cardio respiratory Flashcards
Cardiorespiratory physical examination acronym
IPPA
inspection-visual inspection of patient
palaption
percussion
ausculation
IPPA physical examination, compentnets of Inspection
1 vital signs (HR, RR, BP, SPO2), line and tubes/monitors
2 mechanisms of ventilation (pattern-chest diaphragm other muscles, ratio of isp:esp, depth shallow or normal)
3 thoracic shape (funnel, pigeon, kyphoscolosis,barrel)
4 head neck extremieties (colour, cyanosis, nasal flare, accessory muscle use, Jugular distension, cap refil, clubbingm colour, edema, muscle wasting)
5 speech cough and sputum(effective, productive, wet dry, colour, consitency volume)
how to check HR?
index and middle finger on radial forearm
rate in bpm, rhythm regular or irregular, and strength
Bradycardia
slow resting HR, less than 60 bpm
normal resting HR
60-100bpm
tachycardia
high resting HR, greater then 100 bpm
normal HR children 1 -8 years
80-100 bpm
normal HR infants 1- 12 months
100-120 bpm
normal HR neonates 1 day to 28days
120-160 bpm
3 words to describe HR rhythm
regular- regular consistent pattern
irrigular- irregular but consistent pattern eg bigeminy, trigeminy
irregularly irregular- iregular inconsistent pattern eg a fib
Bradypnea
slow resting RR, less then 12 breaths per minute
Eupnea
normal RR, 12-20 bpm
tachypnea
higher then normal resting RR, greater then 20 breaths per minute
normal RR children 1-8
15-30 bpm
normal RR infants 1- 12 months
25-50 bpm
normal RR neonates 1 -28 days
40-60 bpm
Procedure for obtaining BP
seated upright with arm at level of heart feet flat on the floor, patient should be relaexd ( not relaxed will increase BP)
palpate brachial artery pulse and place cuff 1 inch above. cuff should encircle at least 80% of arm (cuff to small overestimates, cuff to large underestimates)
place stethascpoe on pulse.
pump till pulse is occulded, slowly release
1st kortokoft sound is heard is systolic pressure, second sound is diastolic pressure
hypotention
low BP, systolic less then 90 or diastolic less than 60
s:
normal BP
120/80
90-129/60-79
values hypertention stage 1
130-139/80-89
values hypertention stage 2
> 140/90
critical > 180/110
orthostatic hypotention values
drop of >20 mmHg of systolic pressure going from lying to standing
dizzy lightneheaded due to O2 drop in brain due to gravity
SPo2, how to measure, values
peripheral capillary O2 saturation-percent of how much O2 Hgb is carrying (4 each molecule), measured using pulse oximeter on finger or ear
normal is 95-100
below 90% may warrent further investigation and supplementation
apical breathing
through shoulders, accesory muscle use, indicates severe dyspnea
paradoxical breathing
pattern in reveres, chest recoils on inspiration and expands with expiration
flail chest
multiple fractires in multiple ribs creates a flail segment that gets sucked in during inspiration
ratio of inspiration to expiration
normal is 1:2
obstructive is 1:3- hard time exhaling air, resistance
restrictive is 1:1- can not take as much air in shallow fast breaths
excessive abdominal use to expire
may indicate air trapping and effor to rid lungs of air. obstructive disease
depth of breath
shallow- indicates restrictive disease, often compensated by increasing respiratory rate
Funnel chest
pectus excavatum, sternum sunken
restricts anterior lung expansion
pigeon chest
pectus carinatum, sternum is forward
retrictions in in medial lateral expansion
barrel chest
AP:lateral diameter is 1:1
indicates chronic hyper inflation and air trapping
cyanosis
blue tinge to lips and mucus membranes, indicates respiratory distress
hypoxemia
low arterial blood O2
jugular venous distension
obvious in R sided heart failure, large vein in neck bulges visibly becuase of pressure.
