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PHYSIOTHERAPY UNIT 3:
THE CARDIORESPIRATORY SYSTEM
2010
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THE RESPIRATORY SYSTEM

ANATOMY & PHYSIOLOGY

Consists of 2 systems:
Upper Respiratory System includes nose and pharynx
Lower Respiratory System includes larynx, trachea, bronchi, and lungs

Consists of 2 zones:
Conducting Zone
o Series of interconnecting cavities and tubes
outside and inside the lungs (i.e. nose,
pharynx, larynx, trachea, bronchi, bronchioles,
and terminal bronchioles)
o Function to filter, warm, and moisten air,
which is then conducted to the lungs
Respiratory Zone
o Consists of tissues within the lungs where gas
exchange occurs (i.e. respiratory bronchioles,
alveolar ducts, alveolar sacs, and alveoli)
o Function as the main site of gas exchange
between air and blood

Structures:
The nose
- Filters large particles and traps water to prevent dehydration, moisten air
- Cilia move mucus to pharynx to be swallowed or spit out

The pharynx
- 5 inches extends to cricoid cartilage and
lies posterior to nasal/oral cavities
- Composed of skeletal muscle lined with a
mucous membrane
- Contraction assists in deglutition and is a
passageway for air and food

The Larynx
- Anterior to esophagus composed of nine
cartilage pieces
- Epiglottis consists of elastic cartilage
covered with epithelium
- Elevation of pharynx widens to receive food
and elevation of larynx causes epiglottis to
move down and form a lid over glottis closing it of

The Trachea
- 5 inches long and 2.5 cm in diameter anterior to esophagus
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- Extends to T5 divides into Rt. And Lt. primary bronchi
- Consists of 16-20 cartilage C rings with open part posteriorly
- Mucous consists of epithelium (i.e. pseudostratified ciliated columnar
epithelium), lamina propria (i.e. elastic and reticular fibers)

The Bronchi
- Rt. More vertical, shorter, and wider thus aspiring risk
- Contain rings of cartilage and lined by pseudostratified ciliated columnar
epithelium
- On entering lungs divide into smaller bronchi called secondary (lobar) bronchi
- Secondary bronchi branch into tertiary (segmental) bronchi, which divide in
terminal bronchioles
- The branching is referred to as bronchial tree

The Lungs
- Each enclosed in a double layered serous membrane called pleural membrane
- Superficial layer, attached to thoracic wall is the parietal pleura
- Deep layer, attached to lungs is the visceral pleura
- Interpleural space contains lubrificating fluid causes decreased friction and
causes surface tension
- Costal surface is against the ribs
- Lt. lung contains cardiac notch and is 10% smaller than Rt. Lung
- Rt. Lung is thicker and broader, but shorter to accommodate liver
- Lungs extend to rib 6 anteriorly and T10 posteriorly, with pleura 5 cm lower
anteriorly and T12 posteriorly

Lobes, Fissures, & Lobules

- Both have an oblique fissure extending inferiorly and anteriorly
- Rt. Lung has horizontal fissure
- Lt. oblique fissure separates superior and inferior lobe
- Rt. oblique fissure separates superior and inferior lobe and inferior lobe from
middle lobe, bordered superiorly by horizontal fissure

- Rt. Primary bronchus gives rise to 3 secondary (lobar) bronchi called superior,
middle, and inferior secondary (lobar) bronchi
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- The secondary give rise to tertiary (segmental) bronchi there are 10
- Segment supplied is called a bronchopulmonary segment each containing
many small compartments called lobules
- Terminal bronchioles subdivide into respiratory bronchioles several alveolar
ducts
- Trachea alveolar ducts = ~25 orders of branching

The alveoli
- Around alveolar ducts = numerous alveoli and alveolar sacs
- Alveolus lined by simple squamous epithelium and supported by elastic
membranes
- Type 1 squamous epithelial cells continuous lining of alveolar wall; main
sites of gas exchange
- Type 2 septal cells fewer in numbers and secrete alveolar fluid containing
surfactant
- Lungs = 300 million alveoli with surface area 70 m^2

BLOOD SUPPLY TO THE LUNGS

Lungs receive via pulmonary and bronchial arteries
DeO2 blood through pulmonary trunk Lt. and Rt. Pulmonary artery each
entering respective lung
O2 blood return to heart by 4 pulmonary veins Rt. Atrium

- Unique feature vasoconstriction in response to localized hypoxia

- In all other vessels hypoxia cause vasodilation
- This phenomenon is called ventilation-perfusion coupling perfusion to each
area of lungs matches extent of ventilation to alveoli in the area

PULMONARY VENTILATION
Respiration consists of 3 steps:
(1)Pulmonary Ventilation inhalation/exhalation and exchange of air between
atmosphere and alveoli
(2)External (Pulmonary) Respiration exchange of gases between alveoli and
lungs & the blood in pulmonary capillaries (gain O2, loses CO2)
(3)Internal (Tissue) Respiration exchange of gases between blood in systemic
and tissue (blood loses O2, gains CO2)

Pressure Changes During Pulmonary Ventilation

- Air moves in when air pressure inside the lungs < atmospheric pressure
- Air moves out when air pressure inside lungs > atmospheric pressure

Inhalation
- Before inhalation air pressure inside lungs is equal to atmospheric pressure
- Pressure in alveoli must become < than atmospheric pressure
- Therefore increase in lung volume is necessary

BOYLES LAW: AS VOLUME INCREASES, PRESSURE DECREASES

AS VOLUME DECREASES, PRESSURE INCREASES
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- Increased lung volume is achieved with diaphragmatic & ext. intercostal action
- Diaphragm innervated by phrenic nerves from C3-C5
- Diaphragm descends accounts 75% of air entering
- External intercostals elevate ribs, increase A-P, & lateral diameters 25% of air

- During quiet inspiration IP pressure is always subathmospheric

- Just before inhalation - ~ 4mmHg less than atmospheric
- Volume of pleural cavity also increases thus IP pressure decreases
- During thoracic expansion pleuraes adhere tightly due to subathmospheric
pressure btw them and surface tension thus parietal pleura is pulled out and
visceral pleura must follow
- Alveolar pressure drops thus pressure diference established btw atmospheric
and alveoli = INHALATION
- Accessory muscles include SCM, scalenes, pecs, and back.
- Inhalation is an ACTIVE process!

Exhalation
- Pressure in lungs > pressure of atmosphere
- Exhalation is PASSIVE process result of elastic recoil of chest wall & lungs
(have a tendency to spring back after stretch = elastic fibers & surface
tension)
- Starts with relaxation of inhalation muscles
- Decrease in thoracic volume leads to decrease of lung volume
- Alveolar pressure increases air flows from area of higher pressure to lower
pressure
- Exhalation is ACTIVE when forced!
- Muscles include the internal intercostals and the abdominal muscles increase
pressure in abdominal region and thorax moving ribs down and compressing
viscera thus forcing diaphragm superiorly
- Internal intercostals pull ribs inferiorly
- Although IP pressure is always less than alveolar pressure may briefly exceed
Patm during forceful exhalation such as a cough

Other Factors Afecting Pulmonary Ventilation (Flow Rate):

(1)Surface Tension of Alveolar Fluid
a. Causes alveoli assume small diameter surface tension needs to be
overcome for inhalation surface tension accounts for 2/3 of elastic recoil
(decreases size of alveoli during exhalation)
b. Surfactant decreases surface tension to below pure water
(2)Compliance of Lungs
a. Refers to the efort required to stretch lungs and chest wall
b. High compliance = easily expandable; Low compliance = resist expansion
c. Compliance is related to elasticity and surface tension
d. Causes: scar lung tissue, lung tissue filled with fluid, deficiency in
surfactant, or impeded lung expansion
(3)Airway Resistance
a. Increases during exhalation as diameter of bronchioles decrease
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b. ANS sympathetic cause relaxation of smooth muscle = bronchodilation
and decreased resistance
(4)Breathing Patterns and Modified respiratory Movements
a. Normal pattern = eupnoea
b. Costal, diaphragmatic, & apical patterns all adapts for cough, sneeze,
sigh, yawn, sob, cry, laugh, hiccup, valsava maneuver
c. Most reflexes can be initiate voluntarily

LUNG VOLUMES & CAPACITIES

- At rest normal breath ranges = 12-18 breaths/minute
- Each inhalation/exhalation = 500 ml of air
- Tidal volume = volume of one breath
- Minute ventilation = total air inhaled/exhaled in a minute
- MV = TV * RR

- Spirometer inhalation is an upward deflection and exhalation is a downward

deflection
- 70% of TV reaches respiratory zone, other 30% remains in conduction zone
and is termed anatomical dead space
- Inspiratory reserved volume = the air that does not reach the respiratory zone
- Expiratory reserved volume = additional air exhaled
- FEV1 = forced expiratory volume in 1 second max exhalation following max
inhalation
- The lower pressure in IPP keeps alveoli slightly inflated this air is called
residual volume
- With the pleural cavity opened IPP = Patm air flows out, air remaining is
termed minimal volume
- Inspiratory capacity is the sum of tidal volume and inspiratory reserve volume
- Functional residual capacity is the sum of residual volume and expiratory
reserve volume
- Vital capacity is the sum of inspiratory reserve volume, tidal volume, and
expiratory reserve volume
- Total lung capacity is the sum of vital capacity and residual volume

EXCHANGE OF OXYGEN AND CARBON DIOXIDE

Gas Laws pressure of specific gas in a mixture = partial pressure

Atmospheric air:
Nitrogen 78.6%
Oxygen 20.9%
CO2 0.04%
Other 0.06%
Water Vapor Variable

- Gas difuses across from an area where its partial pressure is > than the area
where its partial pressure is less the greater the diference the faster the rate
of difusion
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- Alveolar air has < O2 and > CO2 than inhaled air gas exchange in alveoli
increases CO2 and decreases O2
- Exhaled air contains > O2 than Alveolar air

External Respiration
- External respiration (i.e. pulmonary gas exchange) = difusion of O2 from air in
alveoli to blood in pulmonary capillaries & difusion of CO2 in other direction
- Converts DeO2 from Rt. Heart into O2 blood returns to Lt. heart
- Blood flows through pulmonary capillaries picks up O2 from alveolar air and
unloads CO2 into alveolar air
- Alveolar air PO2 = 105 mmHg
- Pulmonary Capillaries PO2 = 40 mmHg at rest
- Exercise PO2 < 40 mmHg
- Difusion occurs until PO2 of pulmonary capillary blood increases to match PO2
of alveolar pressure
- PO2 is less in pulmonary veins ~ 100 mmHg

- CO2 is difusing in opposite direction PCO2 of deO2 blood is 45 mmHg at rest

and PCO2 is 40 mmHg in alveolar air
- CO2 difuses from deO2 blood into alveoli until PCO2 of blood decreases to 40
mmHg

Internal Respiration (i.e. systemic gas exchange)

- Lt. Ventricle pumps O2 blood to aorta & through systemic arteries systemic
capillaries
- The exchange of O2 and CO2 btw systemic capillaries & tissue cells = int.
respiration
- PO2 of blood pumped in systemic (100 mmHg) > than PO2 in tissues (40
mmHg) at rest due to constant use of O2 to produce ATP in tissue
- O2 difuses out of capillaries into tissue cells and blood PO2 drops to 40 mmHg
- CO2 difuses in the opposite direction tissue cells are constantly producing
CO2 PCO2 (45mmHg) at rest is higher than systemic capillary blood PCO2 (40
mmHg)
- CO2 difuses from tissue to systemic capillaries until PCO2 in blood increases to
45mmHg
- DeO2 returns to heart and then lungs

Rate of Pulmonary & Systemic Gas Exchange Depends on:

(1)Partial Pressure of diferent gases
(2)Surface are for gas exchange
(3)Difusion distance build up of interstitial fluid slows the rate
(4)Molecular weight & solubility of gases

TRANSPORT OF OXYGEN & CARBON DIOXIDE

O2 Transport
1-3% dissolved in plasma
97% bound to hemoglobin = oxyhemoglobin
Easily reversible reaction
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Relationship btw Hb & O2 Partial Pressure

Higher PO2 = more O2 binds with Hb
Oxyhemoglobin = fully saturated
More binding = ~100% saturated
Pulmonary capillaries = PO2 is high = lot of binding with Hb
Tissue = PO2 is low = not as much binding

Other Factors Afecting Affinity of Hb to for O2

Acidity (pH)
o Increases affinity of Hb for O2 decreases & O2 disassociates
o Acids produced are lactic & carbonic acid
o Decreases O2-Hb disassociate curve shift to the Rt.
o Bohr efect: Increases in H+ in blood causes O2 to unload from Hb & binding
of O2 to Hb causes unloading of H+ from Hb explanation is that Hb can act
as a bufer for H+
o Lowered pH drives O2 of Hb = allows more O2 for tissues
o Elevated pH increases affinity of Hb for O2 = curves shift to Lt.
Partial Pressure of CO2
o As PCO2 rises Hb releases O2 more readily
o Low blood pH results from high PCO2
o As CO2 is in blood much converted to carbonic acid dissociates into H+
and bicarbonate ions
o As H+ increases, pH decreases thus increased PCO2 = acidic environment
o Lactic acid also decreases pH
Temperature
o Temperature increases O2 released from Hb increases
o The acids and heat promote release of O2 from oxy-Hb in metabolically
active tissue
o Hypothermia cellular metabolism slows, need for O2 decreases, O2 bound
BPG
o Helps unload O2 from Hb
o Hormones such a thyroxinem HGH, epinephrine, norepi, & testosterone
increase formation of BPG
o Higher levels in high altitude living individuals

Carbon Dioxide Transport

3 ways:
(1)Dissolved CO2 ~ 7% in plasma upon reaching lungs difuses into alveolar air =
exhaled
(2)Carbamio compounds - ~ 23% binds with a.a. = carbamino compounds most
transported this way is bound to Hb termed carbaminoHb in tissue capillaries
PCO2 is high promoting formation of CO2Hb, but in pulmonary capillaries PCO2 is
low and CO2 rapidly splits apart from globin & enters alveoli by difusion
(3)Bicarbonate ions 70% transported in blood this way CO2 reacts with water to
form carbonic acid, which disassociates into H+ and HCO3-. CO2 is removed from
tissue cells and transported in plasma as HCO3- - as blood passes through
pulmonary capillaries in lungs all these reactions reverse and CO2 is exhaled.
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The lower the amount of HbO2 the higher the CO2 carrying capacity of blood
relationship known as Haldane efect.
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CONTROL OF RESPIRATION
Respiratory Center
Nerve impulses sent from neurons in medulla oblongata and pons of brainstem
Divided in 3 areas:
o Medullary Rhythmic Center = control basic rhythm composed of inspiratory
and expiratory areas. Inhalation lasts 2 seconds and exhalation 3 seconds.
Inspiratory area establishes basic rhythm by generating impulses every 2
seconds to the diaphragm and external intercostals via phrenic nerves and
intercostal nerves. It becomes inactive for 3 seconds to allow passive
expiration. Expiratory area only active during forceful expiration.
o Pneumotaxic Area = coordinates transition btw inhalation & exhalation.
Located in upper pons transmits inhibitory impulses to inspiratory area
turns of area before lungs become too full of air impulses shorten
inhalation when this center is active RR is elevated
o Apneustic Area in lower pons and performs same as pneumotaxic area.
Sends stimulatory impulses to inspiratory area that active it and prolong
inhalation. Results in deep inhalation. Pneumotaxic area overrides apneustic
area

Regulation of Respiratory Center

Cortical Influences on Respiration
Cerebral cortex allows voluntary control over our breathing pattern
We cant stop ourselves from breathing fainting will occur as a protective
mechanism

Chemoreceptor Regulation of Respiration

Chemical stimuli can modulate speed and depth of breathing
Chemoreceptors in 2 locations monitor levels of CO2, H+, & O2 and provide info
to respiratory center
Central chemoreceptors are located near medulla oblongata in CNS respond to
changes in H+ concentration or PCO2, or both in CSF
Peripheral chemorecpetors are located in aortic & carotid bodies sensitive to
changes in PO2, H+, & PCO2 in blood
Aorta vagus (X) nerve & glossopharyngeal (IX) nerves
Increase in CO2 in blood causes an increase in H+ inside cells & a decrease in
CO2, causes a decrease in H+
PCO2 in arterial blood is 40 mmHg if a slight increase occurs a condition called
hypercapnia or hypercarbia central chemoreceptors are stimulated & respond
vigorously to resulting increase in H+ level
Peripheral chemoreceptors respond to a deficiency of O2 as well as PCO2 & H+
PO2 falls from norm of 100mmHg, but still above 50mmHg peripheral
chemoreceptors are stimulated
Severe deficiency of O2 depresses activity of central chemoreceptors and
inspiratory area, which leads to sending fewer impulses to muscle of inspiration
As breathing decreases PO2 falls lower and lower establishes a positive
feedback cycle with possible fatal results
Chemoreceptors work in a negative feedback system regulates CO2, O2, & H+
in blood
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With increased PCO2 decreased pH (i.e. increased H+), or decreased PO2
central and peripheral chemoreceptors causes inspiratory area to become highly
active and rate, depth of breathing, and increase.
Hyperventilation increases inhalation, thus increase O2, decrease CO2, until
PCO2 & H+ are lowered to normal.
If arterial PCO2 < 40 mmHg called hypocapnia or hypocarbia central and
peripheral chemoreceptors are not stimulated no impulses are sent to
inspiratory center area sets its moderate pace until CO2 accumulates and PCO2
> 40 mmHg

Proprioceptor Stimulation of Respiration

With exercise rate & depth of breathing increase, before changes in PO2, PCO2,
& H+ levels occur
Input from proprioceptors, monitor movement stimulate inspiratory area

Inflation Reflex (Hering-Breuer)

Stretch-sensitive receptors called baroreceptors or stretch receptors located in
bronchi/bronchioles
Nerve impulses are sent along vagus nerves to inspiratory & apneustic areas
when these receptors are provoked
Inspiratory area is inhibited directly & the apneustic area is inhibited from
activating inspiratory area, thus exhalation occurs
As air leaves stretch receptors are no longer stimulated, thus inhibition is no
longer occurring
It is mainly a protective mechanism for preventing excessive inflation

Other Influences on Respiration

Limbic system stimulation anxiety stimulates system sends excitatory input to
inspiratory area increasing rate and depth of ventilation
Temperature increase in body temperature increases RR & vice versa; a sudden
cold stimulus causes temporary apnea
Pain severe pain brings on brief apnea, while prolonged somatic pain increases
RR; visceral pain may slow RR
Stretching anal sphincter increases RR
Irritation of airways followed by cough/sneeze after sudden cessation of
breathing
Blood Pressure a rise in BP decreases RR & a drop in BP rises RR

EXERCISE & THE RESPIRATORY SYSTEM

- As CO2 rises blood flow to lungs increases as well
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- O2 difusing capacity (alveolar air to
blood) can increase 3 fold
- Greater surface area available for
difusion of O2 into pulmonary blood
capillaries
- Muscles contract consume O2 and
produce CO2 O2 & pulmonary
ventilation both increase dramatically
(i.e. O2 uptake increases)
- Neural changes that send excitatory
impulses to inspiratory area include:
anticipation, sensory impulses from
proprioceptors, & motor impulses from
primary cortex
- Gradual increase in ventilation due to chemical and physical changes
including: slightly decreased PO2 due to increase O2 uptake, slightly increased
PCO2 due to increase CO2 production, & increased temperature
- Initial decrease, post exercise, is due to changes in neural factors when
movement stops or slows; the more gradual phase reflects the slower return of
blood chemistry levels & temperature to resting rate

Efects of Long Term Exercise

- The respiratory muscles get stronger so they can make the chest cavity larger. The
larger cavity indicates an increased volume, thus increase vital capacity. More
capillaries form around the alveoli, thus increase gaseous exchange. Therefore maintain
a higher intensity for longer.

