CARDIOPULMONARY SYSTEM

o Receives blood supply during diastolic phase

o Left Main Coronary– divides into:
Relevant Anatomy & Physiology: Heart  Left Anterior Descending – anterior and apical
surfaces of the LV, portions of the interventricular
 Situated in the mediastinum, a mass of tissue that serves a
septum
median partition of the (L) and (R) thoracic cavities
 Diagonal
 Organs within the mediastinum: heart, pericardium, aorta,
 Circumflex – lateral and inferior surfaces of the
trachea, esophagus, thymus gland
LV, portion of the LA
 Weighs ~300 grams, roughly the same size as one’s fist, apex
 Marginal
points inferiorly and ~45° to the left
o Right Coronary – RA, most of the RV, part of the inferior
 Heart is situated in the middle of the chest, apex points
wall of the LV, portions of the interventricular septum,
towards the left
conduction system
o Base - ~between 2nd and 3rd rib
o Posterior Descending – commonly a branch of the RCA
o Apex - ~level of the 5th rib, point of maximal impulse
(right-dominant); posterior heart; left-dominant if it
(PMI)/apical beat, auscultated at (L) 5th intercostal space,
originates from the circumflex artery
9 cm from midsternal line/at the midclavicular line
 Cardiac Muscle
o Tricuspid – (R) sternal border of xiphisternal junction at
o Striated, bifurcated ends, with the nucleus in the middle,
the 5th intercostal space
contains gap junctions inside intercalated discs,
o Right Atrium – 2nd intercostal space and angle of Louis
incapable of recruitment
o Aortic valve – (R) sternal border, 2nd intercostal space
o Cell membranes have sodium, potassium, and calcium
o Pulmonic valve – (L) sternal border, 2nd intercostal space
channels
 Heart Tissue o Plateau phase prolongs action potential = prolonged
o Pericardium – double-walled sac that surrounds the
absolute refractory period (no response will be elicited),
heart incapable of full tetanic contraction
 Fibrous – outermost covering of the heart, o Is not capable of developing significant O2 debt
anchors heart to the surrounding tissues and the
 Cardiac Output
central dome of the diaphragm
o Amount of blood that leaves the ventricles/min (L/min),
 Serous – contains pericardial fluid between its
reflects the heart’s performance as a pump
two layers; 15 mL, cushions the heart, minimizes
o Frank-Starling’s Law – when venous return ↑ = EDV ↑ =
friction during heart pumping
preload ↑ = SV ↑ = CO ↑
 Parietal – connects with the fibrous
o Normal = 5250 mL/min
pericardium
o CO = HR (75 bpm) x SV (70 mL/beat)
 Visceral – continuous with the wall of the
o SV = EDV (120 mL) – ESV (50 mL)
heart
o Epicardium – outermost layer of the heart, continuous o Stroke Volume – vol of blood ejected c each myocardial
with the visceral pericardium contraction
o Myocardium – middle and thickest layer, facilitates  Preload – amt of blood in ventricle at end of
diastole from the venous return, load the
pumping action of the heart
ventricles must overcome before contraction
o Endocardium – innermost layer, continuous with the
(directly proportional)
tissue of the valves and endothelium of the blood vessel
 Contractility – ability of the ventricle to contract
 Blood Supply
(directly proportional)
o Provided by the coronary arteries
 Afterload (80 mmHg) – force the LV must
o Sinus of Valsalva – where coronary arteries arise,
generate during systole to overcome aortic
located at the origin of the aorta immediately above the pressure and open aortic valve/load against
aortic valve
 which the LV contracts during left ventricular  Atherosclerosis – affects ages 40-50 in men, ~10 yrs later in
ejection (inversely proportional) women, plaques develop in coronary arteries that result in ↓
Cardiac Conditions blood flow and 02 distribution, body’s chronic compensation is
 In the early part of the 20th century, MI tx included 2 mos of development of collateral circulation
bedrest  Ischemia – inadequate blood supply of O2 to muscles,
 By 40’s-50’s, ambulation began 14 days p an acute episode, completely reversible if transient, but may lead to infarction if
currently the inpatient phase of cardiac rehabilitation prolonged
 Primary Prevention – adoption of lifestyle changes to prevent Angina Pectoris
onset of dse  Reversible ischemic process, temporary inability to supply
 Secondary Prevention – use of techniques to restore, maintain, sufficient O2 to heart muscle
and improve pt’s status p dx of dse  Characterized by sudden onset of relatively diffused ant chest
 It is the leading cause of death, atherosclerosis is m/c cause of pain, usually squeezing or pressure sensation
CHD; atherosclerosis, altered myocardial mm mechanics, o Stable/Chronic Exertion - Precipitated by exercise/stress,