right heart pump can not keep up back up of blood evidendent in jugular vein
Edema in extremities
sign of righ sided heart failure, R side can t pump effectivley back up of blood in venous system, edmema most common in lower extremities becuase of gravity dependent positioniing.
muscle wasting in respiratory disease
indicates muscles not reciveing adequte O2-hypoxia
hypoxia
low o2 levels in tissues
cough
forced expiration against a closed glottis, required to prevent retention, infection, atelectasis
effective- strong with ability to clear
productive/wet-things come up, vs non producrive or dry
persistant- how often?
four things we want to know about sputum
colour
consitency
volume
odour
describe the colour range of sputum
clear- salivia
white-normal, may be associated with asthma
yellow-mucopurlent, possible infection, chronic bronchitism cystic fibroisis, pnuemonia
green-prolent, possible infection, emphysea, advanded pneumonia, bronchietasis, lung abcess
brown flecks- carbon particples, smoker, smoke inhalation
pink frothy- pulmonary edema
frank blood-hemoptysis- Tb lung cancer pulmonary infarction
pink frothy sputum is indicative of what condition
pulmonary edema
frank blood in sputum is indicative of what conditions ( (3)
tuberculosis, lung cancer, pulmonary infarction
describe mucus of cystic fibrosis
lots of thick mucpulent yellow mucus, copius amounts
IPPA: palaption exam includes
1) chest wall expansion
2)diaphragmatic excursion
3) edema
4) pain and crepitus
5) traceal positioning
6) tactile fremitus
describe 2 ways to assess chest wall expansion
1) manual method- look for amount of movment and symmetry between sides, thumbs together-how far apart do they move with breath. assess upper(sternocostal), middle (vertebro costal) and lower (lateral costal)
2) circumferintial method- uses measuring tape to measure diffrence between full inlation and exhalation. measure at axilla, measure at 10th rib. 3 measurments-best of 3
disphragmatic excursion
1) hand placed on apex of belly during inspiration
2) measure diffence with tape measure apex of belly during inspiration
3) diaphragmatic percussions
Edema palpation
pitting vs non pitting
pitting pressure leaves an indent which persits indicates fluid retention that is gravity dependent,Right sided heart failure
non pitting edema-chronic, lymphedema
others: systemic pregnancy
if palaption of chest area increases pain
this indicates oraganic or pain of musculoskeltal orgin
crepitus with breath
bubbles of air in subcutaneous tissue, sub cutaneous emphysema, air leak from chest tube, trauma, pneumothoracx
requires medical attention ASAP
tracheal positioning
should sit between the SC joints,
increase in pressure pushes contralateral
decreae in pressure pulls ipsilateral
tactile fremitus
ulnar border of hand on chest as patient repeats 99, feeling for vibrations.
increased sound transmission indicates more dense tissue (not air) pulmonary edema, consolidation, tumor
decreased sound transmission =hyperinflation, emphysema, pneumothoracm pleural effusion, sound waves attenuate in less dense tissue like air and fluid.