AGING & THE RESPIRATORY SYSTEM

- Airways & tissues become less elastic & more rigid
- Chest wall becomes rigid, thus decrease lung capacity
- Vital capacity decrease ~ 35% by 70 yoa
- Decreases in blood level of O2
- Decreased activity of alveolar macrophages
- Decrease ciliary action of epithelium lining of respiratory tract
- These make aged individuals more susceptible to pneumonia, bronchitis,
emphysema, & other pulmonary complications
- Reduced ability to perform vigorous exercises such as running.

Function Pathophysiological Changes Key Clinical Findings

Breathing Decreased chest wall compliance Decreased VC

Mechanics Loss of elastic recoil Increased RV
Decreased respiratory muscle mass/strength Decreased EFRates
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Oxygenation Increase ventilation/perfusion mismatch
Decrease CO Decreased PaO2
Decreased mixed venous O2 Increase alv-art.O2
Increase physiological deadspace Decreased CO2
Decrease alveolar surface area
Decreased CO2 difusion capacity
Ventilation Decreased responsiveness of central & peripheral Decrease TV
Control & chemoreceptor to hypoxemia & hypercapnia Increased RR
Breathing Increased MV
Pattern Decreased Airway
Clearance
Lung Defense Decreased number of cilia & muscuciliary
Mechanisms clearance Increase risk of infection
Decreased cough reflex Increased risk of
Decreased humoral & cellular immunity aspiration
Decreased IgA production
Sleep & Decreased ventilation drive Increased risk of apnea,
Breathing Decreased to ne of upper airway muscles hypopnea, aspiration,
Decreased arousal snoring
Decreased SO2
Obstructive Sleep Apnea
Exercise Muscle deconditioning & efficiency Decreased Max O2
Capacity Decreased muscle mass consumption
Decreased reserves Breathlessness at low
exercise levels
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FACTORS AFFECTING OXYGENATION

Adequacy of circulation, ventilation, perfusion, & transport of respiratory gases to
tissues are influenced by 4 factors:
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(1)Physiological Factors
a. Cardiac disorders
b. Oxygen carrying capacity disorders
c. Decreased inspired O2 concentration
d. Hypovolemia
e. Increased metabolic rate
f. Chest wall deformities pregnancy/obesity/scoliosis
g. MSK abnormalities
h. Nervous system disorders
(2)Developmental Factors
a. Premature
b. Infants/toddlers
c. School age/adolescents
d. Young/middle adults
e. Older adults
(3)Behavioral Factors
a. Lifestyle nutrition, exercise, smoking
(4)Environmental
a. Pollution

RESPIRATORY CONSEQUENCES OF OBESITY

General Health Hazards
Coronary artery disease, congestive heart failure
Hypertension, type II diabetes mellitus
Hypercholestremia
Choletithiasis
OA, CTS
Venous insufficiency, DVT
Increase all cause mortality

Efects on Respiratory Physiology

Decrease compliance (chest wall>>lung)
Increase airway resistance
Increase work of breathing
Respiratory muscle dysfunction
Ventilation perfusion inequality
Alterations in gas exchange

Pulmonary Function Results

Decreased forced expiratory volume & forced vital capacity
Decreased expiratory reserve volume, functional residual capacity & residual
volume
Decrease in total lung capacity, vital capacity
Decreased maximal voluntary ventilation

Efects on Exercise Physiology

Increase resting O2 consumption (VO2)
Decreased VO2 when adjusted for weight
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Work inefficiency
Increased RR, decreased tidal volume
Normal breathing reserve, dead space, O2 pulse
Increase RHR

Cardiovascular Efects
Increase circulation blood volume
Increase myocardial mass
Increase incidence of diastolic dysfunction
Mild elevation in pulmonary artery pressure

Obesity & Dyspnea

Increase sense of dyspnea

Other Efects
Increase risk of obstructive sleep apnea
Obesity hypoventilation syndrome
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CLINICAL PULMONARY ASSESSMENT IPPA
HISTORY
Goal is to identify & describe key clinical manifestations that will aid in the
identification of the cause of illness

COUGH
Caused by irritation or inflammation of the airways
One of the most common chief complaints
External & internal causes include dust, hot/cold air, foreign bodies, chemical
irritants, secretion, exudates, inflammatory processes, blood, compression of
bronchi, and Lt. heart failure
Cough is documented is strong or weak, as well as brassy, barking, dry, moist,
hoarse, harsh, or bubbling
A brassy cough may indicate compression of the airways by a tumor, a barking or
hoarse cough may indicate the presence of croup
If productive cough is present, the color, consistency, amount, & odor should also
be documented

HEMOPTYSIS
Potentially life-threatening is the expectoration of blood from the respiratory
tract
Blood ranges from blood-tinged sputum to hemorrhage
Etiologies include inflammation, infections, lung abscess, pulmonary embolism,
tumors, and pneumonia

DYSPNEA
The most common manifestation of pulmonary dysfunction is dyspnea
Dyspnea is breathing discomfort that varies in intensity it is derived among
interactions btw multiple physiological, psychosocial, social, & environmental
factors and may induce secondary behavioral responses
Dyspnea is subjective and is described by pt uncomfortable sensation
Manifestations of increase work of breathing, anxiety, restlessness, insomnia,
difficulty concentrating, use of accessories, & orthopnea
Neural activation of the aferent-receptors is responsible for the sensation, while
the cortex & limbic areas in the brain determine pts reaction
Etiology includes pneumonia, pulmonary emboli, ischemia of myocardium,
obesity, anemia, neuromuscular disease, hot humid or cold weather, cancer
Can be acute or chronic chronic dyspnea is consistently present with periodic
exacerbations and may difer in perceived degree of shortness of breath
Often accompanied by fatigue and causes physical deconditioning
Timing of dyspnea, precipitating factors such as: physical activity, emotional
stress, position, exposure to irritants, anemia, pain; associated symptoms such as
cough, chest pain, wheezing; relieving factors such as position change, meds, and
pts description should be documented
The pt rates dyspnea from 0 to 5 (severe shortness of breath) to 10 (worst
imaginable)

ORTHOPNEA/PLATYPNEA/PAROXYSMAL NOCTURNAL DYSPNEA

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Orthopnea is an increase in dyspnea in the supine position
Platypnea is shortness of breath that occurs in the upright position may be
accompanied by an increased RR and shallow respirations may be related to
thoracic surgery, inflammation of pleurae, or Lt. sided heart failure
Paroxysmal dyspnea is the sudden onset of dyspnea & coughing that occurs 1-2
hrs after sleep relieved by sitting up and is usually associated Lt. sided heart
failure

INSPECTION
General appearance, posture, ventilatory pattern, and respiratory eforts should
be continued throughout the assessment, especially during position changes

SKIN
Cyanosis noted centrally (nose, tongue, sublingual area, oral mucosa) and
peripherally (finger tips and toes)
Skin color is described as ashen or pale
It is a blue-gray or purplish discoloration of the skin when blood contains >
5gm/dL reduced Hb
The detection depends on acuity of observer, light intensity, skin pigmentation, &
Hb level; May be present with increased hematocrit
Peripheral cyanosis may be due to cool room temperatures, diabetes mellitus, or
peripheral vascular disease causes vasoconstriction or reduced blood flow
Central cyanosis is a sign of significant oxygen desaturation if present observe
for changes in cognitive function

Digital Clubbing & Hypertrophic Osteoarthropathy

Clubbing sponginess at the base of the nail, angle > 160 degrees btw distal
phalanx & cuticle usually bilateral in fingers & toes
Etiology in conditions that alter cardiopulmonary function, such as CF,
congenital heart disease, Hodgkins disease, bronchogenic cancer, lung abscess,
bronchiectasis, and asbestosis, also local tissue hypoxia, inflammatory bowel
disease, hepatic cirrhosis, and bacterial endocartis. If present in COPD,
bronchogenic cancer should be suspected.
Hypertrophic Osteoarthropathy formation of new bone over distal arms and legs
misdiagnosed as arthritis and is often caused by bronchogenic cancer

Neurologic Function
Level of Consciousness, Orientation, Cognitive Function
This should be determined immediately
Cerebral neurons are very sensitive to hypoxia, a decrease in tissue oxygenations,
and hypercapnia, an increase in arterial carbon dioxide levels. Initially, hypoxia
may alter cerebral function without loss of consciousness causing inattentiveness,
poor judgment, and uncoordinated motor function. More severe hypoxia may
cause global ischemia in the brain and altered neurologic function, including
coma. Seizures and altered motor response to stimuli, including flaccidity &
rigidity
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Hypercapnia has a significant efect on neurologic function, primarily due to the
vasodilation of the cerebral vessels may complain of headache, confusion to
coma, and may develop muscle twitching

Pulmonary System
Examine anterior, lateral, & posterior aspects of the chest comparing both sides

Chest Shape
Shape configuration of the chest best observed in sitting position
Pectus excavatum = funnel chest observed when lower 2/3 of sternum is
depressed, causing a decrease in AP diameter and lung capacity
Pectus carniatum = pigeon breast is an abnormal protrusion of the upper part of
the sternum with an increase in AP diameter
Consider kyphosis, scoliosis, kyphoscoliosis, or ankylosing spondylitis may restring
lung expansion and reduce functional residual capacity, or the lung volume
remaining in the lungs after a normal exhalation
Normally AP diameter is of transverse diameter
An increase in AP = barrel chest and is common in COPD & CF

Nasal Flaring
Noted during inspiration & indicates severe respiratory distress

Pursed Lip Breathing

Observed during increased work of breathing, increases lung capacity by
preventing collapse of the alveoli & smaller airways during expiration
A normal compensatory response or part of the therapeutic regimen for pts with
conditions that collapse the airways such as emphysema
It decreases RR, reduces energy expenditure, and increases time allowed for
alveolar ventilation

RR & Rhythm
Respiratory eforts is evaluated by rate, rhythm, symmetry, & quality of
movement
Normal RR is 12-20 breaths/minute with expiratory period approximately twice as
long as inspiratory period
Prolonged expiratory period may indicate constriction of lower airways, especially
in chronic lung disease or asthma
Tachypnea is defined as an increase in RR with shallow respirations typically when
breathing is 20X per minute or greater causes include restrictive lung disease,
hypermetabolic states, stress, tissue hypoxia, exercise, pleural inflammation, or a
decrease in thoracic volume
Hyperpnea exists where there is rapid, deep breathing > 20-25 breaths per
minute may be normal with exercise, anxiety, high altitudes or metabolic
acidosis other symptoms include dizziness or decreased BP
Bradypnea RR of less than 10 breaths/minute associated with sleep, diabetic
coma, hypothermia, metabolic acidosis, acute renal failure, drug-induced
respiratory depression, or increased intracranial pressure it may precede periods
of apnea or cardiorespiratory arrest and may cause hypoxemia or hypercapnia
24 of 107
Hypoventilation a decrease in tidal volume described as shallow respirations,
may occur with tachypnae or bradypnea decrease in tidal volume may cause
hypoxemia or hypercapnia causes include obesity, neurologic depression from
anesthetics/opiates, pain from surgery or pulmonary infarction, prolonged
bedrest, neurologic dysfunction from neuromuscular disorders, SCI, or
cerebrovascular accidents, or a compensatory mechanism for metabolic alkalosis
Cheyne-Stokes respirations (CSR) pattern of breathing with increasing and
decreasing depth of respiration and intermittent periods of apnea lasting 15-30
seconds normally observed in children and older adults during sleep etiologic
causes include heart failure, uremia, drug-induced respiratory depression, & brain
damage
Ataxic or Biots breathing varying depths & an irregular pattern of respiration
often associated with brain damage
Paradoximal breathing seen in chest trauma attached part of thorax moves in
opposite direction from what it normally does
Increased RR with decreased depth may be due to myocardial ischemia, pleuritic
inflammation of pleurae, thoracic/abdominal surgery, fever, abdominal/liver
enlargement, restrictive lung disease (pneumothorax)
Hyperventilation frequent sighing, cause of dyspnea & dizziness
Poor gas exchange at the alveolar level can occur with a normal RR

Accessory Muscles
These are used to maintain ventilation
Use of these increases RR
They are used when diaphragmatic breathing is depressed & become primary
Scalenes, SCM, Trapz, & Pecs
Hypertrophy may be observed with chronic lung or cardiac conditions or
decreased diaphragmatic breathing

Muscle Retractions
Presence of substernal and/or intercostal muscle retractions
See best in lower chest area during inspiration
Due to increase in IPP needed to overcome airway obstruction
Characteristic of restrictive lung disorders pulmonary fibrosis, atelectasis,
pneumonia, chest wall abnormalities, & lung cancer

PALPATION
Anterior, posterior, & lateral chest from apex to base are palpated tenderness
indicates pleural inflammation

Tracheal Position
Normally located in midline or slightly to the right of sternal notch
Place fingers in sternal notch and move gradually upward
Displaced to unafected side by tension pneumothorax, large pleural efusion, or
tumor
Severe atelectasis, lobar pneumonia, or pulmonary fibrosis will pull to afected
side
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Chest Wall Expansion
Determines degree & symmetry of chest wall movement
Assessed in sitting position with examiner directly in front or behind pt
Decreased in side-lying, prone, or supine in dependent areas of thorax
Posterior chest expansion is determined at level of lower thoracic vertebra while
anterior expansion is determined at the level of the area immediately below the
xiphoid process
Normally move apart 3-5 cm from the midline
Pts with hyperinflated lungs due to emphysema or asthma will have decreased
chest expansion
Bilateral decrease is seen in neuromuscular disorders such as Guillain-Barres
syndrome, emphysema, or in older due to calcification of costal cartilage
Asymmetrical expansion is seen in obstructive disorders such as bronchial
obstruction or restrictive disorders such as pneumothroax, pneumonia, large
pleural efusion, or lobar pneumonia, or if pleural pain with splinting occurs

Tactile Fremitus
Afected by many extrapulmonary conditions
Use terms such as 99 or blue moon
Rough tool
Normally most prominent in upper chest and intrascapular areas and on the Rt.
Side more than the Lt. side
Not palpated over periphery or assessment in individuals on mechanical
ventilation
Increased fremitus indicative of obstructed airways due to alveolar consolidation
secondary to pneumonia or alveolar collapse associated with severe atelectasis,
pulmonary edema, lung cancer, & pulmonary fibrosis
Decreased fremitus obstruction of voice sound transmission by emphysema,
pneumothorax, or pleural thickening

Subcutaneous Emphysema
Palpated over chest wall when air has leaked into the subcutaneous tissue
Best palpated over the clavicular area
May occur when air escape from around a tracheostomy, after thoracic surgery, or
may de due to flail chest

PERCUSSION
Striking of chest wall briskly sets underlying tissues into motion producing audible
sound that can be heard without stethoscope
Used to determine size, borders, & consistency of lungs & estimate diaphragmatic
function
Full or flat sounds due to breast tissue & heart muscle heard over anterior chest
wall
Dullness over area of liver is as high as rib 5 at midclavicular line & over scapula
Documented in terms of location, intensity, pitch, quality, & duration
Limitations = Deeper lesions are not detected depths of 5-7 cm only

Percussion Sounds
26 of 107
Resonance, hyperresonance, tympany, dullness or flatness
Diference in intensity, pitch, duration, or quality
Resonant sounds are heard over normal lung tissue loud, low pitch, sound hollow
Hyperresonant when excess air is present in lung tissue intense, lower, longer;
similar to empty barrel asthma, emphysema, or pneumothroax due to air
trapping as well as over area of pleural efusion
Tympanic lour or intense, musical, medium duration, drum-like detected over
gastric bubble may indicate large pneumothroax or emphysematous bleb
Dull less intense, medium to high pitch, shorter duration, thud-like found when
fluid or solid tissue replaces normal air-filled spaces in lungs or pleural space &
may be due to pleural efusion, hemothorax, emphysema, or consolidation
associated with pneumonia or presence of lung mass
Flat soft intensity, high pitched, short duration, dull causes include massive
atelectasis, large pleural efusion, or pneumonectomy

