Heart Failure

○ Inadequate perfusion of body tissues, result in dysfunction of ventricles

(either or both),
○ Several causes
• Chronic develop slowly over time, valvular stenosis - inc
pressure/demands on ventricle
• Shock - anaphylactic, or any kind, blood loss, rapid blood
transfusions, kidneys fail.
• Any pathology that is going to damage pulmonary vascular (lungs),
impairs blood volume, damages heart muscle/pumping mechanism,
rhythm disturbance, IV fluid overload (too much pressure on heart)
• Acute or
○ Abrupt onset, acutely damaged
○ Lost a lot of blood. Can be right and left.
○ SOB, disnea, pink frothy sputum (need to suction, get some lasix [sp?]),
no dependent edema right away.
○ Crackles all the way up past the bases.
• Chronic
○ Pulmonary edema but better managed, wet lung sounds (crackles at
bases), worse during the day when standing for awhile, when lie down has
PND Paroxyzmal Nocturnal Dyspnea.
○ Orthopnea how high have to be elevated during sleep. Can see how much
pulmonary congestion pt has at night.
• Right Sided (see pic below)
○ Impaired blood flow into pulmonary artery.
○ dysfunction of right ventricle related to a pulmonary disease (blood backs
up into right side of the heart).
○ Right ventricle not pumping well --> Blood backs up into right atrium and
out into circular system, get dependent edema - big puffy legs, edema at
sacral level.
○ Liver becomes congested with blood.
○ Impaired liver func. Liver enlarges. Cardiomegaly
○ Weight loss
• Left Sided - Congestive Heart Failure (see pic below)
○ Systolic dysfunction
• Inabil of heart to generate a good CO (cardiac output)
• Inc in end diastolic volume --> Pressure builds up in ventricle -->
builds up into left atrium --> intolungs --> Pulmonary Edema.
○ Diastolic Left sided
• Inabil to relax, contracts normally tho --> pulmonary symptoms -->
somecongestion into pulmonary vasculature --> also congestion in
peripheral system --> edema in peripheral extremities.
• Other signs: dysnea, hypoxia, trouble profusing organs with
oxygenated blood --> e.g. renal failure.
Alterations in the Pulmonary System
Julie Mann, RN, ACNP

Structures of the Pulmonary System

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• Compose of airways, lungs, chest walls.
• Alveoli
○ Type I - Maintain structure
○ Type II - secrete surfactant - decrease surface tension
preventing lungs from collapsing.
Structures of the Pulmonary System
• Skin, ribs, intercostal muslces protect lungs
○ Pleura, double layered tissue creates potential space with
pleural fluid trapped in between, as we inhale and exhale the
lung tissue expands and there shouldn't be any rubbing
(otherwise will hear harsh sandpaper sounds - if hold breath
and don't hear rub then it's lungs, otherwise could be heart).
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Mechanical Barriers
• Upper Respiratory Tract Mucosa
○ Lining of nose, turbulence in back of throat
○ Regulates temp of air, humidifies air, nose is more effective for
humidification.
• Nasal hair and turbinates
○ Mucosa tracks/removes foreign bodies (bacteria, noxious
gasses, etc)
○ Nasal hairs, turbinates, trap/remove foreign particles/gasses.
• Mucus blanket
○ In trachea/bronchus trap foreign bodies
• Cilia
○ Propel mucus blanket back up to be swallowed or
expectorated.
• Alveolar Macrophages
○ Last level of defense, digest any foreign particles that may
have been able to enter through phagocytosis.
• Irritant Receptors
○ Nares
• Stimulated if there is a foreign object/noxious gas to
sneeze to propel out of sys.
○ Trachea and large airways
• Trigger to cough.

Ventilation vs Respiration
• Ventilation: the mechanical movement of air into and out of the
lungs
○ Ability of chest wall to expand/contract, active and passive.
• Respiration: the exchange of oxygen and carbon dioxide during
cellular metabolism

Function of the Respiratory System

1. Ventilate the alveoli
1. Diffuse Gases into and out of the blood
1. Perfuse the lungs so that the organs and tissues receive blood rich
in oxygen and low in carbon dioxide

Control of the Pulmonary System

• Neurochemical Control of Ventilation
• Mechanics of Breathing
• Gas Transport
• Control of the Pulmonary Circulation

Neurochemical Control of Ventilation

• Respiratory Center in brain stem
○ Transmits signals to lung tissue causing contraction and
relaxtion.
• Peripheral and Central chemoreceptors
○ Located at diff parts of body sensitive to Hydrogen (pH) and
monitor PaCO2, PaO2 in arterial blood
○ In CNS and PNS
• Lung receptors
○ Irritant receptors
• epithelium of conducting airways
○ Stretch receptors
• smooth muscle of airways
 • Send messages about size of volume of lung tissue, inc or
decrease ventilary rate dependent on lung volume.
Bronchioles get smaller.
○ J-receptors (juxtapulmonary capillary receptors)
• near capillaries in alveolar septa
• Sensitive to increases in pulmonary capillary pressure in
alveolar level, initiate more rapid shallow breathing in
cases of increased pressure to exchange more O2 and CO2
ventilation.