diagnosit precussion of chest wall
purpose: determine density of underlying tissue, up to 5 cm in depth
extended finger between ribs-tap firmly with other fingers 2-3 strikes
resonat= normal tissue
dull= nonareated lung tissue
hyperresaonant= hyperinflated lung
percussion diaphargmatic excursion
patient sitting. max exhale and hold as physio percussates makes mark , max inhale and hold physio percussates makes mark
normal distance between is 3-5 cm
define auscultation
art of listening to sounds porduced by the body, pt takes slow deep breaths though MOUTH when assesing, check for dizziness every 2-3 breaths
normal lung sounds resonant
abnormal dull indicates consolifation, plueral fluids, pulmonary edma, pneumonia, atlectasis,
hyperesonant hyperinflation, COPD, acute asthma attack, penumothorax
list R lung segments (9) and where to ausltate
RUL-apical (above clavicle)
RUL-anterior (between clavicle and 4th rib anteriorly)
RUL-posterior (between C7/T3, above spine of scapula-posteriorly)
RML-lateral (mid axillary rib 5, stethoscope beneath orts bra inferiorly)
RML- medial (anterior mid chest, beneath breast tissue between costal cartilages 4 and 6)
RLL-anterior basal ( between ribs 6 and 8 in the mid clavicular area
RLL-superior ( enclosed by T3 to T7 and medial scapular border)
RLL-posterior basal (enclosed by T7 to T10 and mid scapular line)
RLL- lateral basal ( enclosed by T7 to T10, mid scapular to posterior axillary line)
medial basal- can not ausultate
list L lung segments (8)
LUL-apical posterior ( above clavicle anteriorly, posteriorly C7 to T3 above spine of scapula)
LUL-anterior (between clavicle and 4th rib anteriorly)
LUL-superior lingulus,(over 5th rib anterior lateral)
LUL-inferior lingulus ( between costal cartilages 4 and 6 anterior mid chest)
LLL-anterior medial basal
LLL-superior ( posteriorly t3 to T7 and medial border of scap)
LLL-posterior basal (T7 to T10 and medial to mid scapular line)
LLL-lateral basal (T7 -t10 lateral to mid scapular line)
describe vesicular breath sounds
where are they normal?
soft low pitched
Inspiration to expiration 3:1
heard over peripheral lung tissue (not over trachea and bronchi)
indicates normal lung
describe bronchovesicular
where should you hear
Mixture of branchial and vesicular
inspiration to expiration 1:1
inspiration is soft and low pitched
expiration is loud and high ptiched
heard over main stem bronchi in 1st and 2nd intercostal spaces and posteriorly between scapular
bronchial breath sounds
loud high pitched hollow quality
louder on exhalation
inspiration:expiration 1:1 or 1:2
distinct pause between inspiration and expiration
heard over trachea and manubrium
describe crackles as a breath sound
abnormal breath sound
short explosive
inspiratory or expiratory
fine or course
course crackles
air moving retained secretions cuaseing intermittent closing and opening of the airway, wet, insipration and/or expiration, can be in any area of the lung
fine crackles
sudden opening of collapsed alveoli, typically dry, inspiratory, typically in basal lung (area more proone to collapse)
late inspiratory fine crackles
wheeze
abnormal breath sound
differnt pitches-high (bronchospasm), low ( secretions in upper airways)
inspiratory(rare-severe obstructions) expiratory (most)
pleural friction rub
extrapulmonary sound
long low pitcher leathery creaking produced by frictional resistance between layers, may be asociated with pain
stridor
loud musuical high constant pitch, audible from distance without stethoscope, most promminent during inspiration
due to turbelent air flow -upper air way obstruction or narrowed air ways
pulmonary function tests
a group of tests which help evaluate the mechanical functioning of the lungs, researched norm and predicted values are used for comparison, used for determination of presence of restrictive and obstructive diseases, determining severity of condition, determine response to bronchodilator treatment, as an out come measure for disease progresssion or effectiveness of treatment and medications.
obstructive diseases
trouble getting air out, leads to air trapping, lots of junk air and no room for new air
increased airway resistance, narrowed air way leads to increased resisance to air out
chronic bronchitis, emphysema, COPD, asthma, bronchiextasis
increased lung capcities due to air trapping
decreased flow rates FEV1, FEV1/FVC,
restrictive diseases
decreased ability to expand lungs and take air in, stiff chest/lung/ribcage, decreased strength to expand
decreased compliance–> decreased negative pressure–> decreased air entry,
colume of air in lung is reduced
results in increased work of breathing
increase RR that may lead to hyperventiliation (decreased PACO2)
increased accesory muscle use
increased pressure required to maintain lung expansion and ventilation
increaed fatigue ( lots of energy for breathing, depleted O2 deconditioning)
tidal volume
the amount of air taken in or out during normal quiet breathing.
about 500 mL in normal adult
Inspiration
diaphragm moves down on inspiration, the primiary muscle 70%. thoracic space increases and chest wall expands. intrapleural presure becomes more negative and draws air in. diaphragm is its lowest at the end of inspiration
acccessory muscles: external intercostals, SCM, scalenes, pecs
Expiration
expiration is a passive recoil of the lungs and rib cage.
forced expiration/reduced elastic recoil requiers contraction of abdominal wall and internal intercostals. these muscles press the abdominnal organs upwards into the diaphragm reducing the volume of the thoracic cavity. inspiratory muscles are relaxed. throacic volme is decreased intrapleura pressure becomes less negative and forces air out.