Diaphragmatic Movement
The diaphragm itself is not percussed, but the boundary between resonant lung
tissue & dullness of diaphragm is determined
Normal diference btw diaphragmatic position during normal breathing and max
inhalation is 4-8 cm in an adult.
Movement of diaphragm should be symmetric
The diaphragm is normally slightly higher on Rt. Side due to liver, after lobectomy
or pneumonectomy
Diaphragmatic movement is decreased in conditions that increase abdominal
contents (i.e. ascites, pregnancy, hepatomegaly, during pain) and in conditions
with decreased airflow & increased function residual capacity such as emphysema
In emphysema, diaphragm is low & flat & moves minimally with max inspiration
Neuromuscular disease diaphragm remains elevated & immobile during max
inspiration

AUSCULTATION
Best position for auscultation is the upright position
Instructions to breather through the mouth
Pt should lean forward and downward slightly during posterior auscultation
Compare Rt. & Lt. sides with inspiratory & expiratory phases from apex to base
Breath sounds are more intense over posterior lung fields
Deep breathing is encouraged careful of hyperventilation leading to dizziness,
fainting, respiratory alkalosis, especially in elders

Normal Breath Sounds

Documented according to intensity, pitch, duration, quality of sounds,
bronchovesicular breath sounds, & vesicular breath sounds are heard normally
over particular areas
Abnormal breath sounds occur when normal breath sounds are heard in areas
where they are not normally heard
Bronchial breath sounds (i.e. tracheal, tracheobronchial, or tubular breath sounds)
normally located over trachea caused by turbulent air flow through trachea
27 of 107
o Loud, high pitched, harsh or hollow quality, longer expiratory phase, pause
btw insp/exp
o Not normal over peripheral lungs
Bronchovesicular breath sounds over mainstem bronchi anteriorly & in btw
scapulae posterior
o Less intense, lower in pitch, equal insp/exp phases
o Decreased intensity due to increased filtering of sound by lung tissue &
chest wall
o Not normally heard over peripheral lungs
Vesicular breath sounds are over most of the lung fields anterior & posteirorly
o Low pitched, during insp. & initial exp.
o Softer due to gas turbulence through small bronchioles & possibly alveoli
Consolidation of lung tissue caused by liquid or solid exudates filling air spaces
causes increase sound transmission of lung sounds intensity of breath sounds
overrides this
Bronchial breath sounds will be confined to afect area in lobar pneumonia
Bronchial breath sounds are heard over larger area with bronchopneumonia

Decreased or Absent Breath Sounds

May be due to hypoventilation of alveoli & smaller bronchioles, fluid or purulent
exudates in pleural space, or hyperinflation of lungs
Causes of alveolar hypoventilation include excess secretions, decreased
ventilatory efort, a foreign object, respiratory disorders compress lung such as
flail chest, pleural efusion, or pneumothorax, air trapping and increased FRC in
chronic lung disease, neuromuscular disorders such as Guillain-Barre or
myasthenia gravis, or decreased respiratory efort due to pain, injury, or surgery

Adventitious Breath Sounds

Extra sounds that are heard over the normal breath sounds
Described as discontinuous or continuous
o Discontinuous short duration & explosive caused b alveoli popping open
during inspiration
o Continuous longer duration & louder
Crackles (i.e. rales) caused by fluid accumulation in alveoli & heard when
collapsed airways snap open during inspiration
o Defined as fine, medium, coarse
o Defined as moist, wet, dry, crackling, sibilant, & crepitant
o Initially heard at bases & move toward apex as severity increases
o Heard best in dependent portions of lungs
o More fluid in the lungs more intense = coarse
o Normal to hear crackles after max expiration or after prolonged supine
position
o May be heard into expiratory phase especially with chronic bronchitis or
emphysema
o Documented when they are heard Insp/exp; location, if they clear after
position change, cough, or deep breaths
Wheezes produced by airway obstruction & are common in bronchospasm, such
as asthma or severe bronchitis
o Usually heard during expiration, but may be heard during inspiration
28 of 107
o Unilateral wheezes may indicate localized bronchospasm, possibly due to
foreign object
o Classified as sonorous or rhonchi & sibilant wheezes
o Sonorous do not clear with coughing, low pitched, rumbling, heard
primarily during expiration related to excess secretion in upper airways or
external pressure on the airways
o Sibilant higher pitched, originate in smaller diameter lower airways. Heard
thought inspiratory & expiratory phase louder during expiration cause is
narrowing of lower airways
Pleural Friction not related to airflow through airways
o Described as creaking or coarse sounds throughout insp/exp phases
o Heard when pleural membranes are inflamed, including pleural efusion or
after chest trauma
o If hear on Lt. side and continues after breath is held = pericarditis
Mediastinal crunch (i.e. Hammans sign) occurs when crackling sounds are heard
over precordial are of chest synchronous with apical heart beat best heard on
left side & may indicate pneumomediastinum

Clinical Instructor Add ins:

Wheezes due to secretion OR narrowing due to secretion
Monophonic one airway afected
Polyphonic multiple airway afected
o E.g whistle smaller the tube, higher the pitch
Crackles due to:
o Fine end inspiratory = atelectasis
o Coarse air flowing through secretions in alveoli
o Fine pulmonary edema; interstitial edema around alveoli - not really in
lungs
Rx with lasix, not with PT
Pleural Rubs pleural rubbing over each other sounds like balloons rubbing
Bronchial Breath Sounds (abnormally)
o Complete collapse OR consolidation because air is now travelling through a
solid, due to a lot of atelectasis OR secretions
Absent
o True atelectasis because no air flow

Voice Sounds
Normally spoken words are soft & indistinct through stethoscope
Transmitted voice sounds are prevented of spreading through lung tissue, which
intensified sound transmission in cases of consolidation
Abnormal sounds are classified as bronchophone, whispered pectoriloquy, &
egophony
29 of 107

Effects of Smoking on the Cardiovascular System

Pathological Processes are Likely Contributors to

Acute CV Events:
1. Hypercoagulable state
2. Increased myocardial workload
3. Reduced O2 carrying capacity of blood
4. Coronary vasoconstriction
5. Catecholamine release

Chronic CV events include: arthrosclerosis & heart

failure

Primary Mechanisms to Chronic CV:

1. Decreased HDL
2. Compromised endothelial integrity & function
3. Hemodynamic state
4. Oxidant injury
5. Neutrophil activation
6. Enhanced thrombosis
7. Increased myocardial O2 demand
8. CO2 exposure
9. Increased blood viscosity

Smoking 1-5 cigarettes daily increases risk for acute myocardial infraction (AMI)
by 40%
AMI is further increased by amount of tobacco smoked per day
Smoking = known predictor of sudden death by heart failure
Risks increased HR, BP, & myocardial O2 consumption
Acute coronary events caused by rupture of atheromatous plaque or erosion of
coronary vessels;
Pts with higher fibrinogen levels are 2x more likely to develop CAD
30 of 107
Nicotine
Influences CO2 production
Reduction in prostacycline = reduction in inhibitor of platelet aggregation in
hypercoagulable state = thrombosis formation
Imbalance of O2 supply/demand
Increase catecholamine levels, thus increase HR, BP, & O2 demand

Tachycardia & Other Rhythm Disturbances

Sympathetic drive to heart exceeds drive to peripheral blood vessels
Nicotine = direct efect on HR by stimulating intracardiac sympathetic nerves
Smoking impairs inherent arterial baroreflex function

Arthrosclerosis
Primary cause of death in Canada
Caused by narrowing & stifening of arteries
Risk factors smoking, plasma cholesterol levels, hypertension

Other Efects
CO2 interferes with O2 transport for binding sites on Hb but CO2 affinity is 200X
> than O2 affinity in turn afects RBC production
Increase hematocrit levels
Systemic arterial stifening & hypertension
AAA 3-5X increase risk in smokers associated with higher mortality
Increased ventilation = increased dead space = air trapping = no exchange =
increase CO2

Effects of a Sedentary Lifestyle on the Cardiovascular System

Most modifiable risk factor for CV morbidity & mortality

PA results in increased exercise capacity & cardio-resp fitness = decreases all-
cause mortality
Endurance & strength exercise leads to favorable outcomes
Low levels of activity at work & home associated with increase CVD & all cause
mortality
PA leads to increase in exercise capacity, lower myocardial O2 demand, lower HR,
lower BP, MCI reduced by 35-50%
Sedentary leads to decrease arterial compliance, increased diabetes, increased
fasting insulin levels = hypoglycemic

Effects of General Anesthesia on the Cardiovascular System

Increased HR, cardiac sensitivity to catecholamines

Decreased RR, BP, CO, peripheral resistance, myocardial contractility, change in
muscular pattern of inspiration, reduction residual capacity, increase thoracic
blood volume, & reduced airway reflexes
Brief periods of hypertension & tachycardia may be observed
Post-opt shallow, monotonous breathing, with increase chance of collapse
31 of 107
During surgery not all lungs are ventilated with a ventilator lower lobes have
perfusion, but poor ventilation. Axial & anterior & middle better ventilation
Axial & anterior & middle better ventilation than bottom & posterior
Post-opt need retraining of lower lobes due to O2
depletion

Methicillin Resistant Staphylococcus Aureus (MRSA)

What is it?
Type of bacteria commonly found on skin & in noses of the healthy
It is a staph bacteria resistant to the antibiotic methicillin
May develop into serious life-threatening complications such as infection of
bloodstream, bone, &/or lungs

How is it spread?
Primarily skin to skin contact or contact with contaminated items
A person may be a carrier, but not sufer from the illness
Open wounds or infected bodily fluids
Respiratory tract carries MRSA

Progression
24-48 hours symptoms
> 72 hours resistant to Rx

Treatment
With early detection it is usually treatable
Sample is taken & organism is tested against multiple antibiotics
Vancomycin last resort medication

Prevention
Covering wounds, hand washing, & avoiding personal item sharing
Screening methods used & pts found + are isolated
Health care professional should were gloves & gowns
Masks should be worn if pt has pneumonia to prevent spread through sputum
32 of 107

At Risk
Pts with weakened immune systems
Easily spread in health care settings
Diabetes, re-operations, nasal
carriers

Patient Controlled Analgesia (PCA)

A delivery system based on use of sophisticated microprocessor-controlled
infusion pump
Pts self-administer small, predetermined doses of analgesic meds for pain relief
Keyed-access is necessary to set doses
Y shaped tube btw reservoir & IV catheter contains antireflux & antisyphon
valve to avoid accidental overdoses

All PCAs contain:

Initial loading dose important & considered hemodynamic status
Demand (bolus) dose small amount pt receives with button press
Lockout interval - length of time when there is no drug delivery
Background infusion rate constant rate administered regardless of activation
1 hr 4 hr limits

- Respiratory depression
- Limits pts mobility

Peripheral Nerve Catheter

- Nerve block techniques are increasingly used manage post-op pain
- Blocks are placed in brachial plexus, sciatic nerve, interscalenic nerve, or
femoral nerve

Central Neuroaxial Blocks

- Infection risk, neurological complications, anticoagulant interactions
33 of 107

Pharmacology
Morphine
What is it?
Obtained from opium juice secreted by seeds of poppy
Works on several receptors found in N.S.
Opioids term used for all drugs that act on receptors
Relief of pain & respiratory depression most important

How does it work?

Binds to g-proteins in brain & SC region
Increase synaptic nerve terminals
Prevents pain signal transmission
Decrease CNS

Side Efects?
Respiratory depression becomes sedated & sign is pupil constriction
Nausea & vomiting acts on chemotactic trigger zones in brain
Cough suppression, sedation, confusion
Dependence with chronic use
Reduce peristalsis delayed emptying, urinary retention
Histamine release
Little efect on heart & BP may decrease due to pain relief & sedation efect
Hypotension

Precautions?
34 of 107
Pupil size = primary indicator
O2 mask & positive pressure ventilation of lungs if necessary

Dosage
100-200 during surgery, with 1-2mg until pain free after wakening
Much higher doses needed orally
Can be given IV, epidural, or subarachnoid space
Epidural relieve pain for 12-24 hours
Epidural/Subarachnoid severe respiratory depression occurs up to 18 hrs after
administration

Risks
Respiratory depression includes RR, depth, & rhythm, SO2, & might need to
administer an opioid antagonist
Background infusion, nurse/physician-controlled, hypnotics or sedatives, renal,
hepatic, pulmonary, or cardiac impairments, sleep apnea, & obesity
Epidural superior to IV risks must be balanced against positives epidural
hematoma, infection, or neurologic injury; Benefits more apparent in serious
cases
Crosses placental barrier

Clinical Skills Lab Post-Operative Management

Definitions:
Atelectasis diminished volume afecting all or part of a lung or partial collapse of lung
parenchyma. Lung parenchyma although often used to refer solely to alveolar tissue,
term describes any form of lung tissue including bronchioles, bronchi, blood vessels,
interstitium, & alveoli.

Closing Volume is the lung volume at which closure of small airways occurs. This
volume plus the residual volume (the volume of gas Lt. in the lungs following maximum
expiration) is known as the closing capacity (CC)

In the adult, CC is less than FRC, i.e. the volume of gas Lt. in the lungs following tidal
expiration, whereas infants it is greater than FRC. The higher closing volumes apparent
in infants are due to greater chest wall compliance & reduced elastic recoil of lungs than
in adults

Collateral Ventilation is the means by which a distal lung unit can be ventilated,
despite blockage of its main airway

Shunt essentially refers to blood entering arterial circulation that has not taken part in
gas exchange. Anatomical shunt is the venous blood that mixes with pulmonary end-
capillary blood on the arterial side of circulation
35 of 107
As well as bronchial and thebesian venous drainage, it includes blood flowing through
atelectasic lung & areas of consolidation. Shunts also occur in congenital heart disease
where blood moves from Rt. Side of heart directly to Lt. without first passing through
the lungs Rt. To Lt. shunting

All these forms of shunt are termed a true shunt to diferentiate them from ventilation
perfusion mismatch where the normal balance btw lung ventilation & alveolar perfusion
is disturbed. The diference btw these two is important because the amount of
ventilation perfusion mismatch is often given as a percentage shunt Qs/Qt just like a
true shunt.

Low/Reduced Lung Volumes refers to inability to expand lung tissue & includes a
reduction of residual volume, Vt, expiratory reserve volume (ERV), &/or a reduction in
inpiratory reserve volume (IRV)

Two main clinical consequences of reduced lung volumes: a reduction in total lung
capacity (TLC) & vital capacity (VC), as the pt may be unable to increase inhaled
volume sufficiently to expand lung tissue, & a reduction in FRC, as the pt may be unable
to sustain alveolar inflation

Many pts with reduced lung volumes & capacities present with problems of dispose &
decreased exercise tolerance, due to inability to meet ventilator demands of PA (e.g. pts
with ILD may present with dyspnea on ADL)

Alternatively, they may present with the problem of impaired airway clearance due to
the inability to take a sufficient deep breath resulting in reduced expiratory flow &
inefective. Impaired gas exchange & orthopnea may also present

Ventilation/Perfusion Mismatching this is an important cause of hypoxemia afecting

pts on the ICU. Relative ventilation & perfusion, in diferent areas of lung are unequal,
resulting in inefficient gas transfer

The distribution of ventilation in normal subjects varies depending on the mode of

ventilation & positions. In the upright position there is greater ventilation towards the
apex of the lungs than to the bases. In the lateral position, the lower lung is
preferentially ventilated irrespective of which side is lain upon. This is due to the
dependent diaphragm lying higher in the thorax, with increased length of muscle fibers
providing more efficient contraction during inspiration. In the anaesthetized pt,
however, irrespective of the mode of ventilation, the upper lung receives more gas flow

Pulmonary blood flow is greater at the bases than at the apices in the erect subject. The
distribution of flow through the lung is uneven due to the relatively low pressures in the
pulmonary circulation & gravity assumes a very important role. Similarity, in the lateral
position, the dependent lung is perfused more than the upper lung

Although both perfusion & ventilation increase from the apices to the bases the increase
in ventilation is less than that of perfusion &, in order to understand the relationship btw
the two is described as the ventilation perfusion ratio. The resting values are
approximately 4 l/min for ventilation & 5 l/min for pulmonary blood flow, giving a ratio
36 of 107
of 0.8 throughout the whole lung (assuming ventilation & perfusion of all alveoli are
equal). However, some alveoli will receive no ventilation & some will receive no
perfusion. Thus, the ratios will range from zero (efectively the same as a true shunt) to
infinity (efectively the same as dead space)

Hypoxia is deficiency in the amount of O2 reaching body tissues

Signs: rapid breathing, cyanosis, poor coordination, lethargy/lassitude, executing poor

judgment

Symptoms: air hunger, dizziness, headache, mental & muscle fatigue, nausea, hot &
cold flashes, tingling, visual impairment, euphoria

Hypoxemia is the reduction of O2 specifically in the blood; anoxia is when there is no O2

available at all

Causes: Hypoventilation refers to a condition when the O2 (PaO2) content is the blood
decreases & a marked increase in level of CO2 is observed. This lowered PaO2 content
can cause hypoxemia

Low Inspired O2 FiO2 content in blood is called as the fraction of inspired O2 in blood.
A decrease in this fraction of inspired O2 may cause hypoxemia

Lt. to Rt. Shunt this is another cause of hypoxemia. It is a condition when there is a
transfer of blood from Lt. side of heart to Rt. Side. This may occur as a result of a hole in
the following walls: arterial walls, walls separating 2 upper chambers (i.e. Lt. & Rt.
atrium) or wall separating two lower chambers (i.e. Lt. & Rt. ventricles) of heart

Ventilation-Perfusion mismatch condition in which an imbalance btw the volume of gas

expired by alveoli (alveolar ventilation) & pulmonary capillary blood flow is seen
causes hypoxemia

Diffusion Impairment condition in which a marked reduction is seen in O2 movement

from alveoli to capillaries. This restricted movement may trigger hypoxemia
37 of 107

Clinical Skills Lab Post-operative Procedure

Role of Physiotherapists in Perioperative Care

Promote & prevent chronic disease
Early mobilization
Minimize efects of bedrest
Critical care issues
Accelerated d/c continuity of care & education
Increased autonomy & direct referral
Postural drainage
Manual techniques
Breathing exercises
Airway suctioning

