 Pulmonary embolism
 Infection
 Alteration of pulmonary
capillary membrane
Pulmonary Edema
 Assessment
findings:
 Dyspnea
 Wheezing
 Orthopnea
 Restlessness
 Productive cough
(pink, frothy
sputum)
 Cyanosis
 Tachycardia
 Apprehension
 Metabolic acidosis
Pulmonary Edema
 Medical management:
- effort is made to relieve lung congestion
 Drug Therapy
 Inotropic drugs
 Dopamine (Intropin), Dobutamine (Dobutrex), Amrinone (Inocor),
Digitalis
 Diuretics
 Vasodilators
 Nitrates, ACE inhibitors, Ca++-channel blockers
 Morphine
 lessen anxiety, muscle relaxation & reduces work of breathing
 Supplemental O2
 if drug therapy & O2 is inadequate  invasive
measures
Pulmonary Edema
 Medical management:
 Invasive measures
 IABP (Intra-aortic
balloon pump)
 Biventricular pacemaker
 LVAD (Left ventricular
assist device)
 Cardiomyoplasty
 Artificial heart
 Heart transplantation
Pulmonary Edema
 Nursing Management:
 Similar for clients experiencing CHF
 Need close assessment in an ICU
 Establish an IV line for medications
 Monitors the therapeutic & adverse effects of
medication therapy
 Monitor ECG, pulse oximetry, VS q 15-30mins
 Critically ill: may have pulmonary catheter inserted
to measure the pressure readings in he heart
chambers & estimates cardiac output
 Urinary catheter is inserted to monitor UO
 Give proper oxygenation
Disturbances in O2 Transport Mechanism
 Infectious Disorders
 Pericarditis,Myocarditis, Endocarditis, RHD
 Coronary Artery Disease
 Atherosclerosis
 Angina pectoris
 Myocardial infarction
 Congestive Heart Failure
 Pulmonary edema

Arrythmias
Cardiac Dysrhythmias
 A conduction disorder that results in an
abnormally slow or rapid heart rate or one that
does not proceed through the conduction
system in the usual manner
 Normal rhythm: Normal Sinus Rhythm
 Causes of dysrhythmias:
 Ischemic heart disease
 Drugs
 Electrolytedisturbances
 Metabolic acidosis
 Hypothermia
 Degenerative (age-related)
Cardiac Dysrhythmias
 Normal rhythm: Normal Sinus Rhythm
 Characteristics of NSR:
 Heart rate is between 60 and 100 beats/min
 The SA node initiates the impulse (upright P wave before
each QRS complex)
 Impulse travels to the AV node in 0.12 to 0.2 second (PR
interval)
 The ventricles depolarize in 0.12 second or less (The QRS
complex)
 Each impulse occurs regularly (evenly spaced)
Cardiac Dysrhythmias
 Sinus Bradycardia
 Pathway: Normal (SA  AV  BH  BB  PF)
 Rate: ≤60 beats/min
 Seen in healthy athletes, heart disorders, ICP,
hypothyroidism, digitalis toxicity
 Danger: slow rate may be insufficient to maintain cardiac
output
 Treatment: None unless symptomatic  Atropine sulfate
(IV) is given to increase HR
Cardiac Dysrhythmias
 Sinus Tachycardia
 Pathway: Normal
 Rate: 100-150 beats/min
 Occurs in physiologic response to strenous
exercise, anxiety, fear, pain, fever,
hyperthyroidism, hemorrhage, shock, or
hypoxemia
 Treatment: None unless symptomatic: treat
underlying cause
Cardiac Dysrhythmias
 Premature Atrial Contraction
 Electrical
impulse is initiated somewhere in the atria
other than the SA node
 PACs can occur for various reasons:
 Consumption of caffeine
 Use of nicotine/ sympathetic NS stimulants
 In response to heart disease & metabolic disorders
(hyperthyroidism)
 If isolated & infrequent: NO cause for alarm

 Treatment: None or treat underlying cause if known

Cardiac Dysrhythmias
 Supraventricular Tachycardia
 Rate: ≥150 beats/ min
 Heart does not have sufficient time to fill  CO
 Due to  CO  ischemia  Chest Pain!!!
 Hypotension
 Syncope
 Reduced renal output
 Impending heart failure