Inspiratory reserve volume
maximum amount of air that can be inspired above tidal volume, Inspiratory capacity - tidal volume
2- 3L
used during exertion or exercise
Expiratory reserve volume
maximal exhalation after tidal volume expiration ( max expiration - tidal volume)
1L
residual volume
the amount of air left in the lungs after maximal exhalation, cant exhale all the air
cannot be measured by spirometry
1L
total lung capacity
the volume of air in the lungs after a maximal inspiration
residual volume, tidal volume, expiratory reserve volume and inspiratory reserve volume
4-6L
vital capacity
the maximum amount of air that can me exhaled after a maximal inhaltion
expiratory reserve volume, Tidal volume and inspiratory reserve volume
3.8L females 4.8 L males
inspiratory capacity
maximum amount of gas that can be inhaled from resting expiratory level
tidal volume and inspiratory reserve volume
functional residual capacity
amount of air in the lungs after a normal breath out
expiratory reserve volume and residual volume
dead space
volume of ventilated air that does not participate in gas exhange, ventilation with out perfusion
1. anatomical - volume of air that fills the conducting airways (nose trachea bronchi) where gas exhange is not possible because there is no alveoli
2. physiological dead space= antomical dead space plus alveolar dead space. neligible in healthy indiviudals. value increases in lung desease states
does decreased tidal volume indicate restrictive or obstructive disease
restrictive
increased residual volume indicates restrictive or obstructive
obstructive
decreased residual volume O or R
restrictive
increased inspiratory reserve volume indicates O or R
obstructive
decreased inspiratory reserve volume indicates O or R
restrictive
decreased expiratory reserve volume indicates O or R
restrictive
do lung capcities increase or decrease in restrictive diseases
decrease
do lung capcitites increase or decrease in obstructive diseases
increase
forced vital capacity
the total volume of air that can be exhaled after a maximal inhlation indpendent of time
forced expiratory volume (FEV 1 is common)
maximum amount of air that can be expired in 1 second after maximal inhalation
FEV1/FVC
% of of FEV that can be exhaled in 1 sec.
80% is normal
in a restrictive disease both FEV1 and FVC decrease the ratio is normal or greater then normal
<70% is obstructive disease becuase it indicates there is lots of resistance to getting air out, FEV1 reduces beucase hard time removing air.