Mechanics of Breathing
• Major muscles
○ Passive breathing, diaphragm doing the major work.
• Accessory muscles
○ When doing more active forms of breathing, singing, shouting,
difficulty breathing, focused on breathing, more help to
ventilate lung tissue. Sternalcleidal mastoid muscle (sp?) [see
pic below] Scaling muscles, pectoral muscles.
○ No muscles used during expiration. Passive process.
• Elastic properties
○ Of lungs and chest wall, allow lungs to move and ventilate
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Other Determinants
• Alveolar surface tension
○ Ability of alveoli to stay expanded
○ Need surfactant
• Airway Resistance
○ Increased resistance may deter ability to ventilate and
exchange O2 and CO2.
○ Occurs mostly in upper airway (nose, larynx)
• Swelling in nares, obstruction, stuffy nose.
• Work of Breathing
○ Muscular effort it takes for body to ventilate, amount of O2 to
do muscular effort.
○ Normally there's a Low work of Breathing, requires little O2
and energy.
○ WOB increases because of blockages or pulmonary diseases,
requires more O2 and energy to perform work of breathing.

Gas Transport
• Diffusion across alveolar-capillary membrane
○ Oxygen is loaded onto Hemoglobin
○ At tissues oxygen dissociates with hemoglobin and diffuses
across membrane at tissue level.
○ Carbon dioxide more soluble in plasma then O2.
○ CO2 returns to lungs dissolved in plasma as bicarbonate or
bound to hemoglobin

Animations
Video gas transport:
Also in textbook CD.
http://www.youtube.com/watch?v=WXOBJEXxNEo
 http://highered.mcgraw-
hill.com/sites/0072495855/student_view0/chapter25/animation__g
as_exchange_during_respiration.html

Signs of Pulmonary distress

• Dyspnea: difficulty breathing
○ Subjective finding, feeling if have it, need to evaluate even if
can't see.
 ○ Air hunger, breathlessness, SOB, labored breathing,
preoccupied with breathing.
○ Usually caused by some pulmonary disease, between body to
ventilate or respirate AKA Ventilation profusion relationship.
○ Flared nostrils, accessory muscles to breath, sitting in TP
(tripod) position, retracting in intercostal spaces (retraction of
spaces in intercostals)
○ Dyspnea on exertion - only when active. Walk 25 feet or a few
feet?
• Hypoventilation
○ Inabil to alveolar to meet metabolic demands,
underventilating.
• Hyperventilation
○ Exceeding alveolar demands
• Cough
○ Irritant receptors
• Hemoptysis
○ Blood in sputum, coughing up bloody secretions, usually bright
red, usually mixed with sputum --> indicates inflammatory
process in body.

Signs and Symptoms of Pulmonary Disease

• Cyanosis
○ Bluish discoloration in mucus membranes. Increased amount
of desaturated blood.
○ Nail beds, lips, mucosa (mouth, eye)
• Pain
○ Usually from pleura or chest wall.
○ Usually and infection or inflammatory process.
• Clubbing
○ Sign of chronic pulmonary/cardiac condition, bulbous
enlargement of distal part of fingers.
○ Painful, occurs over longer period of time.
○ Observe nail bed! (see pic below)
• Abnormal Sputum
○ First in the day (sputum sample) look for changes in amount
and consistency, also what's in it.
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Abnormal breathing patterns

• Kussmaul Respiration
○ Hyperpnea - rapid inhalation and exhalation. No pause.
○ Sign of acid base disturbance. Get rid of excess CO2.
○ Can't be sustained.