 Treatment: valsalva manuever, unilateral carotid

massage, immersion of face in ice water, meds
(digitalis, adrenergic blockers, calcium channel
blockers)
Cardiac Dysrhythmias
 Atrial Flutter
A single atrial impulse outside the SA node causes
the atria to contract at exceedingly rapid rate
(200-400 contractions/ min)
 “sawtooth pattern” of atrial waves
 Treatment: Cardioversion, digitalis, quinidine,
propanolol, verapamil
Cardiac Dysrhythmias
 Atrial Fibrillation
 Several areas in the right atrium initiate impulses
resulting in disorganized, rapid activity (>400/min)
 Atria quiver rather than contract
 Treatment:
 Ibutilide (Corvert) convert new-onset atrial
 Flecainide (Tambocor) fibrillation into sinus
 Propafenone (Rythmol) rhythm
*** chemical cardioversion – use of drugs to eliminate
dysrhythmia
 Digitalis, quinidine, verapamil, amiodarone, anticoagulant
Cardiac Dysrhythmias
 Heart Block
 Interferenceof the transmission of impulses from
the SA node through the AV node to the ventricles
 Types:
1st degree delay of impulse
2nd degree
3rd degree (complete heart block)
Ventricles develop their own rhythm
independent of the atrial rhythm
30-40 beats/min
Treatment: Pacemaker insertion
Cardiac Dysrhythmias
1st Degree AV Block
 Rhythm - Regular
 Rate - Normal
 QRS Duration - Normal
 P Wave - Ratio 1:1
 P Wave rate - Normal
 P-R Interval - Prolonged (>5 small squares)
 Treatment: None unless symptomatic
Cardiac Dysrhythmias
2nd Degree Block Type 1 (Wenckebach)
 Rhythm - Regularly irregular
 Rate - Normal or Slow
 QRS Duration - Normal
 P Wave - Ratio 1:1 for 2,3 or 4 cycles then 1:0.
 P Wave rate - Normal but faster than QRS rate
 P-R Interval - Progressive lengthening of P-R interval
until a QRS complex is dropped
 Treatment: Pacemaker
Cardiac Dysrhythmias
2nd Degree Block Type 2
 Looking at the ECG you'll see that:
 Rhythm - Regular
 Rate - Normal or Slow
 QRS Duration - Prolonged
 P Wave - Ratio 2:1, 3:1
 P Wave rate - Normal but faster than QRS rate
 P-R Interval - Normal or prolonged but constant
 Treatment: Pacemaker
Cardiac Dysrhythmias
3rd Degree Block
 Rhythm - Regular
 Rate - Slow
 QRS Duration - Prolonged
 P Wave - Unrelated
 P Wave rate - Normal but faster than QRS rate
 P-R Interval - Variation
 Complete AV block. No atrial impulses pass through
the atrioventricular node and the ventricles generate
their own rhythm
Cardiac Dysrhythmias
 Premature Ventricular Contraction
A ventricular contraction that occurs early and
independently in the cardiac cycle before the SA
node initiates an electrical impulse
 No P waves preceeds the wide, bizarre-looking QRS
complex
 Symptoms: flip-flop sensation in the chest
“fluttering”, pallor, nervousness, sweating, faintness
 Occasional PVCs are harmless & they may be
related to anxiety, stress, fatigue, alcohol
withdrawal, tobacco use
Cardiac Dysrhythmias
 Premature Ventricular Contraction
 PVCs suggest myocardial irritability & can lead to
lethal dysrhythmias if the following patterns will be
seen
 Sixor more PVCs per minute
 Runs of bigeminy (every other beat is a PVC)
 2 PVCs in a row (couplets)
 Runs of PVCs (3 or more in a row)
 Multifocal PVCs (originating from more than one location)
 A PVC whose R wave falls on the T wave of the preceding
complex (R-on-T phenomenon)
 Treatment: IV bolus of lidocaine (xylocaine)
followed by IV infusion of the drug
Cardiac Dysrhythmias
 Ventricular Tachycardia
 caused by a single, irritable focus in the ventricle
that initiates the heartbeat (150-250 beats/min)
 May lead to  CO, loss of consciousness, pulseless
 Treatment:
 Lidocaine, procainamide, bretylium, cardioversion,
defibrillation if pulses
Cardiac Dysrhythmias
 Ventricular Fibrillation
 “rhythm of a dying heart”; fatal if not successfully
terminated within 3-5 minutes
 ventricles merely quiver
 assessment:
clientbecomes faint & immediately losses
consciousness
no pulse, apneic, no BP, no sounds,
respiratory & metabolic acidosis develops
Within minutes, pupils become fixed &
dilated, skin becomes cold
DEATH will follow
Cardiac Dysrhythmias
 Ventricular Fibrillation
Emergency care:
 Defibrillation (3 rapid successive shocks of
increasing energy)
 200, 300, 360 joules
 CPR
 airway management
Cardiac Dysrhythmias
Asystole
 Looking at the ECG you'll see that:
 Rhythm - Flat
 Rate - 0 Beats per minute
 QRS Duration - None
 P Wave - None
Cardiac Dysrhythmias
CARDIOVERSION DEFIBRILLATION
Scheduled procedure 1 to Emergency procedure
several days in advance performed during resuscitation
Used to eliminate atrial Used to eliminate ventricular
dysrhythmias (atrial flutter, dysrhythmias (ventricular
atrial fibrillation, SVT) fibrillation, asystole)
Client sedated before procedure Client not sedated but
unresponsive
Uses electrical energy (50-100 Uses more electrical energy
joules) than defibrillation, but (200-360 joules) than
higher levels can be administered if cardioversion
initial outcome is unsuccessful
Delivers electrical energy when Delivers electrical energy
the machine senses the R wave whenever the buttons on the
of the ECG paddles are pressed
Respiratory Anatomy & Physiology
 The UPPER respiratory system consists of:
 1. nose
 2. mouth
 3. pharynx
 4. larynx
Respiratory Anatomy & Physiology
 The LOWER respiratory system consists
of:
 1. Trachea
 2. Bronchus
 3. Bronchioles
 4. Respiratory unit
 The Nose
 This is the first part of the upper
respiratory system that contains nasal
bones and cartilages
 There are numerous hairs called vibrissae
 There are numerous superficial blood
vessels in the nasal mucosa
 The Nose
 The functions of the nose are:
 1. To filter the air
 2. To humidify the air
 3. To aid in phonation
 4. Olfaction
 The pharynx
 The pharynx is a musculo-membranous
tube that is composed of three parts
 1. Nasopharynx
 2. Oropharynx
 3. Laryngopharynx
 The larynx
 Also called the voice box
 Made of cartilage and membranes and
connects the pharynx to the trachea
Chronic Airflow Limitations (CAL)
 A group of chronic lung diseases that
includes:
 Asthma
 Chronic
Bronchitis
 Emphysema