differentiate between normal, restrictive and oabstructive flow volume graphs
normal: most of the air is exhaled in 1 sec, steady decline afterwards
Obstructive: less air is exhaled then normal, takes longer to exhale air, graph scoops, increased scooping indicates increase severity of disease, longer horizontallly
Restrictive: air is exhaled fast, less air to exhale, graph is shorter horizontally
FVC in obstructive diseases
normal or low
FEV1 in obstructive diseases
low, becuase of resistance to air getting out
FEV1/FVC in obstructive diseases
<70% and is diagnositic
FVC in restrictive diseass
low, can not take as much air in therfore less to exhale
FEV1 in restrictive diseases
normal or low
FEV1/FVC in restrictive diseases
normal to high
diffusion capcacity of carbon monoxide
mesures the functioning of gas exchangefrom the lungs to the blood
low: could be a problem with pulmonary or circulatory system eg// emphseyma, fibrosis, anemia
high: problem with circulatory system-not pulmonary eg// polycythemia high RBC count viscous blood
Respiratory muscle strength tests
nose clip, breath trhough tube attached to gage
indicated when resipiratory muscle weakness is expected, when perscribing a inspiratory muscle trainer
inspiration: pt’ attempts a maximal inspiratory effort through blocked mouthpiece, reflex strength of inspiratory muscles
expiration: patient attempts a maximal forced expiratory effort through blocked mouth piece after a full exhalation, reflex strength of patients expiratory muscles
normal blood ph
a measure of the hydrogen ion concentration indicating acidity and alkalinity
7.35-7.45
normal PACO2
35-45 mmHG
controlled by ventilation
normal HCO3
22-26 mEq/L
normal SPO2
95-100%
% of saturation of hemoglobin molecules with ocygen
measured by pulse oximeter
normal PaO2
80-100mmHg
arterial blood gas test
test of arterial blood to measure blood gases and acidity
assess effectiveness of gas exhange in diagnosis of acute respiratory conditions
body tries to maintain homeostasis
patient hypoventilating, how does this effect PaCO2
increased PACO2
patient not breathing in fresh O2 and retaining CO2
respiratory acidosis
patient hyperventilating, how does this effect PaCO2
decreased PaCO2
patient breathing too much
offloading excess Co2
repiratory alkalosis
< 22 mEq/L HCO3-
metabolic acidosis
> 26 mEq/L HCO3-
metabolic akalosis
PaO2 mmHg
mild, moderate, severe hypoxemia
mild 60-80mmHg
moderate 40-60mmHg
severe <40 mmHg
respiratory acidosis values
low Ph and high PaCo2
respiratory aklaosis values
high Ph, low PaCo2
metabolic acidosis values
low HCO3-, low Ph
metabolic akalosis values
high Ph, high HCO3-
if Ph and PaCO2 move in the oppisite direction…
if Ph and HCO3 move in the same directions..
- respiratory
- metabolic
compensated ABG
notmal ph but other components are abnormal
uncompensated ABG
abnormal ph, one component HCO3- or PaCo2 is abnormal while the other is normal
partially compensated ABG
ph is abnormal, PaCO2 and HCO3- are also abnormal
ventilation perfusion ratio
ratio of the amount of air reaching alveoli to the amount of blood reachingi the alveoli
optimal =1
ventilation is the exhange of gases, movement of air in and out of the lugs
perfusion- amount of blood that reaches the alveoli via the capillaries which enables the movment of O2 and CO2 across the alvelolar membrane and capillary membrane
shunt- low VQ ratio , alveoli are perfused but ventilation fails to supplu the perfused region
deadspace- hihg V/Q ratio, air is inhaled but unable to take part in gas exhange
Causes of obstructive lung diseases
smoking-inhibition of cilary motility airway irritation
air pollution
genetics-alpha-1 antirypsin definciency elastin breakdown, floppy lung
infection- repeated/chronic
aging due to increased compliance fo lungs
allergy-asthma attacks
what is COPD, 2 types
progressive airway obstruction that is not fully reversible
associated with RHF
Chronic bronchitis-small airway remodelling
emphseyma-parenchyml destruction- destruction of air ways distal to terminal bronchi, destruction of interalveolar septa cuasing mergin of alveoli into larger air spaces
diagnosistic criteria of chronic bronchitis
productive cough on most days for 3 months out of the year for 2 consectutive years (provided other conditions have been ruled out)
Pathophys of chronic bronchitis
hypertrpphy and hyperpalsia of mucus glands and goblet cells- leading to an increase in mucus. decrease in cilia #’s cuasing secretion retention. chronic inflamatory changes in broncial walls, decreased gas exhange due to formation of misshapen and large aveloar sacs
etiology of chronic bronhitis
chronic irritant exposure ( pollutnats, smoking)
long term irritation of trachea/bronchi
clinical presentation of chronic bronchitis
mucus
I: obese and cyanotic blue bloater, mucus (white to green), commonly ass. with RHF (edema and jugular vein distension), hypoxeimia, dyspnea, chronic productive cough
P: decreased tactile fremitus in areas of air trapping (pillowing) , increase tactilie fremitus in areas of consolidation, possible ankle edema (RHF)
P: hyperresonate in areas of air trapping, dull in areas of consolidation
A: decreased breath sounds in areas of little air movement trapped air, early inspiratory wet crackles-bronchi mucus, possible wheezing due to airway narrowing
ABG: low PaO2, high PACO2
CXR: black in areas of trapping white in oslidations-haziness, cardiomelgaly (enlarged heart due to RHF)
imapct of chronic bronchitis on lung function
airway wall increases due to inflammation and scarring= smaller airways, increase in mucous also decreases airway lumen, damage to cilia increases susceptibility to lung infection, incrase in airway smooth muscle contracton can cuase increase in bronchconstriciton,
what is emphysema
enlargement of airway distal to the terminal bronchioles accompianed by destruction of their walls, air sacs rupture and enlarge (normal many small sacs,) fewer larger sacs.
