CardioPulm Test 2
Stress Testing
Assessment- pt information, med hx (det risk factor & level of supervision needed,
mode of test), insurance, med release
GXT- EKG, BP, VO2, RPE/angina/dyspnea scale, symptoms, protocol, ex capacity
Stress Testing – can be diagnostic (no meds), functional (with meds) or therapeutic
(w/wo meds). If functional, stop at 4-6 METS or 75% of APMHR
Types: Continuous- max or submax, bruce or balke protocol
Functional-3,6,12 min walk tests, march in place
Discontinuous-ADLs, max or submax
NYHA classifications:
I: cardiac disease, no limitations
II: cardicac disease, slight limitations
III: cardiac disease marked limitation
IV: cardiac disease, inability to perform physical activity w/o discomfort
PT Considerations for:
CHF- functional ADL tests, walk tests, cycle or TM test (<5 METS, Naughton
protocol). Meds: digoxin, diuretics, vasodilators, ACE inhibitors, antiarrhythmics.
MI – APMHR not accurate for this population, use of NTG for angina, record meds,
dosage, reaction to ex for 10 min post activity. Do low level ex testing (<5 METS)
with consideration for: low fct capacity, PAD, abnormal signs & symptoms,
supervision for moderate & high risk patients. Recommend 3 non-consecutive
days/week of exercise.
6 objectives of the testing: chronotropic capacity & HR recovery, aerobic capacity,
RPP, exertional symptoms, electrical function, & risk status.
Adverse prognosis indicators: ST segment depr at low level of ex, functional capacity
<5 METS, low peak RPP, drop in BP with exercise.
*Refer to ACSM book for Angina scale (p 666) and medication effects on exercise
(back of book).
HTN- applies to systolic or diastolic at rest or with exercise, consider side effects of
medications (orthostatic hypotension, dizziness). Perform standard GXT, terminate
if SBP is >250 mmHg or DBP is >115mm Hg, headache, ST segment depr or elevation
>2mm, T wave inversion, serious dysrhythmias. Do not test if resting SBP is >200
mmHg or DBP is >105mmHg. Exercise at 40-70% VO2 max to lower htn.
Diagnostics
Echocardiogram- non-invasive transducer for blood flow velocity entering
ventricles or valves; can measure ventricle diameter at snapshots, depicts heart
muscle thickness (for damage if thinning). Inject tiny air bubbles in blood through
heart to detect leaky valves.
Holter monitor- pt wears for more than ex test to monitor HR over course of
day(s).
PET- use a radioactive tracer to look at resting cardiac blood flow; pt is given meds
to induce stress and observe overall blood flow in response to stress. Low false
positive rate (high specificity).
Radionuclide Perfusion Testing – can be combined with SPECT, a radioactive
agent is given at peak stress levels & heart is observed.
SPECT – (single photon emission computed topography) inject radioactive dye,
takes 360 deg photos of heart, measures overall myocardial blood flow.
MUGALab Studies- Norms (Table 8.2 in text)
WBCs- 4500-11,000
RBCs – 4.6-6.2 males, 4.2-5.4 females
Prothrombin time- 11.6-13 sec
Glucose- 70-110
Creatine- .6-1.2
BUN- 8-18 mg/dl
Na+ - 136-143, K+ - 3.8-5 mEq
INR- 2-3
Serous Enzymes
Test
Onset
Peak
Return to Normal
CK- total and MB
3-4 hours
33 hours
3 days
Troponins
3-12 hours
18-24 hours
Up to 10 days
Myoglobin
1-4 hours
3-15 hours
-
LDH
12-24 hours
72hours
5-14 days
Obstructive & Restrictive Lung Disease
Normal lung- delivers O2 for ATP production, remove CO2 from blood. Domeshaped diaphragm. Provides over-ventilation during exercise. Failure of normal
lung inhibits energy, energy reserve, & perfusion during exercise.
COPD (see uploaded file)
Chronic Bronchitis
Emphysema
Asthma
CF-genetic disorder (chromosome 7, CFTR protein is missing) affecting exocrine
glands largely in pulm system resulting in excessive mucous production. Progresses
from obstructive to restrictive. Usually poor prognosis with early death, cor
pulmonale, lung transplant in end-stage.
Characteristics of COPD- Trouble getting air OUT (respiratory tract disease), flow
of air is impeded. FEV1 is most indicative of COPD.