 COPD
 Emphysema
 Chronic bronchitis
 Characterized by bronchospasm, dyspnea &
irreversible tissue damage  respiratory failure
Bronchial Asthma
 Intermittent & reversible airflow obstruction
affecting the lower airway.
 Obstruction is due to:
 Inflammation
 Airway hyper-responsiveness (bronchospasm)
 Constriction
of bronchial smooth muscle due to stimulation
of the nerve fibers
 Etiology:
 allergens, cold air, dry air, airborne particles,
microorganism, aspirin  inflammation
 exercise, upper respiratory illness (viruses),
unknown reasons  bronchospasm
Bronchial Asthma
allergens Histamine,
Leukotriene,
IgE IL-4, Eotaxin
Mast cells
Basophils
inflammation
Blood vessel dilation &
capillary leak
“Atopic or Tissue swelling

Allergic Asthma” Increased secretions &

mucus production
Bronchial Asthma Aspirin
Arachidonic Acid Aspirin & other NSAIDs
inhibit this enzyme

Lipoxygenase Cyclooxygenase

inflammation
Leukotrienes Prostaglandins
Lipoxin Thromboxane
Bronchial Asthma
 Physical assessment
findings:
 Audible wheezing & RR
(acute episode)
 Wheezing is louder during
exhalation
 Dyspnea, cough, use of
accessory muscle of
respiration, barrel chest
(chronic severe asthma)
 Cyanosis, poor O2 saturation
(pulse oximetry)
 Change of LOC & tachycardia
due to hypoxemia
Bronchial Asthma
 Laboratory assessment:
 ABG, elevated eosinophil count, elevated IgE levels
 PuLmOnArY fUnCtiOn teSts – most accurate test for
asthma
 Forced Vital Capacity (FVC) – volume of air exhaled
from full inhalation to full exhalation
 Forced Expiratory Volume (FEV1) – volume of air
blown out as hard and fast as possible during the first
second of the most forceful exhalation after the greatest
full inhalation
 Peak Expiratory Rate Flow (PERF) – fastest airflow rate
reached at any time during exhalation
 Methacholine is inhaled (induces bronchospasm) & then
FVC, FEV1 & PERF is measured then brochodilators will
be given  an  12% of values: asthma
Bronchial Asthma
 Nursing interventions:
Goals:
 To improve airflow
 Relieve symptoms
 Prevent episodes
 Management plan includes
Client education
Drug therapy
Lifestyle management including
exercise
Bronchial Asthma
 Client Education Guide
 Avoid factors that triggers asthma attack
 Use bronchodilator 30 minutes before
exercise to prevent or reduce exercise-
induced asthma
 Proper technique & correct use of metered
dose inhalers
 Adequate rest & sleep, reduce stress &
anxiety; learn relaxation techniques
 Failure of medications to control worsening
symptoms, seek immediate emergency care
Bronchial Asthma
 Bronchodilators:
 β2 agonist
 Albuterol(Ventolin), Bitolterol,
Pirbuterol, Salmeterol, Formoterol
 Methylxanthines
 Theophylline, Aminophylline,
Oxtriphylline]
 Monitor for SE: excessive cardiac &
CNS stimulation (check pulse &
BP)
 Cholinergic antagonist
 Ipratropium (Atrovent)
Bronchial Asthma
 Anti-inflammatory Agents:
 Corticosteroids
 oral– Prednisolone, Prednisone
 inhaler – Budesonide, Fluticasone, Beclomethasone,
Triamcinolone, Flunisolide
 Mast cell stabilizer
 Cromolyn sodium (Intal); helps prevent atopic asthma
attacks (prevent mast cell membranes from opening when an
allergen binds to IgE) but are not useful during an acute episode
 Monoclonal antibodies
 Omalizumab (Xolair), approved in 2003 only – binds to
IgE receptor sites on mast cells & basophils preventing
the release of chemical mediators for inflammation
Bronchial Asthma
 Exercise/ Activity
 Aerobic exercise
(recommended)
 assist in maintaining
cardiac health,
enhancing skeletal
muscle strength, and
promoting ventilation
and perfusion
 Swimming
 Oxygen Therapy
 Often used during an
acute asthma attack
 Bronchitis
 Acute Bronchitis
 Typically begins as an URTI (viruses, bacteria)
 H. influenzae, S. pneumoniae, M. pneumoniae
 Chemicalirritants (noxious fumes, gases, air
contaminants)
 Assessment Findings:
 Fever,chills, malaise, headache, dry irritating
nonproductive cough (initial)  mucopurulent
sputum
 Medical Management:
 Usually self-limiting
 Bedrest, antipyretics, expectorants, antitussives,
Fluids, humidifiers, antibiotics
 Bronchitis
 Acute Bronchitis
Nursing Management:
 Auscultates breath sounds, monitors VS q 4 hrs especially
if client has fever
 Encourage client to cough & deep breath q 2 hrs while
awake & to expectorate rather than swallow sputum
 Provide humidification of surrounding (loosens bronchial
secretions)
 Changes the bedding & clients clothes if they become
damp with perspiration
 Offers fluid frequently
 Prevent infection (teach to wash hands frequently)
 Teach to cover the mouth when sneezing & coughing
 Discard soiled tissues in a plastic bag; avoid sharing of
eating utensils & personal articles
 Bronchitis
 Chronic Bronchitis
 Prolongedinflammation of the bronchi accompanied by a
chronic cough & excessive production of mucus for at
least 3 months each year for 2 consecutive years
 Etiology:
CIGARETTE SMOKING
 Long history of bronchial asthma, RTI, air pollution
 Assessment Findings:
 Chronic productive cough – thick white mucus
(earliest symptom)  yellow, purulent, copious,
blood streaked sputum
 Bronchospasm, Acute respiratory infections,
cyanosis, DOE, RSHF (cor pulmonale)
Chronic Bronchitis
Medical Management
 SMOKING CESSATION
 Bronchodilators,fluid intake, Well-balanced diet,
Postural drainage, Steroid therapy, Antibiotic
therapy
Nursing Management
Focus: educating clients in managing their disease
 Smoking cessation, occupational counseling,
monitoring air quality & pollution levels, avoiding
cold air & wind exposure (triggers bronchospasm)
 Preventing infection, avoid others with RTI,
immunizations, monitor sputum for signs of
infection, proper use of metered-dose inhaler
(MDIs)
Emphysema
 A chronic disease characterized by loss of
lung elasticity & hyperinflation of the lung
 most common COPD
Emphysema
Etiology/ Genetic Risk:
 Major cause:

Smoking
 Alpha1-Antitrypsin
Deficiency (ATT)
 Air pollution (minimal)
 Alpha1 – Antitrypsin Deficiency
(AAT)
 ATT is made by the liver and is normally
present in the lungs
 Function: regulates proteases from working
on lung structures

COPD
If ATT is deficient, develops
even if the person is not exposed to
cigarette smoke or other irritants
Emphysema
 Pathophysiology:
Pathophysiology:
LossLoss
of elasticity
of elasticity

Air trapping
Air trapping

Impaired Impaired
gas exchage
gas exchage

Signs/ symptoms
Signs/ symptoms

Bullae/
Bullae/ blebs
blebs

Pneumothorax
Pneumothorax
 use of accessory muscles in the process of
breathing due to flattening of the diaphragm
Emphysema
Classification
:
 Panlobar or
panacinar
 destruction
of the entire
alveolus
uniformly;
diffuse &
more severe
in the lower
lung areas
Emphysema
Classification:
 Centrilobular or
centriacinar
 openings occur in the
bronchioles and allow
spaces to develop as
tissue walls breakdown;
upper lung sections
 Paraseptal or distal
acinar
 only the alveolar ducts
and alveolar sacs are
affected; upper half of
the lung
“Each type can occur
alone or in combination
in the same lung”
Emphysema
Assessment Findings:
 Exertional dyspnea - 1st symptom
 shortness of breath with minimal activity
 Chronic productive cough with mucopurulent
sputum
 Decreased breath sounds, wheezing,
crackles
 “Barrelshaped chest”
 Use of accessory muscle of respiration
 Toxic CO2 levels Lethargy, stupor, coma
(carbon dioxide narcosis)
Emphysema
 Medical management:
 Meds: Bronchodilators, mucolytics, antibiotics,
corticosteroids (limited basis to assist with
bronchodilation & removal of secretions)
 Physical therapy: deep breathing, CPT, postural
drainage
 Nursing Management:
 Administer O2 via nasal cannula (2-3 L/min)
 High flow of O2 may lead to lost of hypoxic drive
 Teach abdominal breathing (using the diaphragm
effectively), pursed-lip breathing
 Most important risk
factor for COPD is
SMOKING!!!
 Effects of Tobacco Smoke:
 Tobacco smoke triggers the
release of EXCESSIVE amounts
of elastase protease that
breaks down elastin which is a major
component of alveoli
 Impairs & inhibits the action of cilia
ACTIVE smokers – 100%
PASSIVE smokers – 80%
COPD
 Clinical Manifestations
 General appearance
 RR of 40-50 breaths/min
 Presence of “Barrel chest”
 Cyanosis, Clubbing of fingers
 Manifestations of RSHF
(dependent edema)
COPD
 Psychosocial assessment
Socializationmay be
reduced when
friends avoid the
client with COPD
because of annoying
coughs, excessive
sputum, or dyspnea
COPD
 Laboratory assessment
 Abnormal ABG results (hypoxemia, hypercarbia),
Sputum C/S, Hgb./Hct., serum electrolyte levels are
examined because phosphate, K+, Ca++ & Mg++
reduces muscle strength
 CXR to rule out other chest diseases & to
check the progress of clients with respiratory
infections or chronic disease
 Pulmonary Function Test (Vital capacity,
Residual volume, Total lung capacity)
COPD
Interventions:
Mainstays of COPD management:

Airway maintenance
Monitoring
Drug Therapy
O2 therapy
COPD
Airway maintenance:
Keep the client’s head, neck
and chest in alignment
Assist the client to liquefy
secretions and clear the
airway of secretions
Breathing Techniques
COPD
Airway maintenance:
 Controlled coughing
 advise client to cough on arising on the morning, before
mealtimes, before bedtimes
 to cough effectively, the client sits in a chair or on the
side of a bed with feet placed firmly on the floor.
Instruct the client to turn the shoulders inward and to
bend the head slightly downward hugging a pillow
against the stomach. The client then takes a few deep
breaths. After the 3rd to 5th deep breath ( pursed-lip
breathing), instruct the client to bend forward slowly
while coughing two or three times from the same breath
 Chest physiotherapy & postural drainage
Postural Drainage
COPD
 Monitoring:
 Assess COPD client at least q2°
 O2 Therapy:
 The need for O2 therapy & its effectiveness can be
determined by ABG values & O2 saturation by pulse
oximetry
 usually, 2-4 L/min or even 1-2 L/min via nasal
cannula or up to 40% via venturi mask
Low-flow O2 because low arterial oxygen
level is the COPD client’s primary drive for breathing
COPD
Drug Therapy:
 involves the same inhaled and systemic drugs
for asthma
 mucolytics [acetylcysteine (Mucomyst), Guaifenesin]