First Thoughts:
Why are they here?
What has been performed?
Where is their incision?
Are there lines & tubes I should be aware of?
Are the pain meds working?
38 of 107
Am I dealing with an adult or paediatrics?
Observe their position are they sleeping, awake, upright?
**Optimal breathing position is sitting upright with feet on floor!!**
Is the environment safe:
o Tables, chairs
BP decreases with opiates careful of lightheadness

Considerations:
Pain & groggy compliance is difficult

Assessment:
Apical, lateral costal, or diaphragmatic breathing?
Does pt want to move if not try to reposition them in a more upright position
Instruct what your intentions are
Teach breathing exercises:
o Men = more diaphragmatic in nature
o Place pillows under arms
o Instruct them to place their hands supra-umbilical or you place your hands
here
o Dont say push out your stomach they will use their abs
o Sidelying you can attempt in this position for comfort
o Place rolled towel along spinal process to allow for extension
o Lateral costal breathing taught initially tactile stimulation move ribs into
my hands
o Getting arms up later on in post-op can help open chest up
o Lumbar support in sitting is helpful
Teach Coughing:
o Understand & state that it will be uncomfortable
o Need recruit abdominals
o Need big breath close glottis
o Ensure stitches are in place might come undone
o Teach splinted cough with pillow
o Dont lie it will hurt but its important we need to keep sputum out &
clean out your lungs to avoid pneumonia
o If wont cough attempt huffing
o Huffing dont close glottis, helps move air forcefully out, fog up a mirror
o Try to swallow if cant expel it
o Use arms if no extra pillow when walking
o Bending knees can remove pull on incisions

FITT:
5X10 deep breaths (attempt to open alveoli collapsed at bottom better success)
1 big cough
Hold 3-5 seconds (MEV)
39 of 107

Clinical Skills Lab Post-Op Procedures

Procedures:
Remain in contact
Clear instructions
Let them do as much as they can
Height of chair/height of bed
Brakes
Peripheral IV, catheters, tubes
Roll toward all tubes, except chest tubes
View insertion drain =JP drain
Roll sheets back
Roll on their side, support their hand & hip
Push against, bring legs over edge
Lower bed
Check on pt
Rethink lines & tubes before standing
Attach lines & tubes before standing
Attach lines to chair/IV stand
40 of 107
Put shoes on
2nd person to assist if possible
Shift hips to edge
Raise bed = advantage keep feet on ground
Hold hand & IV, support back
Reach back with hands on chair with pillow on it have a seat

Clinical Skills Lab Case Study Interpretation

Assessment:
Hemicolectomy = large incision
Rate pain = talk to nurses
Pain Lt. shoulder = referred from diaphragm
Rt. Colostomy bag dont usually fall of
Crackles = alveoli being open
Auscultation sounds
o Breath sounds
o Adventitious fine crackles, coarse crackles, inspiratory crackles, expiratory
crackles, inspiratory wheezes, expiratory wheezes
o Pleural rubs clicking broken ribs
Analysis
o Typical post-op pt
o Apical breath/shallow altered breathing pattern
o Pain
o Decreased mobility
o Decreased cough
o Referred pain
o Atelactesis in both lower lobes
o Scant describes amount
Rx Goals
o Increase mobility
o Decrease breathing
o Prevent further pulmonary complications
Rx Plan
o Teach breathing
o Mobilize
o Pain coordinate it
o Too high Pain dont mobilize
o Decrease RR
o Normalize V/Q matching
o Abdominal binders controversy, may help with SAT, may help pulmonary
function, ensure not over ribs thus increase lung resistance
Outcome Measures
o SO2/pre-post chest excursion
o NPRS
o RR
o Auscultation
o D/c criteria
41 of 107
COPD
- Expiratory more the issue
- Pursed lip breathing

Best perfusion in base

Best ventilation in apex
Best match in mid-lung zones
Working on Ventilation perfect 1/1 ratio = V/Q

Apical breathing lobes perfusion in bases no ventilation

Shunt perfusion, no ventilation, thus breathing; sitting position;

moving/walking=better breaths

Documentation
S:
- Consent
- HxPI
- PMHx
- General health
- Previous Rx
- Meds
- Social Hx (living status, house template, occupation, PA, environment,
smoking)
- Pain level (aggravating, relief, intensity, type, frequency)
- Diagnostics

O:
- Diagnostics
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- IPPA
- Cough, mobility, ROM/Strength
- Outcome measures
- Pre/post auscultation
- O2 sats
- Rx
- Post-Rx change in pt

A:
- Interpretation
- Problem list
- Response to Rx
- Precaution for Rx if ordered Rx = isnt appropriate explain in doc why not
followed
- Pt. response to Rx

P:
- Goals what is next?
- How will goals be met
- Amount times you plan to see them

COPD & Cardiovascular Disease

- FEV1% predicted is associated with CVD risk in smokers & non-smokers

- FEV1% predicted< 50 = increased arterial stifness
- FEV1% - good marker of environmental & genetic determinants of health
- Pts with COPD > arterial stifness
- Pts with COPD > systemic inflammation & oxidative stress
- Pts with COPD > incidence of hemodynamic abnormalities & chronic hypoxia
- COPD is associated with systemic inflammation = pathogenesis of
comorbidities
- CR-Protein risk factor for CAD, MI, Stroke
43 of 107
- Oxidative stress = imbalance btw production of reactive O2 species &
protective antioxidants unopposed oxidation = apoptosis, cell destruction, &
necrosis & enhances inflammation
- Oxidative stress increases with severity of airflow obstruction
- Ischaemic heart disease risk factors include hypertension,
hypercholesterolemia, smoking, & diabetes = increase production of O2 free
radicals
- Pts with COPD subject to intermittent hypoxia & later stages sustained
hypoxia
- Hypoxia influences atherogenesis increased inflammation, oxidative stress,
up regulation of cell surface adhesion molecules, & haemodynamic stress
- Inhaled corticosteroids = helps reduce systemic inflammation = important
element of CVD pathophysiology

Common Clinical Signs

Tracheal Tug Signs
Campbells Sign
Downward displacement of thyroid cartilage during inspiration seen in COPD
Due to pull on central tendon due to flattened diaphragm

Olivers Sign
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Abnormal downward movement of the trachea during systole that can indicate a
dilation or aneurysm of aortic arch
Elicited by gentle grasp of cricoid cartilage & applying an upward pressure while
the pt stands with neck hyperextended
Due to anatomic position of aortic arch which override Lt. main bronchus, a
downward tug of trachea may be felt in aneurysm is present
Named by William Silver Oliver in 1878

Barrel Chest
Normal elliptical configuration of chest is replaced by a rounded one
A-P diameter enlarges to approximately transverse diameter
Diaphragm = depressed & sternum = pushed forward & ribs = horizontal
Appears continuously in inspiratory position
Late sign of COPD due to augmented volumes due to chronic airflow obstruction
Auscultation for crackles & wheezing
Percussions = hyperresonant = trapped air or dull flat = edema or mucous
Accessory muscle use, intercostal retractions, & tachypnea = respiratory distress
Central cyanosis or peripheral cyanosis
Clubbing
Causes include:
o Asthma
o Chronic bronchitis
o Emphysema
o OA

Hoover Sign
- Refers to paradoxical inspiratory retraction of rib cage & lower intercostals
spaces
- Inward movement on inspiration
- Considered a marker of severe airway obstruction
- Recognizable as inspiratory retraction of lower intercostal spaces
- Occurs with obstructive airway disease
- Caused by alterations in dynamics of diaphragmatic contraction due to
hyperinflation
- Results in traction on rib margins by flatten diaphragm
- Sensitive 58% & Specific 86% for airway obstruction
- Associated with pts BMI, severity of dyspnea, & exacerbation frequency
- Valuable prognostic information & complements other tests
- Loss of bucket handle most often seen in severe pts
- Present in pts with congestive heart failure, asthma, severe pneumonia,
bronchiolitis, & unilaterally diaphragmatic paralysis, pleural efusion, &
pneumothorax
45 of 107

Severity of Airway
Obstruction
Physical
Pursed lip breathing
Hoovers sign
Accessory muscle use
Cyanosis
Laboratory Parameters
Pulmonary function (FEV & FEV/FVC)
Peak expiratory flow rate
Hypoxemia

Edema Its Implications

- Observable swelling from fluid accumulation in body tissues
46 of 107
- Fluid is contained in spaces called interstitial spaces
- Pitting edema = applying pressure to swollen area = persisting indentation
after pressure is release
- Non-pitting no as prevalent due to lymphatic disorders mostly
- Causes systemic disease or local conditions
- Systemic disease = heart, liver, & kidneys
- Occurs primarily due to retention of sodium chloride = increase water retain
age
- Local causes = varicose veins & thrombophlebitis = venous insufficiency
- Kidneys regulate sodium heart failure = retain salt or kidney impairment =
impaired secretion

Edema & Heart Failure

Reflected by decreased CO = decreased flow to kidneys
Kidneys sense reduction of blood volume in body = retain salt & water, though
already too much fluid in body
Build up of fluid in lungs = SOB fluid leaks into alveoli & interstitium =
pulmonary edema
Increase in total body fluid, but decrease volume in arteries
Lt. Heart Failure = SOB & Orthopnea due to pulmonary edema, also due to
hyperinflation
Rt. Heart Failure = chronic lung disease = COPD, causes salt retention = edema =
expanded blood volume in vessels = fluid accumulation in lungs = pulmonary
congestion & SOB
Congestive Heart Failure = as Rt. Pressure increases, Lt. side impeded, thus
decrease Lt. ventricle end diastole volume
Decreased SV & CO = Lt. Heart failure
Cardiomyopathy both ventricles afected thus pitting & pulmonary edema

Venous Insufficiency & Edema

Incompetence of veins due to dilation, or enlargement, of veins, & dysfunction of
valves
Leads to backup of blood & increased pressure in veins = edema
Edema also occurs with DVT & varicose veins

**Systemic diseases cause equal amounts of edema bilaterally!**

Diuretics = Rx
Most potent diuretics = loop diuretics = Lasix, Demadex, Burnex
Excessive loss of K+ occurs thus supplements may be necessary
Pts with impaired kidney function dont need a supplement since their damaged
kidneys retain K+

Pitting Edema Grading

1+ - Slight pitting/2mm, disappears rapidly
2+ - Somewhat deeper pit/4mm, disappears in 10-15 sec
3+ - Deep pit/6mm, may last > 1 minute
4+ - Very deep pit/8mm, lasts 2-5 minutes
47 of 107
Pharmacology
Lasix; generic = furosemide
Description
Potent diuretic = eliminate water & salt from body
Blocks absorption of sodium chloride & water from filtered fluid in kidneys
Increases urine output

Indications
Rx excessive accumulation of fluid &/or swelling of body due to heart failure,
cirrhosis, chronic kidney failure, & nephritic syndrome
Used in conjunction of BP pills to Rx HBP

Side Efects
LBP, dehydration, electrolyte depletion, jaundice, tinnitus, photophobia, rash,
pancreatitis, nausea, diarrhea, abdominal pain, & dizziness
Increased blood sugar & uric acid may occur

Interactions
Aspirin

Prednisone; aka delatsone, orasone, prednicen-M, liquid pred

Description
Oral corticosteroid suppresses immune system & inflammation
Mimic action of cortisol (hydrocortison) naturally produced by adrenal gland
Salt-retaining properties

Indications
Management of inflammatory condition in which immune system plays a role
Arthritis, ulcerative colitis, Crohns syndrome, systemic lupus, allergic reactions,
asthma, & severe psoriasis
Leukemias, lymphomas, idiopathic thrombocytopenic purpura, & autoimmune
hemolytic anemia
Used to suppress immune system & prevent body from rejecting transplanted
organs
Used with a deficient adrenal gland

Side Efects
Salt & fluid retention
Weight gain, HBP, decreased K+, headaches, muscle weakness, moon face, facial
hair growth, thinking & bruising of skin, impaired wound healing, glaucoma,
cataracts, ulcers, worsening diabetes, irregular menses, kyphosis, growth
retardation in paediatrics, convulsions, depression, euphoria, insomnia, mood
swings, personality changes, & psychotic behavior, & osteoporosis

Caution
Adrenal gland atrophies = gradual removal of Rx
48 of 107

Ventolin; generic albuterol or salbutamol

Description
Dilates airways of lungs
Relief & prevention of airway obstruction (i.e. bronchospasm)

Indications
Asthma
Lung conditions such as emphysema & chronic bronchitis (i.e.COPD)

Side Efects
Increased HR, nervousness, tremors, headache, difficulty sleeping, or nausea
Rash, hives, itching, wheezing, or increased difficulty breathing

Interactions
Combining albuterol with loop diuretic may increase hypokalemia (i.e. decrease
K+)
49 of 107

Lines, tubes, & the ICU

Clinical Skills Lab Game
- ECG electrodes & wire attaches to device
- Foley Catheter
- Radial Artery Line
- Catheter bag permanent catheter (SCI) attaches to leg under pants for
bladder contents; dont lift bag over catheter = reverse action
- Femoral Artery tube avoid hip flexion
- Chest tube goes btw ribs 4 & 5 runs in pleural space drains air + fluid
sutured in
o Painful
o Sometimes attached to wall
o Under axilla
o Percussion around it
- o/o airways go upward & turned & drop down directed towards trachea
o put this down & put the suction catheter to it
o used for suctioning
o if increase gag reflex, dont use
- trach plastic comes out
- chest tubes mediastinum where heart sis
- arterial line
o draw arterial blood (arterial blood gases)
o can put meds in there
o arterial BP
- CVP line
o Into Rt. Atrium (put meds)
o Take venous blood
o Measures Rt. Atrium pressure
o TPN (transparental nutrition) can put nutritional supplements into
venous system for people who cant take anything in even by NG tube
- Pulmonary artery line aka SWANGANZ
o Goes into pulmonary auricle
- Endotracheal tube
o Suctioning remove secretions
o Administer O2 keep airway open
o CVP central venous pressure
- Why do we have pressure cuf over arterial line?
o To prevent blood to go back into artery
- Pulmonary artery line measure what CVP cant?
o Pulmonary artery pressure
o CO
50 of 107
o Pulmonary artery wedge pressure
o Both enter same place jugular or subclavian
- PICC line aka peripheral inserted central catheter
o Inserted neck & shoulder
o Chemotherapy
o Shouldnt be doing strength training of upper body
- Intercranial Pressure
o Drill hole for suction in case increase pressure
o At certain pressures no suction
- Hemodyalisis
o Permanent line around shoulder
o Careful of shoulder ROM
51 of 107

COPD - Rx
In hospital & home care

Problem
Increase WOB
o Pursed lip breathing
Increase expiratory time
Decrease hyperventilation
Decrease dyspnea
Decrease EELV
Decrease Vt at rest
Decrease atelectasis creates positive back pressure which helps to
keep airway open (good for bonchiestasis floppy airways)
Remind pt to do PLB during exacerbations
o Positional changes
Forward leaning, sitting, lateral costal
Stabilizes shoulder girdle
Reverse origin & insertion of muscles
Optimizes length-tension relationship of diaphragm
Hands behind head same principles
Increase O2 Demand
o Walking aids
o PLB
o Titrated O2 wean of if able (only if under medical directive)
o Energy Conservation Techniques
Most NB things first, pacing
How to EC in ADL
OT referral home alterations/assistive device
o Deep breathing/retraining in COPD
Increased Secretions
o ACBT in semi-fowlers position
o Deep breathing & coughing
o Acapella/Flutter though not better than CPT
o Vibration/percussion
Orthopnea
o Can get better has other indications from cardiac position (e.g. CHF)
Decreased Mobility
o Mobilization
o Walking aid with O2 carrying capacity
Increased Pitting Edema
o Ankle pumps (increase circulation)
52 of 107
o Elevation
o Educate positioning
o Articular motions knee bends
o TEDS stockings help with swelling efective in reducing DVTs
Atelectasis
Hyperinflated lungs
o Diaphragmatic breathing CONTRAINDICATED
Smoking Cessation Education
Paradoximal Breathing
o Abdominal binder = increases intra-abdominal pressure
53 of 107

Clinical Skills Lab Review Student Seminars

Rx Population/Indicati Contraindicati Evidence Cost Duration Rx

ons ons

ACBT - COPD - Hemolyptisis - Good - no cost - 10-20

- CF - < 2 yoa evidence in minute/sessio
- Excess mucous + combo with n
clearance postural
problems drainage for
-Atelectasis pts with CF
- > 2 yoa - Spirometry
- Secretion
clearance
AD - CF - Cognitive - Good for: - none - specific to pt
- COPD disorders - improved - instruction - 35-45
- Dynamic ciliary - Acute resp. O2 time minutes
collapse disorders - improved
- Coordinated & - Young SAT
motivated children - Improve
> 12 yoa - <12 yoa spirometry
PEP - CF Consideration - Equal to Cost for 10 20
- COPD s: CPT device minutes
- Atelectasis On handouts - Pts prefer
- Increase - Better 65$
secretions compliance
Acapella - CF Consideration -Prefer Cost for 10 -20
- COPD s: acapella over device minutes
- Increase On handouts flutter
secretions 65$
54 of 107

Modified Medical Research Council (MRC) Dyspnea Scale

Purpose
Part of larger questionnaire
Standardize the assessment of pts with occupational respiratory distress
Assesses level of PA necessary to precipitate breathlessness

Description
Self-administered scale
Five descriptive statements regarding PA that precipitate SOB
Grade 0-4 0 = least severe SOB & 4 = most severe SOB

Population
Occupational respiratory ailments
COPD
Interstitial Lung Disease
Asthma
Lung transplants & lung volume reduction
6-80 yoa

Administration
Less than 5 minutes to complete
No gold standard
Interater = 0.92
Not available in healthy populations

Advantages
Consistent with O2 cost diagram & BDI
Quality of life = correlates with MRC = direct relation with pts wellbeing
55 of 107
Longitudinal validity = document therapeutic interventions

CCAC Ontario
- Anyone can make a referral
o Health care professionals
o Personal support
o d/c planner at hospital ensures all is taken care of
- More difficult for pt to do so after hospital d/c, than physician
- 14 in Ontario = really 43, but combined in 14
- Intent is to keep pts in hoes longer & get out of hospital earlier
- Unable to be covered can give pt information & referrals to next pathway
- 2 pieces of equipment covered
- ADP qualification for PT online course
- All is sent to home care manager in hospital, then to home care manage in the
community
- Decreases in services as improvement is observed

O2 Titration Controlled Act

- Can ensure precautions are met & monitor levels
- Cannot adjust it
- Cannot delegate it to another health care professional
- RT can adjust it alter after Rx parameters
56 of 107
- Physician must Rx, parameters, monitored
by physician long-term
- Ensure education on cessation of smoking
while using O2
- Ensure they know appropriate levels for
when they are PA & at rest
- Can perform under medical directive
- Change of scope need training
- RT gives 2 l/min or 40% - delegate to keep
SPO2 > 92%
- Titrate moving from wall to tank
- Automatically qualify for home O2 with
PaO2 < or = 55 mmHg
- If > 60 mmHg not qualified
- 56-60 mmHg may allow undergo
pulmonary function test first to determine
exercise draw blood gases
- Can self-pay for RX
- Palliative care < 1 yr to live = automatic O2
qualification

Management of COPD
1. Prevent disease progression
2. Reduce frequency & severity of exacerbations
3. Alleviate breathlessness & other respiratory symptoms
4. Improve exercise tolerance & daily activities
5. Rx exacerbations
6. Increase health status
7. Decrease mortality

General Rx List
- Educate on disease
- Self-management of dyspnea
- Educate on CCAC for ADL management
- Educate on health failure
- Prevent AECOPD
- Smoking cessation
- Vaccinations influenza & pneumococcal vaccine (5-10 yrs)
- Exercise muscular, endurance, higher intensity is better
- Educate return to activity after acute exacerbation
- Facilitate adherence to pharmacotherapy
- DB elevate RR, decreased Vt, increase with DB of abnormal arterial blood
gases, diaphragm that moves
DB contraindications severe COPD with hyperinflation, decrease RR,
increase Vt 0 unchanged with DB; as well as paradoxical breath
pattern
- Airway Clearance Techniques dependent on:
57 of 107
Pathology
Sputum production
Efect of ACT on lung volumes; Expiratory flow; & Dynamic airway in
each pt.