Centrilobar: affects respiartory bronchioles, males, rare among non smokers, found often with chronic bronchitis
Panlobar: affects terminal and respiratory bronchioles. due to alpha antitrypsin defieciency (genetic) which inhibits elastase, lung is floppy decreased elastic recoil.
pathophysiology of emphysema
develops from obstruction to air flow during exhalation leading to hyperinflation–>destruction of alveloar walls–> decreased elastic recoil–> increased dead space, . decreased gas exhange(alveoli rupture daamage to capillaries and decreased SA).
etiology of emphysema
smoking, pollution, alphaantitrypsin diefeincy
clinical presentation of emphysema
I: thin and wasted pink puffer, muscle atrophy, barrel chest, I:E ratio prolonged 1:3/long exhlaation, pursed lip breathing, increased respiratory muscle use, other signs of resp distress
P: tactile fremitus decreases due to air trapping and pillowing affect
chest wall expansion is decreased becuase lungs are already hyperinflated
P: hyperesonat with precussion
A: decrease breath sounds, may have dry crackles
ABGs: decreased PaO2 normal or increased PACO2
CXR: increased balck area (air trapped), flattened diaphargm, flattened rib angles, narrow mediastinum (thin elongated heart)
impacts of emphysema on lung function
decreased surface area for gas exhang
elasticity of alveloar septa are compromised, air ways collapse early trapping inspired air
hyperventilation-breathing at high lung volumes, diaphragm at a mechanical disadvantage
diagnosis of emphysema
diffusion capcitiy studies Carbon monoxide
spirometry
emphysema and chronic bronchitis
hyperinflation and gas exhange abnormalities
-invcreased airway resistance, early airway collapse leads to to air trapping, short inspiratory muscles
- poor gas exchange
Treatment of COPD
1) pharmacological
2) O2
3) PT
1) bronchodialators for smooth muscle relaxation (ventilin/albuteral) helps to decrease air way resitance
corticosterioids to decrease airway inflammation
2) oxygen is often used during exacerbations, during exercise or for long term use in very chronic individuals, goal is to admin the lowest amount of O2 needed to keep SPO2 around 88-92%
3) pursed lip breathing- slows air flow to create back pressure that stents airways open during exhalation- more CO2 is removed less air is trapped
what is asthma?
chronic inflammatory condition of the airways characterized by hyper responsivemenss of the airways to various stimuli that result in airway narrowing
often reversible with a bronchodialotor
often cooccurs with allergies and eczema
Pathophys of asthma
decreased thresholds od airway smooth muscle reactivity
leads to bronchospasm, bronchial wall edma and inflammationm and increased secretions
narrow airways increase risistance both in and out
intrinsic factors that can trigger an asthma attack
idiopathic, internal, localized immune
drugs, exercise induced, inhaled irritants, respiratory infecions, stress, weather
hypersensitovity
usually adult onset
extrinsic asthma triggers
external: animals, dust, feathers, food, mold, polleen
usually a specific trigger
childhood onset
clinical presentation of an asthma attack
Pulmonary function tests improve post bronchodialtors
Pt reports chest tightness and dyspnea
I: increase in accesssory muscle use, other isgns of respirtory distress
P: tactile fremitus decreases becuase of air trapping, chest wall excursion decreases due to to air trapping
P: hyper resonant due to air trapping
A: decreased breath sounds, possible WHEEEZING due to air way narrowing, possible crackles
ABG: decreased PaO2, increased PaCO2 if severe and decreased Ph or respiratory acidosis
What is bronchectasis?