PNEUMONIA
 one of the most common complications of COPD:

* Teach clients to avoid large crowds and

stress the importance of receiving a
pneumonia vaccination and a yearly influenza
vaccine “flu shot”
COPD
 COMPLICATIONS (COPD)
 Hypoxemia & acidosis – due to impaired exchange of
gases
 Respiratory Infections – due to  mucus & poor
oxygenation (most common: S. pneumoniae, H.
influenzae, Moraxella catarrhalis)
 due to infection, COPD manifestations worsens due to
increasing inflammation & mucus production
 Cardiac Dysrhythmias – results from O2 supply to
the , other cardiac disease, drug effects, or acidosis
 Cor Pulmonale – RSHF caused by pulmonary disease
Bronchiectasis
 An abnormal and permanent
dilatation of bronchi &
bronchioles
 It results from inflammation and
destruction of the structural
components of the bronchial
wall brought about by:
 chronic pulmonary infection
(P. aeruginosa, H. influenzae)
 tumor or foreign body
 congenital abnormalities
 exposure to toxic gases
Bronchiectasis
 The structure of the
wall tissue changes,
resulting in the
formation of
saccular dilatations
which collects
purulent materials
causing more
dilatation,
structural damage
& more infection
Bronchiectasis
Bronchiectasis
 Assessment Findings:
 Chroniccough (copious, purulent, blood-streak
sputum)
 Coughing worsens when the client changes position
 Sputum collected settles in three distinct layers (top
layer is frothy & cloudy, middle layer is clear saliva,
bottom layer is heavy, thick & purulent)
 Fatigue,weight loss, anorexia, dyspnea
 CXR & bronchoscopy – reveals incresed size of
bronchioles, atelectasis & changes in the
pulmonary tissues
 Sputum C/S identify causative microorganism
Bronchiectasis
Medical Management:
 Drainage of purulent material from the bronchi
 Antibiotics
 Bronchodilators
 Mucolytics
 Humidification
 Surgery removal of bronchiectasis if confined
to a small area
Bronchiectasis
 Nursing Management:
 Instruct client in postural drainage techniques
 CPT
 Oral hygiene
Pneumonia
 An inflammatory
process
affecting the
bronchioles &
alveoli
 Most common
cause of death
from an
infection in the
US (Smeltzer & Bare,
2004)
Pneumonia
Causes:
 Usually Infection
 Bacterial pneumonia
“Typical pneumonia”
 S.pneumoniae, P. carinii, S.
aureus, K. pneumoniae, P.
aeruginosa, H. influenzae
 Atypical pneumonia
 Mycoplasma pneumonia,
Chlamydia pneumoniae,
Chlamydia psittaci, Legionella
pnemophila, Mycobacterium
tuberculosis, viruses, parasites,
fungi
Pneumonia
Causes:
 Radiation Therapy (Radiation pneumonia)
 Damage to the normal lung mucosa during radiation
therapy for Breast CA, Lung CA
 Chemical ingestion or inhalation (Chemical
pneumonia)
 Ingestion of kerosene, gasoline or other chemical
 Inhalation of volatile hydrocarbons
 Aspiration of foreign bodies or gastric contents
(Aspiration pneumonia)
 Inhalationof foreign object or gastric contents
during vomiting or regurgitation
Pneumonia
 Bronchopneumonia
 Infection
is patchy, diffuse & scattered throughout
both lungs
 Lobar pneumonia
 Inflammation is confined to one or more lobes of
the lung
Pneumonia
4 General Categories of Pneumonia:
 CAP (Community-acquired pneumonia)
 Illness is contracted in a community setting or within
48 hrs of admission to a healthcare facility
 HAP (Hospital-acquired pneumonia)/
Nosocomial pneumonia
 Occurs in healthcare setting >48 hrs after admission
 Oppurtunistic Pneumonia
(immunocompromised host)
 P. carinii pneumonia (Pneumocystis jirovecii ), Fungal
pneumonia, pneumonia related to TB
 Aspiration Pneumonia
Pneumonia
Pathophysiology:
Microorganisms
-inhalation of droplets
-aspiration of organism from upper