valvular dysfunction, arrhythmias, HTN substernal chest pain for 5-10 mins; cessation of
activity; rest, lingual nitrates
o Unstable/Crescendo/Pre-infarction – also effort-related,
Stages of HTN but pain occur c ↑ frequency, intensity, duration, may
Stage Systolic Diastoli indicate CAD and ↑ risk of MI; less responsive to
c nitrates, require hospitalization and IV nitrates
Prehyperten 120-130 80-89 o Variant/Prinzmetal/Rest – caused by coronary artery
sion
spasm, pain while at rest frequently early morning/upon
Stage 1 130-140 90-100
rising, usually more intense and of longer duration than
Stage 2 140-160 100-110
stable, frequently leads to MI, more common in women
Stage 3 > 160 > 110
than men; unaffected by exertion, may be relieved by
2017 Guideline by AHA/ACC rest and nitrates
Stages of Systoli Diastoli
o Asymptomatic/Silent - ~70% may be silent, usually
Hypertension c c
Elevated 120- < 80 observed via 24-hr Holter monitor, ischemia at cellular
129 levels documented via ECG
Stage 1 130- 80-89  Dx and Tx:
139 o History
Stage 2 ≥ 140 ≥ 90
o ECG: ST segment elevation c variant, ST segment
depression c unstable
Coronary Artery Disease o Exercise Tolerance Test
 Atherosclerotic process, thickening of tunica intima caused by o 24-hr Holter Monitor
accumulation of lipids, insidious onset and process o Beta blockers, nitrates, calcium channel blockers, lipid-
 Left Anterior Descending Artery is m/c affected lowering drugs
 Manifests as one or more of: Myocardial Infarction
o Sudden cardiac death  Necrosis of some portion of cardiac muscle in response to
o Congestive Heart Failure sustained ischemia
o Angina pectoris  Vise-like retrosternal tightening that becomes progressively
o Myocardial infarction intense and unbearable, radiates to jaw, neck, upper back, (L)
 Risk factors shoulder, and arm
o Modifiable: smoking, blood lipid levels, obesity, inactivity  Accompanied by dyspnea, nausea, vomiting, diaphoresis,
o Non-modifiable: age, sex, family hx generalized weakness, unrelieved by nitrates or rest
  Dx
oHx and symptoms
oSerum enzymes
 CK-MB – begins to rise in 2-4 hrs and return to
normal in 48-72 hrs
 LDH – LDH1 > LDH2 within 24 hrs, normal in 7-10
days
 SGOT - ↑ within 24 hrs, normal in 3-4 days
 Troponin – rise in 4-8 hrs, normal in 7 days
o ECG changes
 T wave inversion – ischemia
 ST segment elevation – injury
 Pathologic Q waves – infarction
o Cardiac Catheterization – for dx and interventional
purposes, allows visualization of arterial system and
assessment of myocardium
 Direct intracoronary antithrombotic therapy
(streptokinase, urokinase, tPA) and percutaneous
transluminal coronary angioplasty (PTCA)
 Goal: rapid reperfusion of ischemic/infarcted area
 Complications
o Arrhythmias – abnormalities in impulse generation and
conduction
o Heart Failure – abnormality in effective mechanical
performance of heart muscle; inability of heart to
maintain a CO sufficient to meet O2 demands of tissues
o Thrombus formation – stasis  embolism
o Heart structural damage
 Management
o Cardiac rehabilitation program
o Vocational counselling
o Education on risk factors
o Lifestyle modifications
Sudden Cardiac Death
 Sudden cardiac arrest, from cardiac dysfunction, s prior
symptoms or < 6 hrs duration
 Leading cause is ventricular tachycardia/fibrillation
 No effective CO, prompt initiation of CPR
Congestive Heart Failure – recurring phenomenon by repeated
exacerbation ↑ in frequency and severity
 Inability to maintain CO that is adequate to meet demands d/t
abnormality of function in heart muscle
 Results in ↓ blood flow to tissues and congestion in pulmonary
and systemic circulation
 M/c etiology is ischemic heart disease 2° to CAD, associated c
HTN, valvular disease, CHD
 Changes in myocardial contractility d/t ↓ coronary blood flow,
causing hypoxia
 Ventricular remodeling – compensatory hypertrophy and
dilation of myocardium
 Compensatory mechanisms
o ↑ sympathetic nervous system stimulation - ↑ HR and
contractility
o ↑ Na and H2O retention by kidneys
o Hypertrophy of cardiac muscle fibers – to accommodate
↑ volume
 Types of Heart Failure
o Acute – acute exacerbation of chronic heart failure, rapid
failure happens before compensatory mechanisms can
be effective, symptomatic fall in CO, rapid onset of
symptoms, dyspnea at rest, orthopnea, pulmonary
congestion, edema
o Chronic – gradually, associated c compensatory
mechanisms, pulmonary congestion/peripheral edema
usual reason to seek attention, leading cause of
admission of pts > 65 y/o
o Compensated – maintain adequate CO by compensatory
mechanisms, at rest appears normal, symptoms appear