Signs: Decr flow rates, excessive CO2, hyperinflation of lungs, hypercapnia,
hypoxemia, incr RBC count (>4.6-6.2 males, >4.2-5.4 females), cor pulmonale
Reduced FEV1, FVC, TLC. (FEV1/FVC = usu normal because both are reduced)
Increased: ERV, RV
Tx: exercise for muscle strength, flexibility, endurance (swimming, cycling, walking,
tai chi) body composition, energy conservation, body mechanics to reduce O2 usage,
breathing techniques, secreation clearance, thoracic stretching, posture education,
removal of irritant/hazard/smoking, bronchodilators, anti-inflammatories,
antibiotics. *focus on most difficult ADLs first.
Spirometry- 2 efforts within 150 mL of each, exhalation of >6 sec, volume plateau.
Normally, >70% of predicted.
Exercise Test- for diagnosing exercise induced asthma, must reach 80-90% of max
HR, VE between 40-60% of MVV within 2-4 min of starting, continue 4-6 min after
reaching max HR. If FEV1 falls >10% at any point, + for COPD or from spriometry
post-exercise results.
Restrictive (see uploaded file)
Pulmonary Edema
Pulmonary Effusion
Pneumonia
Idiopathic Pulmonary Fibrosis
Characteristics of restrictive diseases- trouble getting air IN, volume of air is
reduced, reduced CAPACITY.
Signs: tachypnea, hypoxia, incr WOB, dyspnea, worsens with exercise
Reduced lung volumes, TV, TLC, IC, decr DLco (diffusing capacity), cor pulmonale (R
side heart failure)
Increased RR, RV (or can be normal), transpulmonary pressure, WOB (>/= 25%, 5%
is normal)
Symptoms: emaciated appearance, non-prod cough (#1 reason see dr), dyspnea,
hard to exercise
Pulmonary Fibrosis Cases
Sarcoidosis-unknown etiology, pt usually African American female age 20-30,
granuloma formation at site of infection.
Signs & symptoms: weight loss, fatigue, cough, dyspnea, organ dysfunction
X-rays: honeycomb, fibrosis, alveolitis, scarring, swollen/enlarged lymph nodes.
Tx: corticosteroids, immunosuppressants.
Lupus-systemic autoimmune disesase, pt usually women of child bearing age,
chronic, can present with pleural effusions, pleuritis.
Tx: corticosteroids, attn. to pulm function prevention & management.
X-ray: diffuse cloudiness
Rheumatoid Disease- unknown cause, females>males but men have more pulm
complications. 50% of cases have pulm involvement.
Scleroderma-autoimmune, females>males, progressive fibrosis of organs, poor
prognosis.
IPF- see uploaded chart of midterm practical cases.
Environmental Lung Diseasea. Pneumoconiosis- from inhalation of dust, x-rays are diffuse, cloudy,
speckled with widespread fibrotic changes, no effective tx
b. Gas inhalation-hyperemia, edema, epithelial injury, coughing, dyspnea,
cyanosis)
c. Infectious agents
Chest & Spine can contribute to restrictive lung function- kyphosis, scoliosis,
kyphoscoliosis, lordosis, pectus excavatum & carinatum. Females>males,
progressive
Neuromuscular Restrictive Diseases
a. Myasthenia Gravis- autoimmune involving neuromuscular junction,
females (30s)>males (60s), NIV and VC are indicative of changes. Tx:
anticholinesterase drugs, steroids
b. Guillain-Barre- inflammatory polyneuritis with ascending paralysis. Tx:
plasmapheresis, immunoglobulin therapy
c. ALS- dengen of SC & brainstem motor neurons, signs appear >50 y.o.
d. Quadiplegia- C3-5: diaphragm, C5-6: scalenes, T1-11: intercostals, T8-12:
abdominals
Exam 2 Cases
Pulmonary Edema (p. 165-6)
 Causes:
o increased pulmonary capillary hydrostatic pressure d/t LV failure
(cardiogenic)
 increased LA pressure (>30 mm Hg) and then increased
pressure in pulmonary system/loop
 Microcirculation pressure in lung is increased and thus so is
the flow of fluid into the interstitium of the lung.
 Pulm edema floods the alveoli and into the visceral pleura
causing effusions.
o increased alveolar capillary membrane permeability (ARDS)
 Pulm edema fluid has elevated proteins.
 Fluid is in alveoli and interstitium and lung compliance is
decreased.
 WOB is increased and there is restrictive lung dysfunction.
Pulmonary Effusion (p. 162-3)
 Accumulation of fluid in interstitial space between visceral pleura & parietal
pleura encasing thoracic cavity.
 High pressure arteries feed the parietal pleura while low pressure capillaries
feed the visceral pleura. Thus, more fluid leaks into the space for absorption
by lymphatics and visceral capillaries. When this is out of balance and more
fluid builds up, a restrictive impairment occurs and the lungs cannot fully
expand.