D/C Criteria Post-COPD Exaccerbation

- Post-op PT d/c scoring tool objective
criterias
o 5 categories scores from 6-15 - >
13 = d/c
o Interrater = moderately high
o Could facilitate clinical decision
making related to PT d/c planning
o Clinician feedback indicates its use in
practice
o Work in progress
o NEEDS TO BE INDIVIDUALIZED &
BACK AT RESTING STATE

Lines, Tubes, Catheters, & Physiologic Monitoring in the ICU

Name Insert End Purpose Norms Precautions

Tracheal Tube Nose/mout Allows access to Cervical ROM

h upper airway performed
for pts with cautiously &
obstruction, ensure in right
easier position by X-ray
suctioning, &
enable
mechanical
ventilation
Tracheostomy Trachea Same as above Same as above

Chest Tube 3-4 Pleural or Removes Ambulate with

intercostal medistin excess fluid or portable suction;
at al cavity air Inform before
midaxillary discontinuing
suction; Shoulder
ROM,
percussion/vibrati
on to pt tolerance
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Pulse Oximeter On Finger O2 saturation SpO2 > Verify values by
via pulse 97% testing on a
oximetry SpO2 diferent area;
is calculated With norm ensure SpO2 is
oxyHb above 90% & no
SpO2 at drop > 5% from
90% = baseline
PaO2
60mmHg
Peripheral arterial Radial Draw blood Systolic Avoid severe hip
artery, samples to 100-130 flexion if in
dorsalis monitor arterial mmHg femoral
pedis, BP when rapid
femoral, & fluctuations are End BP from baseline
brachial expected, diastolic 4- monitoring
maximal drug 13 mmHg
therapy, & Bring with during
when Mean 9-19 ambulation
vasopressor mmHg
therapy is
anticipated
Central Venous Subclavian, Rt. Measures Rt. Mean 0-8 Caution ROM to
Pressure Catheters jugular, Atrium Atrial pressure mmHg joints near
brachial, or to check Rt. insertion
femoral Ventricle
vein function
Pulmonary Artery Subclavian, Rt. Measures a pts Systolic Same as CVP
Pressure Catheters jugular, Atrium, hemodynamic 15-32
brachial, or Rt. status including mmHg
femoral Ventricle, cardio-
vein pulmonar pulmonary End
y a. pressures, diastolic 4-
flows, & 13 mmHg
circulating
volumes Mean 9-19
mmHg
Calculates
preload,
contractile
state, &
afterload
Pulmonary Artery 4-12 If catheter in
Pressure Catheter mmHg wedged position
wedged notify & they will
deflate balloon &
pull catheter back
proceed with Rx
59 of 107
Intracranial
Pressure monitors
Epidural Beneath Measure 0-15
skull above pressure mmHg at
dura exerted by the rest CPP > 50 mmHg
Subdural/Subarachn brain matter, & ICP < 25 mmHg
oid In non- blood, & CSF Cerebral For secretion
dominant against the skull perfusion removal positions
frontal lobe pressure
(CPP) Monitor
Intraparenchymal In white normal > throughout
matter 60 mmHg
through Intervention
subarachno dictated by
id catheter relationship btw
ICP & mean
Intraventricular Burr hole in Drains CSF to 0-15 arterial blood
ventricle control & mmHg at pressure (MABP)
monitor ICP rest

Jugular Venous Injured side C1 Enable 60-80% Institution

Oxygen Saturation Internal jugular detection of with guidelines
Jugular Vein bulb cerebral O2 normal interventions may
demand & PaCO2 be identified on
consumption, tracing for later
cerebral Decreased interpretation
perfusion, & O2 =
cerebral decreased
ischemia SjVO2
Continuous Femoral or Removal of fluid Within Closely monitor
Arteriovenous subclavian & solutes by preset BP & ECG
Hemodialysis with vessels difusion & pressure
Filtration (CAVHD) (vein & convection limits Keep filter level
artery)
No pump
Continous Femoral or Same as above Within Same as above
Venovenous Subcalvian preset
Hemodialysis with Vein With pump pressure Avoid kinking
Filtration limits tubing that may
interfere with
pump pressure
60 of 107
Intra-Aortic Balloon Femoral a Aorta & Catheter with Usually on
Counterpusation sits balloon ensures bedrest
(IABC) below Lt. adequate BP is
subclavia maintained with Closely monitor
n artery a gas released BP & ECG
with HR
Avoid severe hip
flexion

Closely monitor
pulses in
extremity with
IABC catheter

Rx Instructions for Pursed Lips Breathing

1. Sit in a comfortable position. Relax your shoulders.

2. Take an easy breath in through your nose. Slowly & gently squeeze
you air out through pursed lips. Keep a steady stream of air flowing
though the center of your lips. Concentrate on your breathing out as
long as you can comfortably. Then gently breathing in through your
nose.
3. Remember to relax and to not put much pressure in your chest. Think
of making a candle flicker when you are breathing out.
4. Place your hands on the lower sides of your rib cage when you breathe
in to help remember to fill all around your waist.
5. Use your pulse oximeter to watch the increase in your oxygen
saturation %.
6. Practice in front of a mirror to remind yourself to keep your shoulders
and upper chest still.
7. Practice 10 minutes per day for the first week. Use frequent short
practices during the day. Increase the practice session time by 5-
minute intervals to maximum of 25 minutes total per day by the end
of week 4. One session should last no longer than 10 minutes.
8. Use a daily logbook to record your home sessions and any unexpected
events.
9. Bring your logbook to your physiotherapy appointment.
61 of 107

Chest Physiotherapy
Purpose
- Help pts breathe more freely & get more O2 in the body
- Includes postural drainage, chest percussion & chest vibration, turning, deep
breathing exercises, & coughing
- Used to clear secretions from the lungs

Indications after Ax
- Excessive sputum production
- Efectiveness of cough
- Hx of pulmonary problems Rx successfully with CPT
- Decrease breath sounds or crackles or rhonchi = secretions in airway
- Change in vital signs
- Abnormal CX-Ray atelectasis, mucus plugging, or infiltrates
- Deterioration in arterial blood gas values or O2 saturation

Procedures:
Turning
- Indications
o Inability or reluctance of pt to change body position
o Poor oxygenation associated with position
o Potential or presence of atelectasis
o Presence of artificial airway
- Turning from side to side permits lung expansion
- Elevated head of the bed also promotes drainage
- Turning in the ICU should occur one every 1-2 hours
62 of 107
Coughing
- Helps break up secretions in the lungs
- Allows for mucus to be suctioned out or expectorated
- Pts sit upright & inhale deeply through the nose
- Exhale in coughs
- Repeated several time per day

Postural Drainage
- Indications
o Difficulty with secretion clearance
o Sputum greater than 25-30 ml/day difficulty secreting
o Retained secretions in presence of artificial airway
o Presence of atelectasis due to mucus plug
o CF, bronchiectasis, or cavitating lung disease
o Foreign body in airway
- Use of gravity to assist in efectively draining secretions from lungs & into the
central airway where they can be coughed or suctioned
- Placed in particular positions & held there for 15 minuets
- 4-6 times daily in critically ill
- Percussion & vibration performed in conjunction
- Helps in matching ventilation & perfusion & normalize FRC
- Each position consists of placing target lung segment(s) superior to carina &
held for 3-15 minutes or longer in special situations

Percussion
- Indication
o Same as postural drainage, but used as an additive to PDT
- Rhythmically striking chest wall with cupped hands
- Called cupping, clapping, or tapotement
- Break up think secretions in lungs so they can be removed
- Performed on each lung segment for one to two minutes each

Vibration
- Indication
o Same as postural drainage, but used as an additive to PDT
- Helps break up lung secretions
- Mechanical or manual
- Performed as pt breathes deeply
- Hands are placed against pts chest & creates vibrations quickly contracting &
relaxing arm & shoulder muscles while pt exhales
- Repeated several times each day for approximately 5 exhalations

Risks
- O2 deficiency if the head is kept lowered for drainage
- Increased ICP
- Temporary hypotension
- Bleeding in lungs
63 of 107
- Pain or injury to ribs, muscles, or spine
- Vomiting
- Inhaling secretions into lungs
- Heart irregularities

Normal Responses (i.e. positive responses)

- Increased volume of sputum secretions
- Changes in breath sounds
- Improved vital signs
- Improved chest x-ray
- Increased O2 in blood as measured by arterial blood gas values pt reports of
eased breathing

Contraindications to PDT

All Positions
- ICP > 20 mmHg
- Head & neck injury
- Active hemorrhage with hemodynamic instability
- Recent spinal surgery or acute spinal injury
- Active hemoptysis
- Empyema
- Bronchopleural fistula
- Pulmonary edema with congestive heart failure
- Large pleural efusions
- Pulmonary embolism
- Aged, confused, or anxious pts
- Rib fractures
- Surgical wound or healing tissue

Trendelenburg Position
- ICP > 20 mmHg
- Increased ICP is to be avoided (neurosurgery, aneurysms, eye surgery)
- Uncontrolled hypertension
- Distended abdomen
- Esophageal surgery
- Recent gross hemoptysis
- Uncontrolled airway at risk for aspiration
- Reverse Trendelenburg hypotension or vasoactive meds

Contraindications to Percussion & Vibrations

- Subcutaneous emphysema
- Recent epidural spinal infusion or spinal anesthesia
- Recent skin grafts or flaps on thorax
- Burns, open wounds, & skin infections of thorax
- Pacemaker recently placed
- Suspected pulmonary tuberculosis
64 of 107
- Lung contusion
- Bronchospasm
- Osteomyelitis of ribs
- Osteoporosis
- Coagulopathy
- Complaint of chest wall pain

Monitoring during Rx
- Subjective response
- Pulse rate, dysrhythmia, & EKG
- Breathing pattern & rate, symmetrical chest expansion, synchronous
throracoabdominal movement, flail chest
- Sputum production
- Mental function
- Skin color
- Breath sounds
- BP
- O2 saturation
- ICP

Outcome Ax
- Change in sputum production
- Change in breath sounds of lung fields being drained
- Pt subjective response
- Changes in vital signs
o Moderate change in RR & HR expected
o Bradycardia, tachycardia, or an increase in irregularity of pulse, or fall or
dramatic increase in BP are indications for stopping therapy
- Change of CX-Ray
- Change in arterial blood gas values or O2 saturation
o Oxygenation should improve as atelectasis resolve
- Change in ventilator variables
65 of 107

Myocardial Infarction Biomarkers

Creatine kinase (CK)
Description
AKA creatine phosphokinase (CPK) or phospho-creatine kinase
Enzyme expressed by various cell types
CK catalyses conversion of creatine & consumes ATP = phosphocreatine & ADP
Reversible reaction ATP can be formed from PCr & ADP
Skeletal muscle, brain, photoreceptor cells, hair cells of inner ear, spermatozoa &
smooth muscle, myositis, myocarditis, malignant hyperthermia, neuroleptic
malignagnt syndrome, McLeod sydrome, Hypothyroidism, & injury =
phosphocreatine serves as energy reservoir for ATP & intracellular energy
transport, thus the need for creatine kinase

Clinical Tests
It is found in blood tests = marker for MI, rhabdomyolysis (muscle breakdown),
muscular dystrophy, acute renal failure
Done routinely in ER in pts with chest pain or acute renal failure suspicions
Normal values btw 60 and 400 IU/L
Creatine Kinase (CK or CPK)
66 of 107
o Male: 38 - 174 units/L
o Female: 96 - 140 units/L
Tests are not specific to which type of CK is elevated
Lowered CK = alcoholic liver disease & rheumatoid arthritis
This level is being replaced or used with troponin measures

Troponin
Description
Ordered in pts with chest pain for MI diagnosis or damage to the heart
Often ordered with other cardiac biomarkers (i.e. CK-MB or myoglobin)
Troponin is the preferred test due to specificity for the heart
Helps detect severity of MI & distinguish if chest pain has another cause
Test will be positive even after the initial hours, thus the next day or more

Indication
Test is repeated after the initial ER admission 6-12 hours later
Test may be ordered for individuals with a stable angina if symptoms get worse,
occur at rest, or no longer ease with Rx

Test Results
Normally cardiac troponin levels are so low they cant be measured
Slight elevations = damage to the heart
Results can remain high 1-2 weeks post MI
Test is not afected by muscle damage, injections, accidents, or drugs
Levels may rise following strenuous exercise in healthy population
Not used on their own to diagnose an MI
Physical exam, clinical Hx, ECG are all important
Some do not get elevated troponin levels post MI
Levels may be elevated due to myocarditis, congestive heart failure, severe
infections, kidney disease, & chronic inflammatory conditions

Cardiac
Tests

38-120
Total CK
ng/mL

CK-MB 0-3 ng/mL

CK-index 0-3
67 of 107

Troponin <0.4 ng/mL

Cardiac tests
Coronary Angiogram
Description
Requires cardiologist or interventional cardiologist referral
Performed under oral or intravenous sedation combined with local anesthesia
Right heart catheterization is performed via access through the femoral,
subclavian, jugular, or antecubital vein
Left heart catheterization is performed via access through the femoral or radial
68 of 107
artery
Pressure readings and radiocontrast images are obtained, including right and left
heart, ascending aorta, and coronary arteries

Advantages:
Gold standard for evaluation for the presence of coronary artery disease
Allows functional evaluation of the heart
Can detect small vessel disease
Percutaneous coronary intervention, if indicated, can be carried out at the same
time

Disadvantages:
Invasive and expensive
Mortality 0.08% to 0.75%
Can be associated with significant radiation exposure (3-5 mSv for diagnostic, 10-
30 mSv for interventional)
Contrast administration may cause contrast-induced nephropathy (CIN)
Moderate patient discomfort requiring sedation
Complications can include vascular damage during access procedures, CIN,
arrhythmias, perforation of the heart, stroke, and NSTEMI or STEMI
Relatively contraindicated in patients allergic to radiocontrast dye (may be pre-
medicated)
If possible, metformin should be discontinued prior to the procedure in diabetic
patients, especially if a baseline elevated creatinine is present. Metformin may be
restarted 2 days later if a recheck of the creatinine shows no elevation

Pathological
Abnormal cardiac function
Abnormal intracardiac pressures
Presence of intracardiac shunts
Presence of coronary artery disease

Causes of Pathological Results

Microvascular cardiac disease
Prior NSTEMI or STEMI
Pulmonary hypertension
Significant pulmonary disease with secondary cardiac efects
Coronary artery disease
Pericardial disease
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Electrocardiography (ECG)
Description
12-lead ECG.

Advantages:
Can be quickly performed during symptoms
Noninvasive, easy to perform, universally available, and relatively inexpensive
In the absence of symptoms, may reveal Q-waves, poor R-wave progression, or
ST-T-wave changes that indicate prior myocardial infarction
When obtained during symptoms of chest pain, may indicate whether or not there
is active ischemia or acute myocardial infarction
May identify stigmata of acute pericarditis, pulmonary embolus, or left ventricular
hypertrophy found in other disease processes causing chest pain

Disadvantages:
Test is relatively insensitive and nonspecific in low-risk populations: the probability
of false-positive and false-negative findings is high in the general population
Other ECG abnormalities (eg, left ventricular hypertrophy, left bundle branch
block, Wolf-Parkinson-White syndrome) may mimic or obscure the diagnosis of
ACS
Findings consistent with ischemia may not be present in UA or NSTEMI; ECG may
be normal
Normal result does not exclude ischemia as the cause of chest pain

Pathological
NSTEMI: ST-segment depression over afected area with or without T-wave
inversion. The presence of ST-segment elevation, if prolonged, may indicate
STEMI. Transient ST-segment elevation is a poor prognostic sign in NSTEMI
Various arrhythmias and/or evidence of conduction abnormalities may also be
present
New onset of left bundle branch block or other conduction abnormality may be
present
Severe sinus bradycardia may result from sinus node ischemia
Keep in mind the possibility of a falsely abnormal result

Causes of Pathological Results

Myocardial ischemia causes an abnormal 'current of injury' and changes
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ventricular repolarization; these efects are recorded by the ECG as ST-segment
and T-wave changes, respectively
Abnormal ECG may represent a false-positive finding in an otherwise normal
patient, particularly if the patient does not have identifiable risk factors for
coronary disease, and does not have clinical or other laboratory tests or findings
suggestive of myocardial ischemia or infarction

Medications, disorders and other factors that may alter results

Electrolyte disturbances
Pericarditis
Congenital heart abnormalities
Conduction disturbances
Noncardiac diseases, eg, cholecystitis
Inaccurate lead placement
Inaccurate calibration
Left or right ventricular hypertrophy
Intracranial events such as subarachnoid bleeding
Muscular dystrophies
71 of 107

Pharmacology
Nitroglycerin
Description
Vasodilator; reduces cardiac oxygen demand by decreasing left ventricular end
diastolic pressure and systemic vascular resistance; dilates coronary arteries and
improves flow to ischemic regions; dilates veins more than arteries.