when demand ↑
o Uncompensated – when a severely damaged heart
cannot regain normal CO though compensatory
mechanisms are at work, fluid retention, gradual heart
stretching, diuretics and cardiac glycosides (digitalis)
o Left-sided – more common than right-sided and
frequently leads to right-sided, most frequently seen p
MI, retrograde flow d/t ↑ volume builds, into interstitial
spaces and into alveoli, producing edema, dyspneic,
lungs become stiff and less compliant and dyspnea
worsens
o Right-sided – m/c cause is left ventricular failure and
COPD, ↑ central venous pressure and neck vein
distention, liver engorgement, ascites, peripheral
edema, fatigue, ↓ tolerance of activity, tx towards ↓
circulatory overload, myocardial workload, and O2
demand, ↑ myocardial contractility = diuretics, Na
restrictions, cardiac glycosides, O2 therapy
Pericarditis
 Inflammation of the pericardium, usually caused by bacteria
 Tendency to rub during pumping of the heart
 Constant chest pain, friction rubbing upon auscultation
 Can result to abnormal ↑ in production of pericardial fluid
called pericardial effusion
 Heavily notched/pointed T waves in adults may indicate
condition
Cardiac Tamponade
 Pressure is directed towards the heart d/t fluid buildup,
contraction of the heart is limited
 Complication of pericardial effusion, stab wounds, bleeding into
the pericardial space
Cardiomyopathies
 Alterations in the muscular wall of the heart
o Dilated – ventricular dilation and altered cardiac muscle
contractile function; CAD is the primary cause,
myocarditis, alcohol abuse
o Hypertrophic – diastolic dysfunction with ↑ ventricular
mass; chronic HTN and aortic stenosis
o Restrictive – diastolic dysfunction d/t presence of
excessively rigid ventricular walls, resulting in ↓ in
compliance; diabetes
Relevant Anatomy & Physiology: Respiratory System
Bony Structures
 Thorax – protects vital organs of the cardiopulmonary system
and upper abdominal viscera, provides skeletal attachment for
muscles
 Sternum
 Ribs
 Thoracic vertebrae
Musculature
 Inspiration: principal muscle is the diaphragm, Internal and
external intercostals, scalenes, SCM
 Expiration: mainly passive, relaxation of inspiratory muscles
Lungs
 Each lung has an apex, base, costal surface, and mediastinal
surface.
 Base is concave and rests on diaphragm
o Dome of (R) hemidiaphragm is slightly higher than the
(L) because of liver
 Costal surface is large and convex, conforms to inner contour of
ribcage
 Mediastinal surface is concave, which accommodates the heart
o Cardiac impression is larger and deeper on (L) lung than
(R)
o (L) lung is narrower and longer, (R) is larger, shorter,
wider
 Pleural cavity – space between 2 layers of pleura, contains
serous fluid that reduces friction during ventilation
o Parietal pleura – outer
o Visceral pleura – inner
 Fissures
o (R) – horizontal/transverse and oblique fissures; 3 lobes,
10 segments
o (L) – oblique fissure; 2 lobes, 8 segments
 Conducting Airways
o Upper – nose, mouth, pharynx, larynx
 Nose – filter, humidify, and warm air before
delivery to pharynx
 Pharynx – divided into nasopharynx (continues to
filter and humidify inspired air), oropharynx, and
laryngopharynx (conducts air from oral cavity
into trachea)
 Epiglottis – leaf-shaped cartilage that covers and
protects glottis during swallowing
o Lower
 Begins with the trachea, considered the first-
generation ventilatory passageway, originates
from lower border of cricoid cartilage (C6) and
terminates at level of sternal angle of Louis (T4);
mucous membrane contains both goblet and
ciliated epithelial cells
 Branches into (L) and (R) main stem bronchi
which are the second generation of ventilatory
passageway
 Bronchi further branch into lobar (third
generation), segmental (fourth generation),
subsegmental (fifth generation) bronchi and
continues for 23 generations until they terminate
in the bronchioles
 Most distal conducting airways are respiratory
bronchioles
 Parts of the distal respiratory unit: respiratory
bronchiole, alveolar ducts, alveolar sacs, alveoli
Lung Volumes and Capacities
  Tidal Volume – amount of air inspired and expired during
normal resting ventilation, ~500 mL
 Inspiratory Reserve Volume – additional air that can be further
inhaled p a tidal breath, ~3000 mL
 Expiratory Reserve Volume – quantity of air that can be
potentially exhaled beyond end of tidal exhalation, ~1000 mL
 Residual Volume – volume of air that remains in the lungs p
maximal exhalation of ERV, ~1500 mL
 Inspiratory Capacity – TV + IRV, 3500 mL; amount of air that
can be expired beginning from a tidal exhalation
 Functional Residual Capacity – combined ERV and RV, 2500 mL;