 Tx: identify cause and treat. Effusion resolves secondarily. Sometimes chest
tube for drainage.
o Transudate = low protein & from hydostatic pressure
 Causes- CHF, LVF (L and/or R heart failure also), cirrhosis,
nephrotic syndrome, pericardial disease, myxedema, pulm
emboli, peritoneal dialysis, or atelectasis.
o Exudate= high protein & from increased permeability of parietal
capillaries (either from tumor, infection, etc that increases fluid or
decr lymphatic clearance)
 Causes- bacterial or viral pneumonias, parasitic or fungal
infections, TB, mesotheliomas, bronchogenic carcinoma, lupus,
RA, acute pancreatitis, esophageal perforations, abscess
(abdominal), asbestos exposure, uremia, sarcoidosis or drug
reactions.
Pneumonias (p. 151-4)
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Inflammation that develops into infection of lung parenchyma (respiratory
epithelial cells) usually from something inhaled or aspirated.
If virus reaches alveoli, bigger problems!! (edema, hemorrhage, hyaline
membrane formation, ARDS (resp distress).
Bacterial (abrupt onset) or viral (insidious onset)
o Bacterial symptoms: high fever, chills, productive cough,
tachypnea, dyspnea (WOB), pleuritic pain, leukocytosis.
o Viral symptoms: moderate fever, dyspnea, tachypnea,
nonproductive cough, myalgia (muscle pain), normal WBC count.
o Community acquired
 Causes: bacteria, viruses (5th cause of death in US). Usually
from large exposure or low defense mechanisms.
o Nosocomial acquired
 Acquired 72 hrs after hospitalization and come with new or
more lung filtrate usu from gram neg bacteria.
 Risk factors include: NG tube, intubation, dysphagia,
tracheostomy, ventilation, thoracoabdominal sx, lung injury,
diabetes, chronic cardio pulm disease, uremia, shock, hx of
smoking, older, poor nutritional status.
Tx: Antibiotics, oxygen or mechanical ventilation, postural drainage,
percussion, vibration, & coughing techniques for those with a weak cough.
Idiopathic Pulmonary Fibrosis (IPF) (p. 144-6)
 Inflammation of alveolar wall (epithelial cells, endothelial cells, interstitium,
& capillary network.
 Unknown origin (viral, genetic, immune system disorders) resulting from
acute injury or infection.
 Risk factors: smoking, agriculture/farming, livestock, wood dust, metal dust,
& stone/sand dust.
 Patchy focal lesions bilat that scar & become fibrotic. Destruction to alveolar
spaces and capillary bed.
 Decreases lung compliance & decr lung volumes, increased pulm arterial
pressure (increases RV work). Also incr incidence of lung CA.
 Symptoms: low fever, worsening dyspnea & cough, worsening gas
exchange. Also, repetitive non-productive cough, weight loss, decr
appetite, fatigue, sleep disturbances with loss of REM sleep.
 Signs: dry rales, cyanosis, club fingers. Decr pulm function tests with
incr RR.
 Tx: corticosteroids, cytotoxic drugs. Supporting treatments. Final is lung
transplant (SLT).
Chronic Bronchitis (p. 216-9)
 Inflammation of upper airways (large & small) resulting in mucos
production, which obstructs the airway. (*simple bronchitis= large airways
only and is not obstructive)
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Productive cough for > 3 mos. In each of 2 successive years, and other causes
of mucos production have been ruled out.
Risk factors: smoking, air pollution, middle age, genetics.
Reid index- used to measure mucous gland hypertrophy. (abnormally high is
8:10)
Begins as inflammation & progresses to COPD. Structural changes in lung &
narrowing of airways occur. Lung parenchyma is destroyed and alveoli lose
recoil. Reduces ability of airways to remain open during expiration, leading
to air trapping, hyperinflation.
Symptoms: coughing, “scanty” sputum production, dyspnea
(“heaviness”, “gasping”). May be limited during exercise at first but
becomes worse.
Signs: prolonged expiratory phase (>4 sec), rhonchi, localized
wheezing, “distant breath sounds”. Hyperresonant over some parts of
lung, barrel chest (progressive), widened chest angle, forward leaning
posture (“tripoding”) while resting elbows to assist in breathing,
cyanosis, LE swelling (with RHF), flattened diaphragm. May have bullae
(air filled lung). Decreased FEV1/FVC< .7., decr Pa02 and incr PaCO2.
Emphysema (p. 214-6)
 Alveoli size increases and are not uniform in shape. Destruction of alveolar
walls & enlarged air spaces distal to terminal bronchi.