Indication
Forms part of immediate management regimen and long-term management.

Administration
Do not stop taking suddenly. Dose should be gradually reduced to avoid
withdrawal symptoms
Dissolve sublingual tablets under the tongue. Use while seated at first sign of
anginal attack. Call ambulance immediately if no response after three tablets in
15 minutes
Spray translingual spray under the tongue. Use while seated at first sign of
anginal attack. Call ambulance immediately if no response after three doses in 15
minutes
Keep tablets and capsules in original container and keep tightly closed

Risks/benefits
Nitrates can cause hypotension, particularly if the patient is hypovolemic,
sufers from significant myocardial dysfunction, or is taking medications that can
block increased heart rate response to falls in blood pressure, such as beta-
blockers or calcium-channel blockers. It is therefore recommended that nitrates
be taken while sitting or lying down.

Hypotensive efects can be particularly severe in the face of concomitant

vasodilator therapy, and thus nitrates are relatively contraindicated in patients
who have recently taken sildenafil, tadalafil, or vardenafil.

Vascular adverse efects (notably headache) are common, and may lead to
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patient dissatisfaction. Tolerance with prolonged administration is common.

Nevertheless, rapid symptomatic relief, simplicity of administration, and the

relatively low cost make nitrate medications generally well-tolerated.

Contraindications
Hypersensitivity to nitroglycerin, nitrates, nitrites, or any other component
Sublingual: early myocardial infarction, severe anemia, increased intracranial
pressure

Caution
May aggravate angina caused by hypertrophic cardiomyopathy
Use in acute myocardial infarction requires particular attention to hemodynamic
monitoring and clinical status to avoid the hazards of hypotension and
tachycardia
Tolerance may occur with nitrates. Patients should have a 'nitrate free' period for
10 to 12 hours each day; monitor for withdrawal efects
May cause severe hypotension. Use caution in patients with hypovolemia,
hypotension, and right ventricular infarctions
Use caution in patients with marked anemia, congestive heart failure, and
glucose-6-phosphate dehydrogenase deficiency
Use caution if right ventricular function is impaired for any reason

Side Efects
Common: headache, flushing, palpitations, orthostatic hypotension, syncope,
peripheral edema
Rare: rebound angina, arrhythmias, cardiovascular collapse

Interactions
May cause increased vasodilation and hypotension with other vasodilating or
antihypertensive medications including alcohol, alprostadil, antihypertensives,
anesthetics, anxiolytics, baclofen, diazoxide, hypnotics, monoamine oxidase
inhibitors, phenothiazines, and tizanidine.

Signs of OD
Cyanosis, dizziness, fainting, increase ICP, SOB, tiredness, weakness, weak & fast
heartbeat, fever, seizures
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Coronary Artery Disease

Description
The term acute coronary syndromes
(ACS) includes
o unstable angina (UA) and non
ST-segment elevation
myocardial infarction (NSTEMI)
Patients with symptoms typical of
acute myocardial ischemia, but
without the traditional evidence on
ECG of ST-segment elevation
myocardial infarction (STEMI)

Causes
Pathophysiologic processes: coronary
artery plaque rupture or erosion with nonocclusive thrombus, coronary spasm,
progressive stenosis of the small muscular coronary arteries, inflammation or
infection or both, or secondary UA due to other imbalances of myocardial oxygen
supply and demand, eg, anemia or cardiac arrhythmia; several pathophysiologic
processes may coexist in any one patient

Immediate Action
12-lead ECG can be performed

Patients with chest pain lasting >20 minutes that is suggestive of ACS, recent
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syncope or presyncope, or hemodynamic instability

Administer oxygen, particularly if the arterial oxygen saturation is <90%

Additionally, consider non-cardiac causes (eg, gastrointestinal, pulmonary) of

the presenting symptoms

Key Points
ACS is a heterogeneous group of disorders
Serum cardiac biomarkers may be positive or negative, and distinguish UA
(negative biomarkers) from NSTEMI (positive biomarkers)
The history, physical examination, 12-lead ECG, and initial cardiac biomarker tests
should be integrated to assign patients with chest pain into one of four
categories: a noncardiac diagnosis, chronic stable angina, possible ACS, and
definite ACS

Cardinal features
Unstable angina (UA) is a diagnosis that is largely based on the clinical
presentation of angina pectoris plus at least one of the following features:

o Occurs at rest or with minimal exertion, and usually lasts >20 minutes

o Described as severe and/or of new onset (within the last month)

o Occurs in a crescendo pattern (more severe, prolonged or frequent than in

a pre-existing anginal pattern)

NonST-segment myocardial infarction (NSTEMI) is diagnosed by the presence of

UA features plus:

o Lack of typical findings of ST-segment elevation myocardial infarction

(STEMI) on the 12-lead electrocardiogram (ECG)

o Presence of ST segment depression or T-wave inversion or transient minor

ST elevation implies a higher risk

o Presence of serum markers of myocardial necrosis (creatine kinase methyl

bromide (CK-MB) isoenzyme, and cardiac troponins T or I or both) carries a
higher risk

Etiology
Coronary artery plaque erosion or rupture with superimposed thrombus
Progressive stenosis of small muscular coronary arteries
Coronary vasospasm
Secondary UA due to factors other than, or in addition to, coronary disease, eg,
anemia, tachycardia, arrhythmia
Infection or inflammation
Angina post-myocardial infarction
Syndrome X (microvascular angina)
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Coronary artery dissection
Coronary artery plaque erosion or rupture with superimposed thrombus
Progressive stenosis of small muscular coronary arteries
Coronary vasospasm
Coronary artery dissection
Secondary UA due to factors other than, or in addition to, coronary disease, eg,
anemia, tachycardia, arrhythmia
Infection or inflammation
Angina post-myocardial infarction

Risk Factors
Prior history of cardiovascular disease (80% of patients)
Presence of risk factors for cardiovascular disease: smoking, hypertension,
hyperlipidemia, diabetes mellitus (type 1 or 2), obesity, sedentary lifestyle, family
history of coronary artery disease
Infection or inflammation superimposed on significant coronary disease
Cardiac arrhythmia
Conditions predisposing to anemia

Epidemiology
Approximately 1.4 million patients are admitted to hospitals annually in the U.S.
with UA or NSTEMI. A similar number of cases of UA are believed to go
unrecognized annually
928,000 patients were discharged from U.S. hospitals with a primary diagnosis of
ACS; there were 1.6 million discharges for ACS when a secondary diagnosis was
included; and 879,000 discharges were estimated for 2003
Most common >40 years of age, mean age at presentation is 62 years
Asymptomatic infarction can be found by ECG in 21% to 68% of elderly patients.
The prognosis for these patients is similar to those with symptomatic occurrences
Women present more often with UA, constituting 30% to 45% of patients with UA,
compared to 20% to 30% of patients with NSTEMI and 20% of patients with STEMI.
Recent evidence suggests that patients whose mothers have coronary disease are
more likely to also have coronary disease than those whose fathers have it.
ACS occurs worldwide, but it is much more common in the developed countries.
ACS cuts across socioeconomic groups
ACS is more common in groups with a higher socioeconomic status since
incidence increases with age
Risk factors (especially obesity, dyslipidemias, and diabetes) are more common as
the socioeconomic status increases

Diagnosis

Acute coronary syndrome (ACS) typically presents with a classic history of

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ischemic pain, or angina-type pain, described as deep, poorly localized chest or arm
discomfort, sometimes radiating down both arms, into the jaw, or through to the back.
In contrast with stable angina, ACS is characterized by severe pain that does not
resolve with the usual three doses of nitroglycerin or within 20 minutes, typical
anginal pain that occurs with rest or minimal exertion, new onset angina (less than
one month), or occurring in a crescendo pattern: more frequently, severe, or
prolonged than previously. Women and the elderly, however, frequently have atypical
features, which may include fatigue, gastrointestinal upset, or pulmonary complaints.
A high degree of suspicion is needed to avoid missing the diagnosis in these cases.

Symptoms
Poorly localized, substernal chest or arm pain, often described as aching or
squeezing in nature. Pain may radiate to the arms, to the back, or into the jaw
In patients with a prior history of angina, symptoms may mimic anginal episodes,
but may be more prolonged, severe, or frequent than their usual pattern
Patients with large areas of afected myocardium may have symptoms of 'pump
failure,' such as shortness of breath, nausea, sweating, palpitations, and light-
headedness
Signs
Physical examination may be unremarkable, particularly if the pain has resolved
by the time of presentation, or may be suggestive of ongoing myocardial ischemia
Findings of cardiac compromise may be present: tachycardia, regular or irregular
pulse, rales, or S3 and/or S4 gallop
Electrocardiogram (ECG) shows ST-segment depression and T-wave changes
approximately 50% of the time. Transient ST-segment elevation is associated with
the worst prognosis
Serum cardiac biomarkers may be normal (in UA) or elevated (in NSTEMI) and
help to distinguish the two
Rarely, hypotension may signal that a large area of myocardium is at risk

Associated disorders
Peripheral vascular disease
Atrial fibrillation or other arrhythmias
Congestive heart failure
Aortic aneurysm/dissection
Stroke
Anxiety/depression

Diferential Diagnosis
Pericarditis
Pericarditis is an inflammation of the pericardium. It may be caused by a virus or
bacterial infection, or by an injury, or may occur as a consequence of acute STEMI. It
77 of 107
may occur after a respiratory infection.

Myocardial infarction
Myocardial infarction (STEMI) is myocardial injury associated with ST-segment
elevation on ECG, and elevated serum cardiac biomarkers. It is caused by the acute
occlusion of an epicardial coronary artery.

Pleural pain (pleuritis, pleurisy)

Pleural pain is visceral pain associated with inflammation of the lining of the
lung (pleura)

Pulmonary embolism
Pulmonary embolism is not a disease in and of itself, but rather an often fatal
complication of an underlying venous thrombosis.

Aortic dissection
Aortic dissection occurs when blood flowing antegrade in the aorta separates the
intimal from the medial layer of the artery, and pulses down a false channel.
Dissection can lead to acute rupture of the aorta, and/or to interruption of the blood
flow to critical organs such as the kidneys, bowels, heart, or brain.

Costochondritis
Costochondritis is an inflammatory process of the costochondral or costosternal
joints that causes localized pain and tenderness.

Cholecystitis
Cholecystitis is inflammation of the gallbladder.

Peptic ulcer
Peptic ulcer disease refers to a discrete mucosal defect in the portions of the
gastrointestinal tract (gastric or duodenal) exposed to acid and pepsin secretion.

Gastritis
Gastritis is a common cause of chest pain.
Esophagitis
Esophagitis is inflammation of the lining of the esophagus often due to
gastrointestinal reflux.

Panic attack
A panic attack is a discrete period of intense fear or discomfort accompanied by
multiple somatic symptoms. It is often recurrent and sometimes disabling.

Clinical pearls
Atypical presentations for ACS frequently occur in women, diabetic patients, and
the elderly
Early consultation with a cardiologist is needed to help with the evaluation and
treatment of patients with ACS
At the time of hospital discharge of a patient with ACS, aspirin, beta-blockers, and
statins should be given, unless specifically contraindicated. In those patients with
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impaired left ventricular function, ACE-inhibitors or ARB agents should be
considered

Physical therapy
Cardiac Rehabilitation
Early in the course of an ACS, factors that increase the work of the heart should
be avoided, and the patient should be placed on bed rest
The ability to resume physical activity depends on the response to medical or
invasive therapy for myocardial ischemia

Risks/benefits
With increased activity comes the risk of increased cardiac work and myocardial
ischemia.

Early mobility, however, not only carries psychologic benefits, but serves as
prophylaxis against thromboembolic phenomenon such as deep venous
thrombosis.

In cases where revascularization has occurred, early mobilization is warranted to

avoid problems associated with prolonged inactivity.

Ultimately, increased activity and weight loss both reduce the risks of future
cardiac events.

Initially, activity should be increased slowly, watching for hypotension or

recurrent symptoms suggesting myocardial ischemia.

Efficacy
Regular exercise and risk modification reduces mortality, subsequent coronary
events, and subsequent hospitalizations in patients with coronary artery
disease.

Therapeutic lifestyle changes

Smoking cessation: Goals are complete cessation of smoking and avoidance of
second-hand smoke
Dietary changes for weight loss and for improvement of the lipid profile: Goal is a
body mass index of <25 kg/m2, low-density lipoprotein (LDL) of <70 mg/dL in
patients with myocardial infarction (normal LDL cholesterol: 50-130 mg/dL; <100
mg/dL in patients with atherosclerotic heart disease or diabetes mellitus (type 1
or 2)), and high-density lipoprotein (HDL) of >35 mg/dL
Limited alcohol ingestion
Increased activity/regular exercise regimen
Strict control of diabetes mellitus (type 1 or 2): Goal is a fasting plasma glucose
level of <110 mg/dL or a hemoglobin A1c value of <7
Strict control of hypertension: Goal is a systolic blood pressure of <130 mmHg
and diastolic blood pressure of <85 mmHg
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Stress reduction

Risks/benefits
All lifestyle modifications are associated with improvements in cardiac
outcomes; however, all are difficult to achieve.

Increased activity can be associated with cardiac ischemic symptoms, and any
exercise program warrants monitoring at least initially in patients during
posthospitalization follow-up.

Smoking cessation greatly improves oxygen delivery, reduces symptoms, and

improves prognosis.

Weight reduction reduces the metabolic strain on the heart and improves lipid
profiles. Stress reduction may reduce the blood pressure.

Prognosis
Reported 30-day mortality rates for unstable angina (UA)/non-ST-segment
elevation myocardial infarction (NSTEMI) are between 2.5% and 4.4%
Overall, cumulative mortality at 6 months is approximately 9% in patients with ST-
segment depression acute coronary syndromes (ACS), and 11% at one year,
which is significantly worse than 6-month mortality in patients with acute ST-
segment elevation myocardial infarction (STEMI; approximately 6%) or T-wave
inversions on an electrocardiogram (approximately 3%)
Antithrombotic treatment with and without early invasive therapy is associated in
most studies with a 20% to 35% relative risk reduction
The risk of early stroke is 3% to 6%, and the risk of refractory angina is 3.8% to
5.6%
Risk of myocardial infarction at 6 months is 3.45 to 6.2%, readmission for angina
is 14.5% to 16%, ventricular tachycardia is approximately 1%, and heart failure is
1.0% to 1.7%

Factors afecting prognosis

Presence of heart failure or significant left ventricular impairment is associated
with high 6-month rates of mortality or myocardial infarction
Cardiac troponin I concentration at baseline is also directly linked to mortality
rates at 42 days, with a baseline level of 0 to <0.4 ng/mL associated with a 1%
risk, and levels >9 ng/mL associated with a risk of up to 7.5%
Other factors negatively afecting prognosis include recurrent ischemia,
hemodynamic instability, ventricular tachycardia, or prior CABG surgery
Atypical presentations occur in women, diabetic patients, and older adults and
may delay and impact the initial treatment

Clinical pearls
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Patients in whom there is any elevation of cardiac biomarkers have a dramatically
increased risk of further cardiac events. Aggressive evaluation of these patients is
warranted, usually with cardiac catheterization
Patients in whom biomarkers are negative (that is, 'myocardial infarction ruled-
out') and who have a negative stress test are often not pursued for risk factor
modification. They should receive further evaluation and management
If myocardial ischemia is not established, remember to continue to evaluate the
patient for the true cause of their discomfort
81 of 107

Myocardial Infarction
Description
Myocardial infarction (MI) or ST-segment
elevation MI (STEMI) is a disorder in which
necrosis of the myocardium occurs due to an
inadequate supply of oxygen. The syndrome is
usually caused by a sudden and complete, or
nearly complete, occlusion of at least one
coronary artery
Arterial occlusion is usually caused by rupture
of an atherosclerotic coronary artery plaque
with subsequent acute thrombosis
Unless death occurs within approx. 30min (e.g. from arrhythmia), myocardial
necrosis is always evident
Treatment of choice is restoration of blood flow to the myocardium in the shortest
possible period of time, either pharmacologic (e.g. thrombolysis) or by mechanical
means (e.g. primary angioplasty)

STEMI is distinguished clinically from acute coronary syndromes, such as non-STEMI

(NSTEMI) and unstable angina, by the presence of characteristic electrocardiogram
(ECG) changes, and carries diferent prognostic and treatment implications

Immediate action
Time is critical - approx. half of all deaths from MI occur within 1h of the onset of
symptoms
If the patient becomes unconscious, administer cardiopulmonary resuscitation
(CPR)
Administer oxygen
Administer nitroglycerin sublingually if the systolic blood pressure is >90mmHg
Administer morphine for pain
Obtain a 12-lead ECG

Key points
Rapid re-establishment of coronary perfusion is key to preventing/minimizing
myocardial damage, and lowering morbidity and mortality
Diagnosis is most often established by suggestive history, physical examination,
and 12-lead ECG findings
Studies show that simple therapies such as the administration of aspirin, beta-
blockers, angiotensin-converting enzyme (ACE) inhibitors, and statins to reduce
82 of 107
recurrence, morbidity, and mortality are severely under utilized

Cardinal features
The presence of either of the following satisfies the definition of diagnostic criteria for
acute, evolving, or recent myocardial infarction (MI):

Typical rise and fall in biochemical markers of myocardial necrosis, plus at least one of
the following: ischemic symptoms, classically, acute onset of squeezing substernal
chest pain or pressure, often radiating to one or both upper extremities, to the neck or
jaw, or through to the back, difficulty breathing or shortness of breath, nausea,
lightheadedness and/or weakness, feeling of impending doom; electrocardiogram (ECG)
showing classic evolving changes, including ST-segment elevation, T-wave inversions,
and late development of Q-waves over the afected myocardium (ST-segment
depression, nonspecific T-wave inversions, or a lack of ECG findings in a patient with
otherwise classic presentation should alert the provider to the possibility of an evolving
non-ST-segment elevation myocardial infarction (NSTEMI, an acute coronary syndrome);
or the patient has had a recent coronary angioplasty

Diagnostic criteria for established MI:

Development of pathologic Q-waves on serial ECG, with or without a history of
symptoms, with or without a rise and fall in biochemical markers (which may
have already resolved by the time of patient presentation)

Clinical presentation:
Patients sometimes present with an episode of severe and/or prolonged anginal-
type chest pain that does not resolve on standard therapy, after a period of
change in the established pattern of chronic stable angina, and evidence of a
recent acute coronary syndrome characterized by increased frequency,
severity, or duration of myocardial ischemic symptoms
In many patients the first presentation is sudden cardiac death
30% of patients die from acute MI, half in the first hour after the onset of
symptoms
Heart failure, pulmonary edema, hypotension, syncope, or arrhythmias may be
presenting features
In relatively asymptomatic patients, the presenting complaint might be
exhaustion or malaise

Etiology
The most common cause is coronary thrombosis (blood clot), usually occurring
on an atherosclerotic plaque (which often shows evidence of a recent plaque
rupture). Involved plaques are often not severe (<50% diameter stenosis) prior
to rupture and thrombus activation.