volume of air that remains in the lungs at the end of a tidal
exhalation
 Vital Capacity – three volumes under volitional control (TV +
IRV + ERV)
 Total Lung Capacity – TV + IRV + ERV + RV
 Forced Expiratory Volume in 1 second (FEV1) – ≥ 70% of total
FVC; volume of air that can be forcefully exhaled during the
first second of a forced vital capacity maneuver
Pulmonary Conditions
 Pts c COPD benefit from treadmill walking programs (Pierce et
al., 1964), exercise training and education are major
components of rehab
 Obstructive Lung Diseases ♦
o ↑ in resistance to airflow d/t partial/complete
obstruction at any level, from trachea and larger bronchi
to terminal and respiratory bronchioles
o ↓ maximal airflow rates during forced expiration, usually
measured by FEV1
o Only ~10% of pts c COPD are non-smokers, but only a
minority of smokers develop COPD
o Occur in 2 general conditions:
 Chest Wall Disorders - neuromuscular diseases
such as poliomyelitis, severe obesity,
kyphoscoliosis
 Chronic Interstitial and Infiltrative Diseases –
pneumoconioses and interstitial fibrosis of
unknown etiology
 Restrictive Lung Diseases ♪
o ↓ expansion of lung parenchyma and ↓ total lung
capacity
o ↓ total lung capacity, expiratory flow rate is (n) or ↓
proportionately
♦ Emphysema (Pink Puffers)
o Irreversible enlargement of airspaces distal to terminal
bronchiole, destruction of their walls s obvious fibrosis
d/t ↓ alpha antitrypsin
o Clearly associated c smoking, women and African-
Americans more susceptible
o Classified according to anatomic distribution
 Centriacinar (Centrilobular) – central/proximal
parts of acini (respiratory bronchioles), distal
alveoli spared; lesions more common and severe
in upper lobes
 Panacinar (Panlobular) – uniformly enlarged
respiratory bronchioles to terminal alveoli; occur
more commonly in lower zones
 Distal Acinar (Paraseptal) – proximal part is
normal, predominantly involves distal parts;
more commonly occurs in upper half of lungs
 Airspace Enlargement c Fibrosis
(Paracitricial/Irregular) – acinus is irregularly
involved, associated c scarring; asymptomatic
and clinically insignificant
o Manifestations do not appear until at least 1/3 of
functioning parenchyma is damaged
o First symptom: dyspnea, insidious but steadily
progressive
o In some, coughing/wheezing is c/c, cough and
expectoration extremely variable
o Barrel-chested and dyspneic, prolonged expiration, sits
forward hunched over, pursed-lip breathing
o Dx: Expiratory airflow limitation measured through
spirometry
o May over-ventilate and remain well-oxygenated
♦ Chronic Bronchitis (Blue Bloaters)
 Persistent cough c sputum production for at least 3 mos in 2
consecutive yrs, common among habitual smokers and
inhabitants of smog-laden activities
 Many pts affected also have emphysema, can lead to cor
pulmonale
 Earliest feature: hypersecretion of mucus in large airways
associated c hypertrophy of submucosal glands in trachea and
bronchi
 ↑ in goblet cells of small airways  excessive mucus
production
 Cardinal symptoms: persistent, productive cough
  Dyspnea on exertion eventually develops, hypercapnia,  Usually affects lower lobes and most severe in more distal
hypoxemia, mild cyanosis bronchi and bronchioles
Emphysema Bronchitis  Severe, persistent cough; expectoration of foul-smelling,
Age 50-75 40-45 sometimes bloody sputum, dyspnea and orthopnea in severe
Dyspnea Severe, early Mild, late cases
Cough Late, scanty Early, copious  Symptoms often episodic precipitated by URTI or introduction
Infections Occasional Common of new pathogenic agents
Respiratory Terminal Repeated  Paroxysms of cough when pt rises in the morning
Insufficiency Clinical Term Site Pathologic Etiology Signs/Sympt
Cor Pulmonale Rare, terminal Common Changes oms
Airway (n), slightly ↑ ↑ Emphysema Acini Airspace Tobacco Dyspnea
Resistance enlargement, smoke
Elastic Recoil Low (n), high wall destruction
Chest Hyperinflation, Prominent vessels, Chronic Bronchi Mucous gland Tobacco Cough,
Radiograph small heart large heart Bronchitis hyperplasia, smoke sputum
hypersecretion production
Appearance Pink Puffer Blue Bloater
Asthma Bronchi Smooth muscle Immunologic Episodic
♦ Asthma hyperplasia, al/Undefined wheezing,
 Causes recurrent episodes of wheezing, breathlessness, chest excess mucus, cough,
tightness, cough inflammation dyspnea
Bronchiectas Bronchi Airway dilation, Persistent or Cough,
 Widespread, variable bronchoconstriction, partially reversible
is scarring severe purulent
airflow limitation infections sputum, fever
 More discouraging and disabling than lethal ♦ Cystic Fibrosis (Mucoviscidosis)