airways
-Seeding from the bloodstream
Alveoli
-Inflammatory reaction takes place
-Exudate formation
-Impaired gas exchange
-Atelectasis, consolidation (inflammation &
exudates), hypoxemia, bronchitis, CHF, empyema,
pleurisy (inflammation of the pleura), septicemia,
hypotension, shock, DEATH
Pneumonia
 Assessment Findings:
 Fever
 Chills
 Productive cough,
sputum (rust colored)
 Discomfort in the
chest wall muscles
 General malaise
 Pain during breathing
(patient exhibits
shallow breathing)
Pneumonia
 Diagnostic Findings:
 Wheezing, crackles,
decreased breath
sounds
 Cyanosis (nail beds,
lips, oral mucosa)
 Sputum culture
reveals infectious
microorganism
 CXR shows areas of
infiltrates &
consolidation
 WBC
 Cyranose 320
Pneumonia
 Medical Management:
 Prompt
initiation of antibiotic therapy for bacterial
pneumonia
 Hydration to thin secretions
 Supplemental O2 to alleviate hypoxemia
 Bed rest, CPT, bronchodilators, analgesics,
antipyretics, & cough expectorants or suppressants
 F&Ereplacement 2° to fever, dehydration &
inadequate nutrition
 Severe
respiratory difficulty – intubation along with
mechanical ventilation
Pneumonia
 Nursing Management:
 Auscultate lung sounds & monitor the client for
signs of respiratory difficulty
 Checkoxygenation status (pulse oximetry) &
monitor ABGs
 Position: semifowler’s position
 Encourage  fluid intake
 Monitor I&O, skin turgor, VS & serum electrolytes
 Administer antipyretics as indicated
 Encourage at-risk & elderly clients to receive
vaccination against pneumoccocal & influenza
infections
Pleural Effusion
 Abnormal collection
of fluid between the
visceral & parietal
pleurae as a
complication of
 Pneumonia
 Lung CA
 TB
 Pulmonary embolism
 CHF
 Normal: 5-15ml
Pleural Effusion
General Classification
 Transudative effusion
(protein-poor, cell-poor)
 HYDROthorax- accumulation of
water/serous fluid
 Exudative effusion (protein
rich fluid)
 PYOthorax or Empyema-
accumulation of pus
 Hemothorax- accumulation of
blood
 Chylothorax- accumulation of
lymph and lipoprotein
Pleural Effusion
Assessment Findings:
 Fever
 Pain
 Dyspnea
 Dullness over the involved
area during chest percussion
 Diminished or absent
breath sounds
 Friction rub
 CXR & CT scan – shows
fluid accumulation
Pleural Effusion
 Medical management:
 Maingoal: eliminate the cause & relieve
discomfort
Antibiotics
Analgesics
Cardiotonic drugs to control CHF if
present
Thoracentecis
Insertion of a CTT
Surgery if cause by CA
Pleural Effusion
Thoracentesis
Nursing Guidelines:
 Explain the procedure to the client
 Reassure the client that he or she will receive local
anesthesia. Explain that the client will still experience
a pressure-like pain when the needle pierces the
pleura & when fluid is withdrawn
 Assist client to an appropriate position (sitting with
arms and head on padded table or in side-lying
position on unaffected side)
Thoracentesis
cont… Nursing Guidelines:
 Instruct the client not to move during the
procedure, including no coughing or deep
breathing
 Provide comfort, Inform client about what is
happening
 Maintain asepsis
 Monitor VS during the procedure – also monitor
pulse oximetry if client is connected to it
 During removal of fluid, monitor for respiratory
distress, dyspnea, tachypnea or hypotension
 Apply small sterile pressure dressing to the site
after the procedure
Thoracentesis
cont… Nursing Guidelines:
 Position the client on the unaffected side. Instruct
client to stay in this position for at least 1 hour and
to remain on bed rest for several hours
 Check that chest radiography is done after the
procedure
 Record the amount, color and other characteristics
of fluid removed
 Monitor for signs of increased RR, asymmetry in
respiratory movement, syncope or vertigo, chest
tighness, uncontrolled cough or cough that
produces blood-tinged or frothy mucus (or both),
tachycardia and hypoxemia
Pleural Effusion
Nursing Management:
 Ifwith CTT, monitor the function of the
drainage system & the amount & nature of
the drainage
Pleural Effusion
Pleural Effusion
Pleural Effusion
Pleural Effusion
 When caring for a client with chest
tubes, the nurse should be aware of the
following:
 Fluctuation of the fluid in the water-seal chamber
is initially present with each respiration.
Fluctuations cease when the lung reexpands. The
time for lung reexpansion varies. Fluctuations
also may cease if:
The chest tube is clogged
The wall suction unit malfunctions
A kink or dependent loop develops in the
tubing
Pleural Effusion
 When caring for a client with chest
tubes, the nurse should be aware of the
following:
 Bubbling in the water-seal chamber occurs in the
early postoperative period. If bubbling is
excessive, the nurse checks the system for leaks.
If leaks are not apparent, the nurse notifies the
physician
 Bloody drainage is normal, but drainage should
not be bright red or copious
 The drainage tube(s) must remain patent to
allow fluids to escape from the pleural space
Pleural Effusion
 When caring for a client with chest
tubes, the nurse should be aware of the
following:
 Clogging of the catheter with clots or kinking
causes drainage to stop. The lung cannot expand,
and the heart and great vessels may shift
(mediastinal shift) to the opposite side. The nurse
must be alert to the proper functioning of the
drainage system. Malfunctions need immediate
correction
 If a break or major leak occurs in the system, the
nurse clamps the chest tube immediately with
hemostats kept at the bedside. He or she notifies
the physician if this occurs
Fractured Ribs/ Sternum
 Common injury resulting from a
hard fall or a blow to the chest
 Automobile & household accidents
(frequent cause)
 Sharp end of the broken rib may
tear the lung or thoracic blood
vessels
Flail Chest
 Complication of chest trauma
occurring when 2 or more
adjacent ribs are fractured at two
or more sites, resulting in free-
floating rib segments
Fractured Ribs/ Sternum
 Paradoxic movement of the chest:
 The chest is pulled INWARD during inspiration,
reducing the amount of air that can be drawn
into the lungs
 The chest Bulges OUTWARD during expiration
because the intra-thoracic pressure exceeds
atmospheric pressure. The patient has impaired
exhalation
Fractured Ribs/ Sternum
 This paradoxical movement will lead to:
 Increased dead space
 Reduced gas exchange
 Decreased lung compliance, retained airway secretions
 Atelectasis, Hypoxemia
 Assessment findings:
 Severe PAIN on inspiration & expiration & obvious
trauma
 Shortness of breath
 Hypotension & inadequate tissue perfusion 2° to 
CO
 Respiratory acidosis
 CXR – confirms the diagnosis
Fractured Ribs/ Sternum
 Medical Management:
 Immobilize the fractured ribs
 rib belt or elastic bandage is used
especially in multiple rib fractures
 it can lead to decreased lung expansion
followed by pulmonary complications
(pneumonia & atelectasis)
 Pain: Analgesics (codeine), regional nerve
block
 Support ventilation, clear lung secretions
 Antibiotics
 ET intubation & mechanical ventilation
Fractured Ribs/ Sternum
 Nursing Management:
 Apply the immobilization device
 Stress the importance of taking deep
breaths every 1-2° even though
breathing is painful
 Plan & implement care based on
respiratory needs of clients with more
severe injuries
 Assess, monitor the client for signs of
respiratory distress, infection & pain
Pneumothorax
 Accumulation of air
in the pleural space
it can lead to partial or
complete collapse of the lung
 Types:
 Spontaneous
pneumothorax
 Open pneumothorax
 Tension pneumothorax
Pneumothorax
Spontaneous
pneumothorax
 Most common type of closed
pneumothorax
 Air accumulates within the
pleural space without an
obvious cause (no
antecedent trauma to
 thorax)
Rupture of a small bleb on the visceral
pleura most frequently produces this type
of pneumothorax
Pneumothorax
 Open pneumothorax
 usually caused by stabbing or gunshot wound
Pneumothorax
 Tension pneumothorax
 pressure in the pleural space is POSITIVE
throughout the respiratory cycle
 occurs in mechanical ventilation or resuscitation
 air enters the pleural space with each inspiration
but cannot escape
 causes  intra-
thoracic pressure
& shifting of the
mediastinal
contents to the
unaffected side
(mediastinal shift)
Hemothorax