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• Chenye Stokes Respiration

○ Crecendo decendo, increases in depth until it reaches max,
then decreases til period of apnea (no respiration) for 15-60
seconds.
○ Often with neurological condition, malignancy on brain, or end
of life patter of respiration.
○ Can last for awhile.
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Hypercapnia
• Increased CO2 in arterial blood (PaCO2)
○ Usually from hypoventilation, may be initially overlooked.
People's respiratory rate may not change initially.
○ Only way to tell is through ABS (arterial blood gas)
○ See in people with respiratory acidosis
○ Decrease in drive to breath
• Caused by depression of resp. center
• Recreational/illicit drugs
• diseases of the medulla or trauma of CNS.
○ diseases of the neuromuscular junction or resp. muscles, eg
muscular dystrophy, mylestinia gravus (sp?)
○ thoracic cage abnormalities
• Chest injury or congenital condition, or deformity.
○ large airway obstruction
• Tumor or real severe sleep apnea.
○ increased work of breathing
• Emphysema

Hypoxemia
• reduced O2 in arterial blood (PaO2)
○ decreased oxygen content in tissues
• Tissue b/c hypoxic
• Decreased O2 in air itself (mountains)
• Most common cause: high altitude.
○ Hypoventilation
○ diffusion abnormalities
 •Edema --> inc pressure at capillary level, hard for O2
blood to cross over capillary membrane (pulmonary or
peripheral).
○ abnormal ventilation-perfusion ratios
• Atelectasis, collapsed lung tissue (can't ventilate)

Acute Respiratory Failure

• Inadequate gas exchange
○ Hypoxemia, acidotic (pH is low) due to inadequate gas
exchange.
○ Many other conditions/diseases can lead to Acute respiratory
failure.
○ results from
• direct injury to the lungs, airway or chest wall (trauma
occurs)
• indirectly due to injury to another body system (spinal cord
injury, neurological injury)
• PaO2 <50mmHg or PaCO2 >50mmHg with pH <7.25

Conditions Caused by Pulmonary Disease/Injury

• Pulmonary Edema
○ excess water in lung
○ lung kept dry (drained) by lymph sys and surfactant
• Drains extra fluid when there is extra pressure
○ most common cause is heart disease
○ vs pleural effusion - fluid in the pleural potential space
• Aspiration
○ passage of fluid or solid particles into the lungs
• Commonly in right middle lobe (because right bronchus
drops straight into right middle lobe)
• Can lead to pneumonia setting in.
• Atelectasis
○ collapse of lung tissue
○ 2 types: compression or absorption
• Conpression - external pressure on lung tissue (tumor in
chest cavity)
• Absorption - usually from hypoventilation, not breathing
deeply or coughing as should be, lung tissue stays
collapsed. Can be seen on CXR (chest Xray).
○ Expand lung tissue through incentive spirometers (ICS).
 • Cough and deep breath (ppl don't want to do because it
hurts).

Pneumothorax
○ presence of air or gas in the pleural space
• No more negative pressure, lung tissue collapses.
• Need to insert chest tube to create negative pressure, re-
expands lung.
• Pneumothorax
○ Open
• Stabbed in chest, pleura filled with air, air comes in and
out (communicating pneumothorax)
○ Tension
• Fractured rib, gunshot, etc, flap covers, air cannot get back
out. Need to open air space with a giant needle like in the
movies.
○ Spontaneous
• Sudden pleural pain, HR up, some dyspnea, severity
depends on how much tissue is lost.
• Diminished breath sounds over where tissue develops, see
in thin male athletic individuals.
• May have some hyper resonance over open area during
percussion.
○ Traumatic (secondary)
• Open, tension, spontaneous.
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Pulmonary Disorders

Acute Respiratory Failure:

Acute Respiratory Distress Syndrome
• Body undergoes overwhelming inflammatory response, damages
alveolar capillary membrane, end up with pulmonary edema.
• 18% of ICU patients - need mechanical respiration, high
concentration O2, ventilated, intubated.
• A fulminant (process that has an end of life scenario) form of
respiratory failure
• Some of the Causes:
○ Burns
○ Pneumonia
○ CABG
○ Pancreatitis
○ Massive Blood transfusions
○ Drug overdoses
○ inhalation of smoke or noxious gas
○ embolus
○ high concentration of supplemental O2

ARDS - Mechanism of Injury

• Acute injury to the alveolocapillary membrane
○ severe pulmonary edema
○ Shunting of blood and O2 away from Alveolar capillary
membrane leading to...
○ Hypoxemia
○ Lungs become less compliant, full of pulmonary edema, work
of breathing goes up dramatically.
○ End up with fibrosis of lung tissue, less able to expand,
respiratory failure gets worse.
• Wide spread inflammation leads to systemic inflammatory
response
○ can progress to MODS (Multi-Organ Dysfunction Syndrome)

Acute Respiratory Failure

Classic Signs and Symptoms
1. Hyperventilation
2. Respiratory Alkalosis
3. Dysnea and hypoxemia
4. Metabolic Acidosis
5. Respiratory Acidosis
6. Further Hypoxemia
7. (MODS) Hypotension, decreased CO, death
• Diagnosed by physical exam ABG, CXR (diffuse edema throughout
lungs), physical exam.
• Can only do supportive therapy, need to catch early.