 Hallmarks: ↑ airway response to a variety of stimuli,  Exocrine gland dysfunction that results in abnormally viscid
inflammation of bronchial walls, ↑ mucus secretions secretions
o Atopic – evidence of allergen sensitization; m/c type,  Hereditary disease transmitted as an autosomal-recessive trait
classic example of IgE-mediated hypersensitivity (mutation of CF gene [cystic fibrosis transmembrane
reaction, usually beings in childhood triggered by conductance regulator] in the long arm of chromosome 7)
environmental allergens, skin test c offending antigen  Abnormally viscous mucus secreted by tracheobronchial tree
results in immediate wheal-and-flare and hyperplasia of mucus-secreting glands  airway
o Non-atopic – no evidence of allergen sensitization, skin obstruction, recurrent infection, bronchiectasis, hyperinflation
test is usually (-), commonly triggered by respiratory  Dx: Sweat test, ↑ levels of NaCl (> 60mEq/L), genotyping for
infections d/t viruses CFTR mutations for pts c borderline sweat chloride results
 Chest tightness, dyspnea, wheezing, cough c/s sputum  ↓ FEV1, ↑ RV, hypoxemia, hypercapnia
production, ↑ airflow obstruction, difficulty c exhalation,
 Pancreatic insufficiency, GI dysfunction  meconium ileus at
elevated eosinophils
birth, malabsorption, reproductive problems
 Status asthmaticus - most severe form, severe acute paroxysm
♪ Idiopathic Pulmonary Fibrosis
persists for days/weeks, extreme airway obstruction may cause
 Cause unknown, begins insidiously c gradually increasing
severe cyanosis/death
dyspnea on exertion and dry cough
♦ Bronchiectasis
 Most pts 40-70 yrs old at presentation, mean survival of ≤3 yrs
 Permanent dilation of bronchi and bronchioles caused by
 Late: hypoxemia, cyanosis, clubbing
destruction of muscle and elastic tissue resulting from or
 Progression is unpredictable c gradual deterioration despite
associated c chronic necrotizing infections
medical tx
 Develops in association c a variety of conditions (postinfectious
conditions caused by M. Tuberculosis, S. Aureus, H. Influenzae,
♪ Pneumoconioses
congenital conditions such as CF)
  Originally non-neoplastic lung reaction to inhalation of mineral  Water enters spaces of alveoli
dusts, now includes those induced by organic particulates,  Unequal pressures at blood vessels pushes water out of
chemical fumes, vapors capillaries
 Air pollution in urban areas, cigarette smoking predisposes to  Associated c left-sided heart failure, MI, mitral valve stenosis
accumulation of dust  Dyspnea, non-productive cough
o Coal Workers’ Pneumoconiosis (CWP) Pulmonary Embolism
 Benign disease, little decrement in lung function  Lodging of particles in venous circulation, more on base of the
 Some evidence suggests exposure to coal dust ↑ lungs, fatal condition
incidence of chronic bronchitis and emphysema,  M/c cause: DVT, can be caused by venous stasis, clotting
independent of smoking disorders, oral contraceptives, air
o Silicosis  Sudden acute pain, dyspnea
 Slowly progressing, nodular, fibrosing Pleuritis/Pleural Effusion
pneumoconiosis  ↑ amounts of pleural fluid, associated c CHF
 Inhalation of crystalline silicone dioxide (silica)  Causes: CHF, cardiac failure, renal failure, liver cirrhosis
 Most prevalent chronic occupational disease in  Cardinal sign: Dull/sharp pain
the world
 Deep breathing and coughing, doorstop breathing, pleural
 Chest radiograph: fine nodularity in upper zones
friction rubbing
of the lung but pulmonary functions are either (n)
Pneumothorax
or moderately affected
 Air leaking into pleural space
 Late dyspnea, ↑ susceptibility to TB
 Forms: Traumatic, iatrogenic, spontaneous
o Asbestosis
 Sudden sharp pain, deVere dyspnea, mediastinal shifting, ↓or
 Chronic deposition of inhaled fibers from
absent breath sounds
asbestos (crystalline hydrated silicates) 
Atelectasis
inflammation and fibrosis
 Dyspnea usually first manifestation, provoked by  Loss of lung volume expansion
exertion/even at rest, accompanied by  Forms:
productive cough o Primary – d/t incomplete inspiration d/t weakness
 Appear 10 yrs p exposure, more common p 20 o Secondary – d/t obstruction
yrs or more  Cough and sputum production, fever
♪ Pneumonia Severe Acute Respiratory Syndrome
 Intra-alveolar infection of lung parenchyma  Caused by coronavirus, transmission through direct contact c in
 M/c cause: Streptococcal the past 10 days
 Can be bacterial, viral, aspiration  High-grade fever, hyperthermia, dry cough, myalgia, lethargy,
 Chills, fever, chest pain, cough sore throat
♪ Tuberculosis
♪ Bronchogenic Carcinoma
 Caused by Mycobacterium Tuberculosis
 Tumor arising from bronchial mucosa
 Hallmark: Hemoptysis
 Types:
 Incubation period of 2-10 wks, maximally infectious during first
o Small Cell
2 wks (isolation in (-) pressure room)
o Oat Cell
 Long-term medication (6-12 mos)
o Squamous Cell – m/c
 Fever, weight loss, cough, lymph nodes enlargement,
hemoptysis  Unexplained weight loss, hemoptysis, dyspnea, weakness and
fatigue, hoarseness
Pulmonary Edema Evaluation
 Initial contact often happens indirectly, chart review is first o Cheyne-Stokes Respiration – periodic breathing: gradual
point of contact hyperpnea, hypopnea, and apnea; dying, coma,
o Read hx and physical and admission note associated c poor prognosis; usually CNS involvement
o Read last medical note o Kussmaul’s Respiration – hyperventilation (↑ rate and
o Scan remainder of chart depth), underlying cause is metabolic acidosis
o Read reports from medical specialists/consultants o Biot’s Respiration – “irregular irregular” breathing:
o Review pertinent lab tests hyperpnea (or normopnea) and apnea; poor prognosis,
o Review medications neuron damage, TBI
o Review psychosocial information o Ataxic Breathing – sudden change in depth
 Anatomical landmarks: American Thoracic Society Dyspnea Scale
o Anterior – midsternal and midclavicular lines Grad Degree Description
o Lateral – Anterior, mid-, and posterior axillary lines e
0 None Not troubled c breathlessness except c
o Posterior – Vertebral and mid-scapular lines
strenuous exercise
 Visual Inspection 1 Slight Troubled c SOB when hurrying on level/walking
o Nasal flaring – outward movement of the nares c up a slight hill
inspiration 2 Moderate Walks slower than people of same age on level
o Cyanosis d/t breathlessness/has to stop for breath when
 Central – insufficient gas exchange c/in the lungs, walking at own place on level
O2 saturation < 80%; face, lips, tongue 3 Severe Stops for breath p walking about 100 yards/p a
 Peripheral – O2 extraction at the periphery is few minutes on level
excessive, associated c low cardiac output 4 Very Too breathless to leave
states; usually occurs in cooler body parts Severe house/dressing/undressing
o Nail clubbing – loss of angle between nail bed and DIP Borg’s Scale - subjective
(Schamroth’s sign) Grade Description
 Chest Wall Configuration 0 Nothing at all
o AP to lateral diameter is 1:2 or 5:7, angle of ribs > 90° 0.5 Very, very slight
o Barrel chest - ↑ AP diameter as ribs become more (just noticeable)
1 Very slight
horizontal; most commonly observed in pt c COPD
2 Slight
o Pectus excavatum – funnel chest; depressed lower
3 Moderate
sternum, can result into restrictive lung disease
o Pectus carinatum – pigeon chest; prominent upper 4 Somewhat severe
sternum 5 Severe
o Flail chest – chest wall moves inward c inspiration 7 Very severe
9 Very, very severe (almost
 Breathing Pattern – normally between 12-20 bpm; normal ratio
maximal)
of inspiratory to expiratory time is 1:2
10 Maximal
o Eupnea – normal breathing cycle
 Auscultation – art of listening to the sounds produced by the
o Apnea – temporary halt in breathing
body
o Tachypnea – rapid, shallow breathing pattern, > 20 bpm
o Breath sounds
o Bradypnea – slowed breathing, < 12 bpm
 Normal
o Orthopnea – difficulty breathing when lying flat;
 Bronchial (tracheal) – high-pitched,
pulmonary edema, CHF
hollowed; heard in both inspiration and
o Dyspnea – shortness of breath
expiration, louder on expiration with
pause between phases; over manubrium
  Bronchovesicular – high-pitched c equal
inspiratory and expiratory cycles but s
pause; superior to clavicles,
suprascapular, parasternal, interscapular;
over main stem bronchi: 1st and 2nd ICS
anteriorly and between scapulae
posteriorly
 Vesicular – soft, low-pitched; over
remaining peripheral lung fields; mainly
inspiration c initial 1/3 of expiration
audible s pause between phases
 Abnormal
 Bronchial (tubular) – consolidation
pneumonia, compression of lung tissue;
when peripheral lung tissue becomes
airless; louder expiration
 Decreased – hyperinflation d/t
emphysema, depth of
respiration/thickness of chest wall
 Absent – loss of lung compliance d/t
fibrosis (can lead to decrease or absence)
 Adventitious – extraneous noises over
bronchopulmonary tree
 Crackles – discontinuous, low-pitched
primarily during inspiration; peripheral
airway process
 Rhonchi – low-pitched but continuous
sounds in both inspiration and expiration;
snoring quality; obstructive process in the
larger, more central airways
 Wheezes – continuous, high-pitched;
hissing or whistling primarily during
expiration; bronchospasms. Movement of
air through secretions
 Voice sounds – low-pitched, muffled or mumbled
 Bronchophony - ↑ vocal transmission,
louder and clearer; ↑ lung density e.g.