 Accumulation of
BLOOD in the pleural
space

 frequently found w/ an
open pneumothorax
resulting in a
hemopneumothorax
Pneumothorax/ Hemothorax
Assessment findings:
 PAIN, Dyspnea
 Diminished/absent breath sounds on affected
side
 respiratory excursion on affected side
 Hyperresonance on percussion
 vocal fremitus
 Tracheal shift to the opposite side (tension
pneumothorax accompanied by mediastinal
shift)
 Weak, rapid pulse; anxiety; diaphoresis
Pneumothorax/ Hemothorax
Assessment findings:
 Diagnostic tests
 Chest x-ray reveals
area and degree of
pneumothorax
 ABG
Pneumothorax/ Hemothorax
Nursing interventions:
 Provide nursing care for the client with an ET
tube
 suctionsecretions, vomitus, blood from nose,
mouth, throat,
 monitor mechanical ventilation

 Restore/promote adequate respiratory function

 Assist with thoracentesis and provide appropriate
nursing care
 Assist with insertion of a CTT to water- seal
drainage and provide appropriate nursing care
Pneumothorax/ Hemothorax
Nursing interventions:
Pneumothorax/ Hemothorax
Nursing interventions:
 Continuously evaluate
respiratory patterns and
report any changes.
 Provide relief/control of pain.
 Administer narcotics/
analgesics/ sedatives as
ordered and monitor effects
 Position client in high-Fowler’s
position.
Myasthenia Gravis
 A neuromuscular
disorder in which
there is a
disturbance in the
transmission of
impulses from nerve
to muscle cells at the
neuromuscular
junction, causing
extreme muscle
weakness
Guillain-Barré Syndrome
 Symmetrical,
bilateral,
peripheral
polyneuritis
characterized
by ascending
paralysis
Pablo Jimenez's daughter, Ilsse, 17, helped
him exercise his arm to regain strength he
has lost as the result of Guillain-Barré
syndrome, which struck him several months
ago. Jimenez is a director for SER Jobs for
Progress, which helps low-income families get
job training.
 Amyotrophic Lateral Sclerosis
(Lou Gehrig’s Disease)
(Maladie de Charcot)
 Progressive motor
neuron disease,
which usually leads
to death in 2-6 years
Acute Respiratory Distress Syndrome
“Noncardiogenic pulmonary edema”,
“Adult respiratory distress syndrome”,
“Shock lung”
 An acute respiratory failure with the
following indications
 Hypoxemia that persists even when 100% O2 is given
 Decreased pulmonary compliance
 Dyspnea
 Non-cardiac-associated bilateral pulmonary edema
 Dense pulmonary infiltrates on x-ray (ground-glass
appearance)
Acute Respiratory Distress Syndrome
Etiology:
 Often ARDS occurs after an acute traumatic
event with no previous pulmonary disease
 Aspiration (near drowning, vomiting)
 Drug ingestion/ overdose
 Hematologic disorders (DIC, massive
transfusions)
 Direct damage to the lung (inhalation injury)
 Metabolic disorders (pancreatitis, uremia)
 Shock, Trauma, Major surgery, Embolism,
Septicemia
Acute Respiratory Distress Syndrome
Pathophysiology:

Body responds to injury by reducing

blood flow to the lungs
Platelet clumping Gas exchange
-Respiratory & metabolic
Release of histamine, acidosis
bradykinin, serotonin Surfactant
-Lungs become stiff &
Inflammation of
non-compliant
alveolar membranes
Pulmonary edema microatelectasis
Acute Respiratory Distress Syndrome
 Assessment Findings:
 Severe respiratory distress
develops within 4-8° after the
onset of illness or injury
 RR, shallow, labored
respirations, use of accesory
muscles, cyanosis
 Respiratory distress
unrelieved w/ O2
administration
 Anxiety, restlessness, mental
confusion, agitation,
drowsiness
Acute Respiratory Distress Syndrome
 Medical Management:
 Initial
cause must be diagnosed & treated
 Administration of humidified oxygen
 ET or tracheostomy tube insertion
 Mechanical ventilation (PEEP, CPAP)
 Client’spulmonary status, determined by ABG findings &
pulse oximetry results, dictates the oxygen
concentration & ventilator settings
 Complications associated with PEEP include tension
pneumothorax & pneumomediastinum
 Colloids(albumin) for pulmonary edema
 Adequate nutritional support: enteral feeding (tube
feeding), parenteral (hyperalimentation)
Acute Respiratory Distress Syndrome
 Nursing Management:
 Focus:promotion of oxygenation & ventilation,
prevention of complications that includes:
 Deteriorating
respiratory status, Infection, Renal failure,
Cardiac complications
 Assess lung sounds hourly & suction as needed to
maintain a patent airway
 Provide explanations & support
 Provide alternative methods for the client to
communicate if hook up to a ventilator
Pulmonary Embolism
 Obstruction of
one of the
pulmonary
arteries or its
branches caused
by a thrombus
that forms in the
venous system or
right side of the
heart
Pulmonary Embolism
Thrombus Embolus
Virchows Triad: Traveling blood clot, air, fat
venostasis, vessel Deep vein of lower X, MI,
injury, endocarditis, bone fractures,
hypercoagulability surgery, prolonged bed rest,
trauma, post-partum state,
debilitating dses
Occlusion of the PA

Infarction (necrosis
or death of the lung
tissue)
Pulmonary Embolism
Pulmonary Embolism
 Assessment Findings:
 Pain, tachycardia, dyspnea, fever, cough, blood
streaked-sputum
 Larger areas are involved: more pronounced S/Sx
 Severe dyspnea, Severe pain, Cyanosis,
Tachycardia, Restlessness, Shock
 Massive pulmonary infarction: SUDDEN DEATH
will occur
 CXR – may reveal areas of atelectasis
 Lung scan, CT scan, pulmonary angiography –
identify & detect the involved lung tissue
Pulmonary Embolism
 Medical & Surgical Management:
 Administration of IV heparin
 Administration of thrombolytic drugs
 Urokinase, streptokinase, t-PA
 Anticoagulants are given after thrombolytic therapy

 CBR, O2, analgesics

 Pulmonary embolectomy
 Insertion of umbrella filter device (greenfield filter)
 Insertedusing a catheter into the right internal jugular
vein & threaded downward to an area below the renal
arteries
 Teflon clips (inferior vena cava)
Pulmonary Embolism
Pulmonary Embolism

The AngioGuard is an
umbrella-shaped
filter with 100-
micron-wide holes.
Courtesy Cordis
Lung Resections
 Lobectomy
 removal of one lobe of a lung; treatment for
bronchiectasis, bronchogenic carcinoma,
emphysematous blebs, lung abscesses
 Pneumonectomy
 removal of an entire lung; most commonly done as
treatment for bronchogenic CA
 Segmentectomy/ Segmental resection
 segment of lung removed; most often done as treatment
for bronchiectasis
 Wedge resection
 removal of lesions that occupy only part of a segment of
lung tissue; for excision of small nodules or to obtain a
biopsy
Lung Resections
Lung Resections
 Nursing interventions: PREOPERATIVE
 Provide routine pre-op care.
 Perform a complete physical assessment of the
lungs to obtain baseline data.
 Explain expected post-op measures: care of
incision site, oxygen, suctioning, chest tubes
(except if pneumonectomy performed)
 Teach client adequate splinting of incision with
hands or pillow for turning, coughing, and deep
breathing.
 Demonstrate ROM exercises for affected side.
 Provide chest physical therapy to help remove
secretions
Lung Resections
 Nursing interventions: POSTOPERATIVE
 Provide routine post-op care
 Promote adequate ventilation
Perform complete physical assessment of
lungs and compare with pre-op findings.
Auscultate lung fields every 1-2 hours.
Encourage turning, coughing, and deep
breathing every 1-2 hours after pain relief
obtained.
Perform tracheobronchial suctioning if
needed.
Lung Resections
 Nursing interventions: POSTOPERATIVE
 cont… Promote adequate ventilation.
 Assess for proper maintenance of chest drainage
system (except after pneumonectomy).
 Monitor ABGs and report significant changes.
 Place client in semi-Fowler’s position
 If pneumonectomy is performed, follow
surgeon’s orders about positioning, often on
back or operative side, but not turned to
unoperative side).
 If Lobectomy, patient is usually positioned on
the UNOPERATIVE SIDE
Lung Resections
 Nursing interventions: POSTOPERATIVE
 Provide pain relief.
 Administer narcotics/analgesics prior to turning,
coughing, and deep breathing.
 Assist with splinting while turning, coughing,
deep breathing.
 Provide client teaching and discharge
planning concerning
Need to continue with coughing/deep
breathing for 6-8 weeks post-op and to
continue ROM exercises
Importance of adequate rest with gradual
increase in activity levels
Lung Resections
 Nursing interventions: POSTOPERATIVE
 cont… Provide client teaching and
discharge planning concerning
High-protein diet with inclusion of
adequate fluids (at least 2 liters/day)
Chest physical therapy
Good oral hygiene
Need to avoid persons with known
upper respiratory infection
Lung Resections
 Nursing interventions: POSTOPERATIVE
 cont… Provide client teaching and
discharge planning concerning
Adverse signs and symptoms
recurrent fever, anorexia, weight loss,
dyspnea, increased pain, difficulty
swallowing, shortness of breath,
changes in color, characteristics of
sputum, & importance of reporting to
physician
Avoidance of crowds and poorly
ventilated areas.
Lungs