 Symptoms: cough, SOB, hyperventilates with exercise, finger clubbing,
wheezing, hyperinflated lungs, small heart?
 Risk factor: smoking (kills cells)
 3 Types:
o Centrilobular- upper lobes and posterior lung, hyperdilation
o Panlobular- lung bases, dilation of all airspaces in acinus
o Distal acinar- under apical pleura, dilation of air spaces, presence of
bullae (can lead to pneumothorax).
CHF (p. 104-112)
 Symptoms: dyspnea (OOB), paroxysmal nocturnal dyspnea (PND),
orthopnea (SOB while lying down), peripheral edema, cyanotic
extremities, weight gain, rales, S3 heart sounds, tachycardia, jugular
vein distension, hepatomegaly, decreased exercise tolerance.
 Signs: incr RR
 Breathing patterns: rales/crackles on inspiration, tachypnea (quick &
shallow), Cheyne-Stokes (waxing & waning depth with apnea recurring).
 Heart sounds:
o S3 (may be normal in children & young adults)- hallmark of CHF. S3 is
filling of LV where there is fluid overload or scar tissue. Early diastole.
o S4- presystolic, vibrations of ventricle wall from an exaggerated atrial
kick (rapid influx of blood).
o Murmurs- systolic, need to help them with afterload reduction.
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May experience extreme dyspnea after changing positions sometime related
to orthostatic hypotension & incr HR (blood pools in LEs or muscle
deconditioned).
Peripheral edema- causes by incorrect signaling by pressoreceptors to
kidney to retain fluid spurred by inadequate pumping by heart. Common
sites are abdomen, sacrum, ankles
Pulsus alternans- alternating strong & weak pulses at radial or femoral
arteries.
Exercise impairment- skeletal muscle changes, classified according to NYHA
functional classification (I-IV).
Echo- EF, LV structure, other structural abnormalities?
PT- TM walking, cycling, hallway walking, calisthenic or strength
training. 6MWT (>300 m is good).
QOL- MN Living with HF Questionnaire- one study found quad strength
was most powerful predictor of QOL in elderly with CHF. Another study
found BW was. Depression is a factor for increased mortality.
Asthma (p. 209-14)
o Reversible episodic obstructive disease characterized by airway
inflammation & remodeling.
o Risk factors: low or high birth weight, prematurity, maternal/parental
smoking, high salt intake, pet ownership, obesity.
o Hypocapnia- asthma attack (low CO2)
o Hypercapnia- during sever asthma attack requiring treatment
o Symptoms: wheezing, chest tightness, SOB, worse at night or after
exercise, exposure to allergens
o Signs: wheezing, air trapping
o Diagnostics – air expelled in first second of FEV1 & low FEV1/FVC ratio,
methocoline test.
o Tx: short-term relievers (dilators) or long-term controllers (corticosteroids).
o PT- use of meds prior to PT, secretion clearance techniques, breathing
techniques, exercise & strength training, thoracic stretching, posture
education.
Bronchiectasis (p. 220-4)
 Found in areas of limited health care; irreversible dilation of one or more
bronchi with chronic inflammation and infection. Airways become distorted
(thickened, herniated, dilated). May be related to immunity disorders.
 Idiopathic, though sometimes related to prior lung infection/injury.
o Localized- d/t inhaled foreign object or airway tumor preventing
clearing of mucous distally.
o Diffuse- try to identify underlying systemic cause.
 3 Types:
o Cylindrical- smooth, parallel walls.
o Varicose- distorted, bulging brochi.
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o Saccular- progressive incr in dilation toward lung periphery.
Mechanisms: bronchial wall injury, traction for lung fibrosis, or lumen
obstruction.
o Wall injury- from accumulation of bacteria following
inhalation/infection.
o Traction from lung fibrosis- airway is pulled outward resulting in
fixed dilation of airways.
o Lumen obstruction- slow growing tumors, histoplasmosis, or TB.
Symptoms: cough with chronic sputum (3 layers), may have blood in
sputum (avoid chest PT if present), breathlessness, tiredness.
Signs: signet ring sign, tram-tracks sign, nodules (dried mucous in
airways), crackles over involved lobes, rhonchi when mucuous
retention, dull percussion, diminished breath with mucous plugging.
Tx: Ig replacement therapy, steroids, antibiotics, bronchodilators,
hydration, clearance techniques.
Spirometry- may be normal in localized type, in diffuse, FVC, FEV1, FEF
reduced by 25-75% with incr RV. Obstructive-restrictive mix. Also
check for asthma & GERD.