consolidation
 Egophony - ↑ transmission of vocal
vibrations, “eee” is distorted as “aaa”,
coexists c bronchophony
 Whispered – low-pitched vibrations
muffled by normal lung parenchyma
 Whispered pectoriloquy – whispered
sounds become distinct and clear, can be
present when bronchophony and
egophony are absent; identifying smaller
or patchy areas of lung consolidation
o Extrapulmonary sounds
 Friction rub – rubbing or leathery sounds during
both inspiration and expiration; rubbing of
parietal and visceral pleura such as inflammation
or neoplasm, usually associated c pain
o Heart sounds
 Pt position: supine and sitting – all areas, side-
lying – apex using bell
 S1 – “Lubb,” closing of AV valves, duration: 1.10
s, loudest at apex, systolic phase:
 Isometric/isovolumic contraction –
ventricles contract s movement, all 4
valves are closed
 Ejection – specific phase when S1 is
heard; closed AV valves, open semilunar
valves
 S2 – “Dupp,” closing of semilunar valves and end
of ventricular systole
 Isometric/isovolumic relaxation – specific
phase when S2 is heard; all 4 valves are
closed
 Ventricular filling – open AV valves, closed
semilunar valves
 S3 – faint, low-frequency sound, reflects early
ventricular filling p AV valves open; abnormal in
pt > 40 y/o; ideal position is (L) side-lying;
ventricular failure, tachycardia, mitral
regurgitation
 S4 – dull-sounding, rapid ventricular filling p atrial
contraction; may be heard c left ventricular
hypertrophy; systemic HPN, cardiomyopathies,
coarctation of the aorta
 Murmurs – vibrations from turbulent blood flow,
swishing sound
 Systolic – AV valve insufficiency,
semilunar valve stenosis
 Diastolic – AV valve stenosis, semilunar
valve insufficiency
 Continuous – starts in S1 and lasts
through portion or all of S2
 Gra  SA Node – upper part of the RA; heart’s primary
de pacemaker, makes the atria contract; highest
I Faint Requires concentrated effort to rate of rhythmicity, greatest frequency of
hear firing/min = 60-100 impulses/min
II Faint Audible immediately  AV Node – lower part of the RA; fires 40-60
III Louder than II Intermediate intensity impulses/min
IV Loud Intermediate intensity;
 Bundle of His – transmits impulses from AV node
associated c palpable vibration
to the ventricles
(thrill)
V Very loud Thrill present  (L) & (R) Bundle Fibers
VI Audible s  Purkinje Fibers – located in the inner ventricular
stethoscope walls in a space called the subendocardium,
* Grade III+ usually associated c cardiac pathology makes the ventricles contract; fires 20-40
 Mediate Percussion – assess density of underlying organs impulses/min
o Resonant – loud/high amplitude, low-pitched, longer o Normal ECG
duration, heard over air-filled organs e.g. lungs  P wave – sinus node and atrial depolarization
o Dull – low amplitude, med to high-pitched, short  PR/PQ segment – AV node conduction
duration, heard over solid organs e.g. liver  QRS complex – atrial repolarization/ventricular
o Flat – high-pitched, short duration, heard over muscle depolarization
mass e.g. thigh  ST segment – initiation of ventricular
o Tympanic – high-pitched, medium duration, heard over repolarization
hollow structures e.g. stomach  T wave – completion of ventricular repolarization
o Hyper-resonant – very low-pitched, prolonged duration,  U wave – ventricular relaxation
heard over tissue c ↓ density (↑ air: tissue ratio);
abnormal in adults; lungs c emphysema
o Diaphragmatic Excursion – 3-5 cm, difference between
lowest level of diaphragm on max inspiration and lowest
area of resonance p expiration; ↓ in pt c COPD
 Chest Wall Excursion (Chest Expansion Symmetry) – 3.25 in
(8.5 cm) in young adults between 20-30 y/o
Count-off Method – only applicable when rhythm is normal
o Upper Lobe – suprasternal notch
1 small square – 0.04 secs (40 ms)
o Middle Lobe – xiphoid process
1 large square – 0.2 secs (200 ms)
o Lower lobe – back
5 large squares – 1 sec
 Tactile fremitus – transmitted vibrations from spoken R-R interval - Heart Rate Relationship
words/vocalization (↑ = less air, ↓ = more air) R-R Interval Heart Rate
 Tracheal Deviation – index finger in medial aspect of (bpm)
suprasternal notch 1 300
 Contralateral – pneumothorax, pleural effusion, 2 150