Embolization of material into a coronary artery, e.g. from a valvular

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endocarditis, mural thrombosis, or paradoxical emboli

Trauma causing coronary artery laceration or dissection, including iatrogenic

trauma during angioplasty

Vasculitis, e.g. systemic lupus erythematosus and other collagen vascular

diseases

Vasospasm, e.g. with cocaine or amphetamine use and/or variant Prinzmetal's

angina

Proximal extension of a thoracic aortic aneurysm into a coronary artery ostium

Spontaneous dissection of a coronary artery (a rare occurrence in young

pregnant women)

Degenerative or infiltrative coronary artery disease, e.g. amyloidosis

Congenital abnormalities, e.g. anomalous origin of left coronary artery (intra-

arterial course)

Conditions which suddenly increase myocardial oxygen requirements or

decrease supply, e.g. hypovolemic shock and carbon monoxide poisoning

Coronary thrombosis

Coronary embolization

Coronary dissection

Vasculitis

Coronary vasospasm

Extension of thoracic aortic aneurysm

Degenerative coronary artery disease

Congenital anomalies

Conditions leading to mismatch of myocardial oxygen supply and demand, e.g.

carbon monoxide poisoning

Risk Factors
Smoking
Dyslipidemias (especially elevation of low-density lipoprotein (LDL) cholesterol
and/or reduction of high-density lipoprotein (HDL) cholesterol)
Hypertension
Diabetes mellitus, type 1 or type 2
Obesity
Physical inactivity
Male gender increases the risk of MI in men between the ages of 40-65 years
Strong family history
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Acute triggering events such as sudden intense emotion or extreme physical
exertion occur in up to half of MIs
Inflammation, as evidenced by an increase in high sensitivity C-reactive protein
(cardio-CRP, hsCRP)
Recent noncardiac surgery
Hypoxemia
Cocaine or methamphetamine abuse should be strongly suspected in any young
person presenting with acute MI

Epidemiology
>500 cases per 100,000 of population.

>1100,000 cases per year in the US

Approx. 225,000 deaths per year in the US

Most common >40 years of age

Peak occurrence is between 50-70 years of age

Asymptomatic infarction can be found by ECG in 21-68% of elderly patients. The

prognosis for these patients is similar to those with symptomatic occurrences

Between the ages of 40-65 years, MI is most common in males

>65 years of age, there is no diference between males and females

Genetic predisposition: recent evidence suggests that patients whose mothers

have coronary disease are more likely to also have coronary disease than those
whose fathers have it

Worldwide, but much more common in developed countries.

Cuts across socioeconomic groups

Risk factors (especially obesity, dyslipidemias, and diabetes) are more common
as socioeconomic status increases

Diagnosis

The classic presentation of acute myocardial infarction (MI) is pain, similar to

angina pectoris, but more severe and lasting longer. The combination of characteristic
pain persisting for >20min and diaphoresis strongly suggests MI. Approx. a quarter of
patients will exhibit signs of sympathetic nervous system activation: pallor,
tachycardia, and hypertension. The electrocardiogram (ECG) initially shows ST-
segment elevation, followed by a typical evolution over several days to the presence
of Q-waves over the area of the infarct. Serum cardiac biomarkers are released into
the blood stream, and detectable over a period of 4-72h, although troponin levels can
remain elevated for 7-10 days. It is important to note that patients can present
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without chest pain, and may exhibit only some of the above characteristics. However,
the diagnosis of acute ST-segment elevation MI (STEMI) is based on characteristic ECG
changes and the presence of serum biochemical markers of myocardial necrosis.

Symptoms
Main symptom is chest pain that is characteristically described as retrosternal,
and crushing or squeezing in nature. Alternative descriptions include 'heaviness'
or 'aching'
Pain can also be epigastric or in the upper back
Radiation is often present: inner aspect of arms (left more than right), shoulders,
neck, teeth, or jaw
Lasts at least 20min, unresponsive (or only partially so) to nitroglycerin
OTHER: weakness, fatigue, restlessness, diaphoresis, palpitation, nausea,
vomiting, hiccupping, SOB, anxiety, abdominal pain, dry mouth

Up to one-third of patients do not experience classic substernal chest pain - this is

especially true of older patients, females, diabetics, and surgical patients.

Signs
Diaphoretic or cool skin, pallor, or other signs of vasoconstriction
Hypertension (initially due to pain and adrenergic discharge) may be followed by
hypotension in larger infarcts or inferior wall infarction
Restlessness
Apical systolic murmur, caused by mitral regurgitation secondary to papillary
muscle dysfunction may be present
Tachycardia (sinus or tachyarrhythmia) or bradycardia (sinus or secondary to
heart block - especially in inferior infarctions as a manifestation of the Bezold-
Jarish reflex)
Irregular rhythm (premature auricular contractions (PACs) and premature
ventricular contractions (PVCs), Wenckebach atrioventricular (AV) block, other
arrhythmias)
Signs of left ventricular failure and/or right ventricular dysfunction/failure in large
infarcts
Rales, other evidence of pulmonary congestion
Signs of low cardiac output, e.g. hypotension, poor carotid pulses, and pulsus
alternans
Confusion, especially in elderly patients
Apical systolic murmur, S3 or S4 may be present
Conduction disturbances on ECG
'Nonspecific' repolarization abnormalities useful in identifying MI if classic ST-
segment elevation/T-wave inversion is not present
ST-segment depression, isolated T-wave inversion, and new onset bundle branch
block are less specific, but may be supportive of a diagnosis of MI

Associated disorders
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Peripheral vascular disease
Atrial fibrillation or other arrhythmias
Congestive heart failure
Aortic aneurysm/dissection
Pericarditis
Pulmonary embolism
Stroke
Anxiety/depression

Diferential diagnosis
Pericarditis
Pericarditis is an inflammation of the pericardium, which is the sac that surrounds
the heart. It may be caused by a viral or bacterial infection, injury, neoplasm,
uremia, or as a consequence of recent MI or cardiac surgery. It often occurs after an
upper respiratory infection.

Pleural pain

Pleural pain is pain that is related to the covering (pleura) of the lung.

Pulmonary embolism
Pulmonary embolism is not a disease in and of itself, but rather an often fatal
complication of underlying venous thrombosis.

Aortic dissection
Aortic dissection is dissection of the thoracic aorta.

Costochondritis and chondrosternal inflammation

Costochondritis is an inflammatory process of the costochondral or costosternal
joints that causes localized pain and tenderness.

Cholecystitis
Cholecystitis is inflammation of the gallbladder.

Peptic ulcer
Peptic ulcer refers to a discrete mucosal defect in the portions of the gastrointestinal
tract (gastric or duodenal) exposed to acid and pepsin secretion.

Esophagitis
Inflammation of the lining of the esophagus, often due to gastrointestinal reflux.

Panic attacks
A panic attack is a discrete period of intense fear or discomfort accompanied by
multiple somatic symptoms. It is often recurrent and sometimes disabling.

Physical therapy
Cardiac Rehabilitation Therapy
Early in the course of acute MI, factors that increase the work of the heart should
be avoided
87 of 107
After about 12h, however, physical activity such as sitting and dangling the feet,
and getting up to a chair should be encouraged
Ambulation should resume within 2 days whenever possible
Working with physical therapy or cardiac rehabilitation services, if available, is
probably more efective than self-initiated programs

Risks/benefits
Early mobility not only carries psychologic benefits, but is associated with
decreased pulmonary capillary wedge pressure, and serves as prophylaxis
against thromboembolic phenomenon such as deep venous thrombosis.

Patient and caregiver information

While bed rest may be indicated for the first 12-24h, early ambulation is
important in preventing complications from MI
Initially, activity should be increased slowly, watching for hypotension or recurrent
symptoms suggesting myocardial ischemia

Efficacy
Early activity is associated with positive psychologic benefits, and potentially
improved hemodynamics, as well as reduced thromboembolic complications.

Therapeutic Lifestyle Changes

Cessation of smoking
Weight loss
Reduction of fat consumption (especially saturated fats)
Carefully monitored exercise program
Treatment of hypertension
Treatment of hyperlipidemia
Treatment of diabetes mellitus types 1 and 2
Compliance with prescriptions, e.g. beta-blockers, aspirin, thienopyridines, ACE
inhibitors, and lipid-lowering agents
Mind-body practices to reduce stress

Risks/benefits
Lifestyle changes help speed recovery and help prevent future attacks. Smoking
cessation greatly improves patient prognosis. Weight reduction may help
promote a more favorable lipid profile and thereby reduce risk of adverse
cardiovascular events. Weight reduction may reduce strain on the heart. Stress
and anxiety reduction may reduce the need for medical intervention by reducing
blood pressure. Exercise increases exercise tolerance, and reduces blood
pressure, lipids, stress, and weight.
88 of 107

Patient and caregiver information

Patients should be instructed about their disease process, and medication use and
side-efects; and risk factor modification including smoking cessation
Remind the patient of the positive efects on prognosis and general health
Smoking cessation: some patients may require pharmacologic support to
successfully quit smoking. The use of transdermal nicotine is a safe and efective
potential strategy. Multiple strategies are more likely to be successful. They may
include group sessions, counseling with the physician, and pharmacologic
intervention
Weight reduction: some patients may require nutritional consultation and
supervision to achieve the goals with respect to diet. In some cases, enrollment in
a weight reduction program may be indicated
Stress reduction: patients may need help in dealing with their stress, and may
benefit from relaxation techniques and other methods of stress control
Exercise: patients may be fearful of increasing exercise level with angina, and
may be resistant to a regimen that may require a significant change in lifestyle
and must be long-term to be efective

Prognosis
One-year mortality after acute myocardial infarction (MI) is as high as 21%,
particularly if left ventricular function is significantly impaired (<30% ejection
fraction)
The smaller the amount of myocardium afected, in general, the better the
prognosis.

Factors afecting prognosis

The single most important predictor of long-term prognosis after MI is severity of
left ventricular dysfunction. Other factors are:

Age

Significant comorbidities (diabetes, hypertension)

Presence of high-grade ventricular arrhythmias

Completeness of revascularization

Evidence of continuing ischemia

Compliance with secondary prevention strategies, including those for risk factor
modification
89 of 107

Anatomy of the Heart

Location
Rests on diaphragm, near midline
Inside mediastinum (from sternum to vertebral column, rib 1 to diaphragm, btw
lungs)
2/3 of its mass lie to the Lt.
Anterior surface deep to sternum & ribs
Inferior surface btw. apex & Rt. Border & rests on diaphragm
Rt. Border faces Rt. Lung & extends from inferior surface to base
Lt. Border (i.e. pulmonary border) face Lt. lung & extends from base to Apex

Pericardium
Surrounds & protects heart
Consists of:
o Fibrous pericardium though, inelastic, dense irregular connective tissue
Prevents overstretching of heart & anchors it to mediastinum
o Serous pericardium thinner, delicate double layer around heart
Parietal layer fused to fibrous pericardium
Visceral layer inner layer = epicardium adheres to heart
Btw parietal & visceral = lubricating serous fluid = pericardial fluid
Space = pericardial cavity

Layers of Heart Wall

3 layers
o Epicardium = visceral layer of serous pericardium
o Myocardium = 95% of heart responsible for pumping action
Cardiac muscle fibers swirl diagonally around heart in bundles
o Endocardium = smooth lining for chambers of heart & covers valves
Continuous with endothelial lining of vessels

Chambers
4 chambers
2 superior = atria
o auricles on anterior surface increase capacity of atrium to hold more blood
2 inferior = ventricles
Surface of heart = sulci grooves that contain coronary blood vessels & fat
o Deep coronary sulcus encircles most of heart & marks separation btw atria
& ventricles
o Anterior Interventricular sulcus anterior surface btw Lt. & Rt. Ventricles
o Posterior interventricular sulcus posterior surface btw. Lt. & Rt. Ventricles

Rt. Atrium
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Rt. Border of heart
Receives blood from
o SVC
o ICV
o Coronary sinus
Posterior wall is smooth
Anterior wall is rough due to pectinate muscles
Interatrial septum
o Oval depression = fossa ovalis remnant of fetal circulation
Blood passes from Rt. Atrium into Rt. Ventricle through tricuspid valve (i.e. Rt.
Atrioventricular valve)

Rt. Ventricle
Forms most of anterior surface of heart
Inside contains raised bundles of cardiac muscle fibers = trabeculae carneae
o Part of conduction system
Cusps of tricuspid valve connected to chordae tendinae in turn connected to
trabeculae carneae called papillary muscles
Separated from Lt. ventricle by interventricular septum
Blood passes from Rt. Ventricle through pulmonary valve (i.e. pulmonary
semilunar valve) into an artery called pulmonary trunk
o Pulmonary trunk divides into Rt. & Lt. pulmonary arteries

Lt. Atrium
Forms most of the base of heart
Receives blood from lungs through 4 pulmonary veins
Anterior & posterior wall are smooth
Blood passes from Lt. atrium into Lt. ventricle through bicuspid (i.e. mitral) valve
(i.e. Lt. atroventricular valve)

Lt. Ventricle
Thickest chamber
Forms apex of heart
Contains trabeculae carneae & has choradae tendae that anchor bicuspid valve
cusps to papillary muscles
Blood passes from Lt. ventricle through aortic valve (i.e. aortic semilunar valve) to
ascending aorta
Some blood flows into coronary arteries through holes in the aorta
91 of 107

Heart Valves & Circulation of

Blood

Atrioventricular Valves
Tricuspid & bicuspid valves
When open, rounded ends project into ventricle
When ventricles are relaxed, papillary muscles are relaxed, chordae tendineae are
slack, & blood moves from higher pressure in atria to lower pressure in ventricles
though open valves
Ventricles contract, pressure of blood drive cusps up until edges met and close
opening, papillary muscles contract pull on chordae tendinae to prevent valve
cusps from everting (i.e. opening into atria)

Semilunar Valves
Aortic & pulmonary valves
Made up of three crescent moon-shaped cusps
o Each cusp attached to arterial wall
They allow ejection of blood into arteries & prevent backflow into ventricles
Free borders of cusps project into lumen of artery
Ventricles contract pressure builds up in chambers, semilunar valves open when
pressure in ventricles exceeds pressure in arteries = ejection of blood from
ventricles into pulmonary trunk & aorta
Ventricles relax blood starts to flow back toward heart backflow blood fills
valve cusps which causes valves to close tightly

Systemic & Pulmonary Circulations

These are arranged in series, the output of one becomes input of other
Lt. side = systemic circulation
o Receives oxygen rich blood from lungs
Lt. ventricle ejects blood into aorta
Systemic tissues arteries give rise to smaller diameter arterioles, & finally
capillaries
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Systemic venules carry deoxygenated blood larger veins Rt. Atrium
Rt. Side = pulmonary circulation
o Receives deoxygenated blood from systemic circulation
Blood from Rt. Ventricle flows into pulmonary trunk pulmonary arteries
pulmonary capillaries gas exchange pulmonary veins Lt. atrium

Coronary Circulation
Myocardium has own blood vessels coronary/cardiac circulation
Coronary arteries from ascending aorta & encircle heart
Blood flows in when heart relaxes, high pressure of blood in aorta propels blood
through coronary arteries into capillaries, & into coronary veins

Coronary Arteries
Lt. coronary artery passes inferior to Lt. auricles & divides into anterior
interventricular & circumflex branches
Anterior interventricular branch (i.e. Lt. anterior descending artery)
o In anterior interventricular sulcus & supplies both ventricles
Circumflex branch
o In coronary sulcus & distributes O2 blood to walls of Lt. ventricle & atrium
Rt. Coronary artery supplies small branches to Rt. Atrium
o Divides into posterior interventricular branch follows posterior
interventricular sulcus & supplies two ventricles
o Marginal branch in coronary sulcus Rt. Ventricle
There are many anastamoses in case on coronary artery is blocked