Obstructive Pulmonary Diseases

• characterized by: airway obstruction that is worse with expiration
• either more force to exhale or emptying of lungs is slowed, or both
• Unifying symptom: dyspnea
• Unifying sign: wheezing
• COPD (emphysema, chronic bronchitis, asthma [may be considered
COPD])

Obstructive Pulmonary Disease

Asthma
• Inflammation resulting in hyperresponsiveness of the airways
(narrow), occur on a variable reoccurance rate.
○ Some ppl have a trigger that causes it, others will have chronic
aspirations all the time, sometimes just at night (awaken early
with dyspnea, coughing episodes).
• Causes recurrent episodes of:
○ wheezing
○ breathlessness
○ chest tightness
○ coughing
○ symptoms particularly at night or early morning
• Can be asymptomatic during remission, pulmonary function test
may be normal, but during exacerbation of asthma will have SOB,
chest constriction, expiratory wheezing, dyspnea, non-productive
cough.
• Severe, will have wheezing in inspiration, expiration, use accessory
muscles to breath.
• Exposure to irritant or allergen triggers episode. Causes swelling
and spasm (further narrows bronchiole opening).
• Changes happen to underlying endothelial tissue every time there
is an episode --> Over time damages bronchioles, process is not
reversible. <-- treated with drugs.
• Adult onset - can develop a sensitivity to new allergen.

Asthma
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COPD
Emphysema
• Abnormal permanent enlargement of gas-exchange airways and
accompanied by destruction of alveolar walls
○ Airways become distended, alveoli are damaged.
• Obstruction occurs d/t changes in lung tissue
• Loss of elastic recoil
• Leads to hyperinflation (hyperventilation) of alveoli and
development of blebs (pockets of air in tissue, can burst and are
painful, not stable, can break easily)
• Barrel chest appearance (a lot of trapped air in lung tissue)
• Hard for people to exhale air (pink puffers, purse lips to slow down
exhalation)
• Very oxygenated, just can't get extra O2 out. Can have excess CO2
(not always) Don't give high volumes of O2!
• Anything that damages alveolar membrane can lead to
Emphysema.

Emphysema

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Respiratory Tract Infections

Pneumonia
• Acute infection of the lower resp. tract
• Several pathogens can cause it, bacteria and viruses change.
Fungal pneumonias.
• Community Acquired Pneumonia
○ Pick up out in world
• Nosocomial Pneumonia - hospital
• Aspiration pneumonia - food/liquid/pills wrong pipe.
• Pneumococcal pneumonia (common), strep infex, set off immune
response which is accompanied by inflammatory response -->
pulmonary edema. Dyspnea, air hunger, cough.
• Viral pneumonia

Pneumonia
• virulent microorganisms overwhelm natural body defenses
• release of multiple inflammatory mediators and activation of
immune response damages bronchial airways and alveolocapillary
membranes
• fill with infectious debris and exudate
• leads to further lung damage

Pneumonia
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Pulmonary Vascular Disease

Pulmonary Embolism
• Occlusion of a portion of the pulm. Vasculature by an embolus.
Sometimes main artery (more severe)
• Clot breakage to heart, to pulmonary circulation, occlusion, can't
meet metabolic needs, ischemia.
○ Abrupt onset of dyspnea and SOB.
• Risk factors:
 ○ Venous stasis (bed rest, sitting on airplanes for long time)
○ Hypercoagulability (more prone to develop clots)
○ Injuries to endothelial cells that line vessels (develop thrombus
that travels through body)
• Put on blood thinners, supportive O2 therapy.

Disorders of the Upper Airway in kids

Croup
• Acute Laryngotracheobronchitis
• parainfluenza A. (pathogen) causes most cases.
• incidence higher in winter
• More often in male than female children.
• airway obstruction in subglottic region (upper airway, children are
small so it is easier to obstruct airway)
• mucosal edema and secretions (gather in obstructed airway)
complicate
• Kids 6 mo to 5 years
• Stridor (hoarse, rough sounding breath sound) on inspiration
• Seal-like barking cough
• Wake up in the middle of the night with this.
• Generally does not require medical intervention, tell parents to
wrap in blanket and take outside to let cool air to open airway,
otherwise use cool humidified air.