tumor 3 100
 Ipsilateral – atelectasis
4 75
 ECG Interpretation – Dr. Willem Einthoven
5 60
o Main function is to monitor electrical activity of the heart
o P wave
o Pacemaker/Nodal cells – can generate their own action
 Conduction of electrical impulse through atria
potential, found in the heart’s intrinsic conduction
 Precedes QRS complex
system:
 2-3 mm high
  0.06-0.12 secs  Depression – 0.5 mm below baseline; may
 Usually rounded and upright indicate myocardial ischemia &
o QRS Complex unstable angina
 Follows PR interval o Leads
 5-30 mm high, differs for each lead used  Precordial leads – unipolar; back-front and right-
 0.06-0.10 secs/half of PR interval left
 Beginning of Q wave to end of S wave/beginning  V1 – RSB, 4th ICS
of R wave if Q wave is absent  V2 – LSB, 4th ICS
 Q wave – first negative deflection p the P wave  V3 – between V2 and V4
 R wave – first positive deflection p P or Q wave  V4 – 5th ICS, (L) MCL
 S wave – first negative deflection p R wave  V5 – between V4 and V6
 Variety – qRs, rS, QS, Rs, rsR, qR, Qr
 V6 – 5th ICS, (L) MAL
o T wave
 Limb leads – bipolar; up-down and right-left
 Ventricular recovery/repolarization, peak
 aVF – (L) foot
represents relative refractory period of
 aVL – (L) arm
ventricular repol
 aVR – (R) arm
 Follows S wave
 Leads II, III, and aVF signify activity of the inferior
 0.5 mm in leads I, II, III, up to 10 mm in
wall of the heart
precordial leads
o Abnormalities
 Usually round and smooth
 Usually upright in leads I, II, and V3-V6, inverted  Dysrhythmia – abnormal rhythm
in lead aVR, variable in others  Arrhythmia – absence of a rhythm
o PQ/PR Interval – 0.12 – 0.20 secs  T wave inversion – abnormality in the ventricles
(myocardium); may indicate myocardial
 Length of SA – AV conduction
infarction
 Prolongation causes ↓ HR
 Bundle Branch Block (either left or right) - QRS
 M/c cause of prolongation is AV node block
complex looks like a bishop’s miter/double
 Represents electrical events that take place in
peak/bigeminal and prolonged (>0.12 ms)
the atria
 AV Node Block – m/c cause of PR interval
o QT Interval – electrical depolarization and repolarization
prolongation
of the ventricles; conduction from AV node to Purkinje
 1st Degree – mildest form, delayed but all
fibers
impulses still reach Purkinje fibers
 Represents electrical events that take place in
the ventricles  2nd Degree – partially damaged AV node,
o ST Segment – found within the QT interval, flatline some impulses do not reach Purkinje;
causes dropped wave, wherein QRS
between S and T waves; latency period between
occurs p 2 P waves
ventricular depolarization and repolarization
 Prolongation means that ventricular  3rd Degree – complete heart block; QRS
repolarization is delayed occurs p 3 P waves
 ST displacement – not all are significant, only  Atrial Fibrillation
those measuring ≥ 2 mm (1 small box = 1 mm)  No distinguishable P wave, only QRS
 Elevation – above baseline, immediately complex
after R wave; may indicate myocardial  Caused by firing of individual myocardial
infarction & variant angina cells
 Leads to stasis, which can lead to
thrombus formation
  Flutter – more severe form of fibrillation
o IN SUMMARY:
1. Determine the rhythm. P-P and R-R intervals
2. Determine the rate. Count-off method.
3. Evaluate the P wave.
4. Determine the duration of the PR interval.
5. Determine the duration of the QRS complex.
6. Evaluate the T waves.
7. Determine the duration of the QT interval.
8. Evaluate any other components.
 Arterial Blood Gas Analysis
o PaO2 – >75 mmHg, partial pressure of O2 in arterial blood
o M/c site of extraction is the radial artery
o pH – 7.35-7.45, “per hydrogen”
 Signifies acidity/alkalinity of blood, expressed in
negative logarithm of H+
 ↑ means less hydrogen, alkalosis
 ↓ means more hydrogen, acidic
o PaCO2 – 35-45 mmHg, partial pressure of CO2 in arterial
blood
 Neutralizes effects of excessive alkalinity
o Bicarbonate (HCO3) – 22-26 mmol/L = mmol L-1 = mEq/L
 buffer, neutralizes effects of excess acid
o Buffering Systems
 Respiratory – regulates PaCO2
 Metabolic – regulates HCO3
o How is the pt?
o Assess oxygenation
o Determine pH
o Determine respiratory component
o Determine metabolic component