Coronary Veins
Most of deoxygenated blood from myocardium drains in large vascular sinus on
posterior surface inside coronary sulcus = coronary sinus
Coronary sinus empties into Rt. Atrium
Veins bringing blood into coronary sinus include:
o Great cardiac vein in ant. Interventricular sulcus
Lt. coronary artery
o Middle cardiac vein in post. interventricular sulcus
Rt. Coronary artery
o Small cardiac vein in coronary sulcus
Rt. Atrium & ventricle
o Anterior cardiac veins
Drain Rt. Ventricle & open directly into Rt. Atrium
93 of 107

Cardiac Muscle
Tissue & the Cardiac Conduction System
Histology of Cardiac Muscle Tissue
Compared to skeletal muscle fibers
o Shorter in length & less circular in transverse section
o Exhibit branching = stair-step appearance
o Ends of fibers connect to neighboring fibers by irregular transverse
thickening of sarcolemma called intercalated discs
o Discs contain desmosome = hold fibers together & gap junctions, which
allow muscle action potentials to conduct from one muscle fiber to its
neighbors
o Gap junctions allow entire myocardium of atria or ventricles to contract as a
unit
o Increase mitochondria
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Autorhythmic Fibers: The

Conduction System
Inherent & rhythmical electrical activity is reason for lifelong beat
Network of specialized cardiac muscle fibers = autoryhthmic fibers = self-
excitable
Repeatedly generate APs that trigger heart contractions
Autorhythmic fibers
o Act as pacemakers setting the rhythm
o Form conduction system path for each cycle of cardiac excitation
Chambers work in coordinated manner = efective pump
Cardiac APs propagate through conduction system:
1. Begins in Sinoatrial node in Rt. Atrial wall inferior to SVC
a. Does not have a stable resting potential
b. Repeatedly depolarize to treshold spontaneously = pacemaker potential
c. At treshold = AP, which propagates throughout both atria via gap
junctions in intercalated discs of atrial muscle fibers = atrial contraction
2. Reaches Atrioventricular node in interatrial septum
3. AV node AP enter atroventricular bundle (i.e. bundle of His)
a. Allows conduction from atria to ventricle
4. Enters Rt. & Lt. bundle branches extend through interventricular septum
toward apex
5. Purkinje Fibers = rapid conduction of AP at apex upward to remainder of
ventricular myocardium = ventricular contraction = pushes blood toward
semilunar valves
95 of 107

Action Potential &

Contraction
of Contractile
Fibers
An action potential occurs in a contractile fiber as follows:
1. Depolarization
a. Stable resting membrane potential (-90mV)
b. When brought to treshold voltage gated fast Na+ channels open flooding
Na+ inside = rapid depolarization
2. Plateau
a. Maintained depolarization due par to opening of voltage gated slow Ca2+
channels in sarcolemma Ca2+ moves in = contraction
b. Also voltage gated K+ channels are found in sarcolemma
c. Lasts about 0.25 seconds
3. Repolarization
a. Recovery of resting membrane potential
b. After delay additional voltage gated K+ channels open.
c. Outflow of K+ restores negative resting membrane potential
d. Ca2+ = closing = contributes to repolarization

ATP Production in Cardiac Muscle

Relies almost exclusively on aerobic cellular respiration
96 of 107
The Cardiac Cycle
Pressure & Volume Changes During the Cardiac Cycle
Atria & ventricles contract & relax in each cycle = forces blood higher pressure to
lower pressure areas
As an area contracts, blood pressure within it increases

Atrial Systole
0.1 seconds the atria are contracting, ventricles are relaxed
o depolarization of SA node causes atrial depolarization = P wave
o Atrial depolarization = atrial systole
o Atrial systole contributes a final 25 mL of blood to volume already in each
ventricle (105 mL)
o End of atrial systole = end of ventricular diastole (relaxation)
o Thus, ventricles each contain 130 mL at diastole (i.e. end of relax) = end-
diastolic volume (EDV)
QRS marks onset of ventricular depolarization

Ventricular Systole
0.3 seconds ventricles are contracting, atria are relaxed in atrial diastole
o ventricular depolarization causes ventricular systole
o pressure rises inside ventricles = blood up AV valves = forcing shut
o 0.05 seconds both AV & SL valves closed = isovolumetric contraction
o cardiac muscles are contracting, but not yet shortening
o continued contraction = pressure increases
o ejection of blood from heart begins
o SL valves open = ventricular ejection = 0.25 seconds
Lt. ventricle ejects 70 mL into aorta& Rt. Ventricle ejects same volume in
pulmonary trunk
o Remaining volume in each ventricle at end of systole = 60 mL = end-
systolic volume (ESV)
o Stroke volume volume ejected per beat from each ventricle = EDV-ESV
At rest = 130mL-60mL = 70mL
T Wave marks onset of ventricular repolarization

Relaxation Period
0.4 seconds atria & ventricles = relaxed
o ventricular repolarization causes ventricular diastole = lower pressure =
flow inside
o backflowing blood closes SL valves
o another period of isovolumetric relation
Ventricles continue to relax pressure falls quickly, when below atrial pressure
AV valves open = ventricular filling begins
Blood that has been building up in atria during ventricular systole then rushes
rapidly into ventricles
97 of 107

Cardiac Output
CO volume of blood ejected from Lt. ventricle (or Rt.) into aorta (or pulmonary
trunk)
CO = SV * HR
Norm SV = 70mL/min
Norm HR = 75 beats/min
Norm CO = 5.25 L/min
This volume is close to total blood volume, thus your entire volume flows through
circulations each minute
Cardiac reserve diference btw a persons max CO & CO at rest
o Norm 4-5X CO resting value
o Athlete 7-8X CO resting value

Regulation of Stroke Volume

At rest, SV = 50-60% of EDV because 40-50% remains in ventricles (ESV)
3 factors regulate SV & ensure Rt. & Lt. ventricles pump out equal amounts
o preload degree of stretch on hear before contraction
o contractility forcefulness of contraction of individual ventricular muscle
fibers
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o afterload pressure that must be exceeded before ejection from ventricles
occurs

Preload Efect of Stretching

a greater preload (i.e. stretch) on cardiac muscle fibers prior to contraction
increases their force of contraction
The more the heart fills with blood during diastole, the > the force of contraction
during systole = Frank-Starling law of the heart
Greater the EDV, the more forceful the next contraction
Two key factors determine EDV
o Duration of ventricular diastole
o Venous return
Volume of blood returning to Rt. Ventricle
HR increase diastole is shorter
Less filling time = smaller EDV ventricles may contract before adequately filled
Venous return increases greater volume of blood flows into ventricles = EDV
increased
HR exceeds 160 beats/min, SV usually decline due to short filling time, EDV is
less, & preload is lower
Slow resting HR = larger SV because filling time is prolonged & preload larger

Contractility
The strength of contraction at any given preload
Substances that increase contractility are positive inotropic agents
o Stimulation of sympathetic division of ANS, hormones such as epinephrine,
nor epi, increased Ca2+ in interstitial, drug digitalis
Substance that decrease contractility are negative inotropic agents
o Inhibition of sympathetic division of ANS, anoxia, acidosis, anesthetics,
increased K+ in interstitial

Afterload
Ejection of blood from heart begins when pressure in Rt. Ventricle exceed pressure
in pulmonary trunk & when pressure in Lt. ventricle exceeds pressure in aorta
The pressure that must be overcome before a semilunar valve opens is the
afterload
An increase in afterload causes SV to decrease, thus more blood remains in
ventricles at end of systole
Increased afterload is seen in hypertension and atherosclerosis

Autonomic Regulation of Heart Rate

Nervous system regulation of heart originates in cardiovascular center in medulla
oblongata.
Limbic system & cerebral cortex send information
Cardiovascular center directs appropriate output by increasing or decreasing
frequency of nerve impulses in both sympathetic & parasympathetic branches of
ANS
Limbic system = anticipatory reaction
Physical activity = proprioceptors
99 of 107
Chemoreceptors monitor changes in blood
o Hypoxia, acidosis, alkalosis all depress cardiac activity
o Epinephrine, norepinephrine enhance hearts pumping efectiveness
o Exercise, stress, excitement = hormone release
o Thyroid hormones enhances cardiac contractility & HR
o Elevated blood levels of K+ or Na+ decrease HR & contractility
o Excess Na+ blocks Ca2+ inflow during cardiac APs, thus decreases
contraction
o Excess K+ blocks generation of APs
o Moderate increase in interstitial Ca2+ = speeds HR & strengthens heartbeat
Baroreceptors monitor stretching of major arteries & veins
Parasympathetic nerve impulses reach heart via Rt. & Lt. vagus nerve extend to
SA, AV nodes & atrial myocardium
Sympathetic cardiac accelerator nerves extend to SA, AV nodes & myocardium
Age, gender, physical fitness, & body temperature all influence HR

Exercise & the Heart

Aerobics elevates CO & accelerates metabolic rate
Whether demand in O2 is met depends mainly on adequacy of CO & proper
functioning of respiratory system
After several weeks of training increase maximal CO increases maximal rate of
O2 delivery to tissues
O2 delivery also rises due to skeletal muscles increased capillary networks in
response to training
Hypertrophy of the heart also occurs with training
o Resting CO is the same though SV is increased, but HR is decreased
Regular exercise helps reduce BP, anxiety, & depression, control weight, increase
bodys ability to dissolve blood clots by increasing fibrinolytic activity
100 of 107

Clinical Skills Laboratory

Infection Control

Objectives:
1. Review changes in PIDA routine practices
2. Review PIDAC additional precautions (i.e. isolation)
3. Unveil new signage to support Routine Practice & Additional Precautions (RPAP)
4. Examine the cost of Healthcare Associated Infections (HAI)

Basics of Infection Control

Chain of infection
Routine practice
o Based on premise that all blood body fluids, secretions, & excretions are
potentially infectious
Transmission based precautions
o When routine practice is not sufficient to prevent disease transmission
additional precautions required

Chain of Infection
1. Contact
2. Droplet
3. Airborne
4. Vehicle
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5. Vector
6. Parenteral

Infectious agent reservoir portal of exit mode of transmission portal of

entry susceptible host
In West Nile Virus portal of exit = blood
H1N1 portal of exit = mouth & nose; mode of transmission = droplets
Chicken Pox airborne light, thus dont have to be close to someone to get it
its airborne
Vehicle e.g. eating

5 Elements of Routine Practice

1. Risk Ax
a. Each health care provider has a responsibility to;
i. Perform a risk Ax before each interaction
ii. Understand & follow organizational policies & procedures
iii. Is there an exposure risk? Yesuse routine practices
iv. Are the dx or Undx symptoms? Yesuse routine practices + additional
precautions
v. Are there organizational policies or procedures for this interaction?
Yesfollow procedures
2. Hand Hygiene
a. New role coordinator/data support
b. Corporate Initiative
c. Ministry Mandate
d. Public reporting of rates
e. Alcohol Hand Sanitizer quick & easy, viable, kills on contact, moisturizes
f. Water takes longer, sinks, soap doesnt kill, more drying on hands, more
efective with Cdif
g. 4 Moments
i. Before initial pt/pt environment contact
1. Protect pt/pt env. From harmful organisms
ii. Before aseptic procedure
1. Protect pt. against harmful organisms, including pts own
iii. After body fluid exposure risk
1. Protect yourself & health care env. From harmful pt organisms
iv. After pt/pt environment contact
1. Protect yourself & health care env. From harmful pt organisms
3. PPE personal protective equipment
a. Will I be exposed to body fluids?
i. PPE
b. Will my hands be exposed to blood, excretions, secretions, or contaminated
items?
i. Gloves
c. Will my face be exposed to a splash, spray, cough, or sneeze?
i. Mask
d. Will my clothes be exposed?
i. Gown
e. Selection is base on risk Ax
102 of 107
f. Used to break chain of transmission
g. Used alone or in combination to prevent exposure
h. Put on prior to interaction & remove immediately
i. PT may weak PPE when ambulating a pt in the hallway
j. Gloves, gowns, masks/respiratory, eye protection
How to:
Removing Personal Protective Equipment
1. Gloves First
a. Use glove to glove, skin to skin technique
2. Gown of
a. Discard in hamper with minimal air disturbance
3. Clean hands
4. Overhead mask
5. Mask
6. Hand hygiene

This is the minimum requirement. If suspect contamination during removal of any piece
of PPE, perform hand hygiene

Transmission in Health Care Environment

48 reports of HCW infected with H1N1
26 cases provided detailed risk factor information
13 cases acquired virus in health-care setting
o 1 case HCW HCW
o 12 cases patient HCW
o 3/12 wore full PPE 100% of the time
o How many HCW infections could have been prevented? ALL of THEM

4. Environmental Controls
a. Accommodation
b. Availability of Products
i. Hand hygiene facilities
ii. PPE
c. Cleaning & Disinfection
d. Sharps Containers
e. Monitoring air exchanges
f. Pt placement first choice = private room; second choice multiple pt room
= maintain a spatial separation
i. For pts who have a cough & other symptoms of febrile respiratory
illness or influenza like illness:
1. Instruct pt weak mask outside of room
2. Instruct pt hand hygiene & respiratory etiquette
3. Maintain spatial separation of 2 meters
g. Hospital disinfectant is efective for cleaning
i. Clean & disinfect
ii. Allow to dry
h. Aerosol-Generating Procedures
i. High risk respiratory procedures
ii. Ensure curtain is pulled in multi-pt room
103 of 107
5. Administrative Controls
a. Education
i. Staf
ii. Pt/visitor
iii. Respiratory etiquette
b. Immunization
c. New contact precautions sign
i. ARO, scabies, lice, diarrhea, draining wound not contained in dressing,
undiagnosed rash
ii. Wear gloves for every entry into room
iii. Wear gown if there will be contact with pt or environment
iv. No gown if check of pt visually, speak to pt without touching
anything, hand hygiene to follow
Scenarios:

1. You enter a room in contact precautions to see if the pt is awake. What PPE will
you weak? GLOVES
After speaking with pt he requests your assistance in using the phone at the
nursing station, Which actions will you take? LEAVE ROOM TAKE GLOVES OFF,
WASH HANDS, WERE ALL EQUIPMENT & GO BACK IN

2. Pt presents to ER with temp of 38.5C SOB, & productive cough, what do you wear?
ALL PPE
3. Child comes to your unit with scattered vesicular type rash. What are your
actions? AIRBORNE SIGN CLOSE DORR TO NEGATIVE PRESSURE ROOM OR ROOM
WITH HEPA FILTER, WEAK GLOVES, GOWN, & N95 RESPIRATOR AS WELL AS
CONTACT PRECAUTIONS BASED ON YOUR RISK AX

MRSA methicillin resistant staph aucocullus; common in nose, axilla, & rectum
VRE varomicin resistant entrococcus

Cost of HAI
Hand hygiene prevention cost
o 1 cent per wash
o Pt with MRSA Colonization
8,841 per pt
o PT MRSA Infection
25, 000
Our rating
o Average
Our goal
o Excellent

Root Causes of Transmission & Outbreaks?

Time collection of admission swabs for ARO
High numbers of ARO in hospital
Hands
PPE

104 of 107

Summary of PIDAC Revisions

1. Droplet precautions modified to 2 meter distance
2. All staf are to mask & wear eye protection when conduction an aerosol
generating procedure
3. Contact percaustions
a. Gloves in every room
b. Based on risk ax gown work if in contact

Can pts in isolation come out of their rooms?

3 Cs
o compliant
o cognitive
o clean/contained
not to visit public areas
pt wears clean gown & hand hygience

Going home with AROs

fact sheet are available on intranet
give health teaching on hand hygiene & disinfect home

How many infections are preventable 30-50%

What name give to Routine Practices
When are routine practices required? All the time/for every pt
What is the most important procedure in routine practices? Hand hygiene
What are two acceptable methods of hand hygiene? Alcholo & soap
Which hand hygine method kills germs? Hand sanitizer
Name one type of additional precaution? Contact/Droplet/airbone/vectoborne/vehicle
borne
What types of fluids do routine precautions account for? All body fluids
Name 3 of practices that are used as part of routine practices?
105 of 107

ECG Waves What do they mean?

Electrical activity of the heart
One square in terms of time = 0.04 seconds
Large square = 0.02 seconds

ECG Analysis
Heart Rate
Rhythm
Axis
Hypertrophy
Infarction
Strips = 6 seconds with line in middle indicating 3 seconds
Simple way = 6 seconds = 30 large boxes
Count number of QRS in large boxes * 10 = 50 beats on chart
R wave dont need to memorize
HR = 300 divided by large boxes btw 2 QRS

Heart Rate
Normal Sinus Rhythm
106 of 107
o Rhythm: regular all waves look same
o Rate 60-100
o Configuration: normal
Sinus Tachycardia
o Rhythm : regular
o Rate 100-150
o Configuration: normal
o Normal in exercise, stress response, paediatrics
Sinus Bradycardia
o Rhythm: regular
o Rates 40-60
o Configuration: Normal
o Normal in sleeping, very fit, beta-blockers

Rhythm Atrial Arrhytmias

Atrial Flutter
o Spot in Rt. atrium extra firing
o P wave alterations
o See extra P waves all look the same
o Rhythm: regular or irrgular (depends on AV conduction ratio)
o Rate: atrial: 250-400
Ventricular: varies with number of impulses conducted to venricles
o P wave: sawtooth defections called flutter waves
o QRS: normal
o Atrium is shaking not emptying completely = clots forming in area able to
be transported in other areas
Atrial Fibrillation
o Multiple spots in either Rt. Or Lt. atrium extra firing
o Rhythm: ventricular rate vaies with number of impulses conducted to
ventricles
o P wave: wavy deflections
o QRS normal still nice & narrow
o Causes heart disease in general

Rhythm Ventricular Arrhythmias

- More serious than atrial arrhytmias
-
Premature Ventricular Contraction (PVC)
o Extra spot in a ventricle = extra firing
o Wave cant look the same since the path is altered
o Get big wide QRS some have normal then a bad one
o Deflection down
Ventricular Fibrillation
o Shaky mess on strip
o No real contraction
Ventricular Flutter
o Same type of result

ST Elevation indicates myocardial infraction

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ST Depression indicates ischemia