irriversible abnormal destruction and dialation of medium sinzed bronchi and bronchioles + increased serections resulting in airflow obstruction and secretion retention,
commonly associated with chronic inflammation and infection within these airways
extreme form of chronic broncitis
treatment for asthma
prevent triggers
control attacks pharmalogically: bronchodilators and corticosteriods inhaled
for exercised induced asthma: keep patient upright, use inhaler if prescribed, lean forward and teach pursed lip breathing
Pathophysiology of bronchectasis
destruction of bronchial wall cuasing permenanent dialation of airways, ciliated walls are replaced by non ciliated mucus secreting cells, poolnig of secretion lead to reoccurent infections and may cuase atelectasis distal to obstruction ( may lead to restrictive findings, increased difficulty to expand)
Etiology of Bronchectasis
post infection ( necortizing bacterial pneumonia, congential disorders ( cystic fibrosis, cillary defect, airway defects), bronchial obstruction (aspiration,Ca), other ( connective tissue diseases, systemic disorders, imunodefeicneis,idiopathic- increases in lifetime infection risk), tuberculosis
Clinical presentation of Broncheiectasis
I: thin and fatigued, digital clubbing, increased accesory respiratory muscle use, other signs of respiratory distress, severe cough, increase in mucus foul smelling, purlent, may contain blood)
P: decreased chest wall excursion due to airtrapping, tactile fremitus increaes over consolidation/mucus and decreases of areas with trapped air
P: resonat over air trapping, dull over mucus obstructions
A: decreased breath sounds, wheezing, coarse crackles
CXR: dilated airways, dark fields of air trapping, flattened diaphragm, high resolutions CT for diagnosis
treatments for broncheictasis
antibiotics, bronchodialaotors, regular secretion clearnace techniques
what is intersitial pulmonary fibrosis?
thickening of the interstium of the alveolar walls which porgresses to fibrosis or scarring creating stiff less compliant lugs
Pathophys of pumonary fibrosis
decreased lung comliance, increased elastic recoil, increased fibrolansts results in increased collagen leading to fibrosis or scaring, decreased diffusion capacity ( increases thickness of diffusion membrain)
etiology of pulmonary fibrosis
idopathic, environmental exposure to inorganic dust/toxic gas and certain drugs, geneticm some connective tissue disorders (RA), conditions that can lead to inflamttion and scarring og lungs (pneumonia, TB, lung cancer)
Clinical presentaton of pulmonary fibrosis
wieght loss
I: dsypnea, increase RR and shallow breaths, dry unproductive cough becuase of irritation, clubbing, cyanosis
P: decreased chest expansion, increased tactile fremitus
P: dull on precussion
A: Auscultation late fine inspiratory crackles-popping open of alveoli
ABG: low PAO2 (not enough in ) and PACO2 (becuase of hyperventilation
CXR: small contracted lungs, raised diaphargm, diffuse reticular markings, high resolution CT more accurate on diagnosis
treatment for pulmonary fibrosis
O2 therapy, pulmonary rehab, lung transplant,
What is sacoidosis?
a disease invovling granuloma (collections of inflammatory cells that form a lump) developmment in the lungs, skin , lymph nodes and other organs
complicated pathology
unknown cuase
can present with restrictive or obstrucive signs
what is atelectasis
collapse of alveoli or lung tissue (sub segmental, segmental or lobar distribution)
Pathophysiology of atelectasis
poor ventilation
post surgical/ansesthetic
obstruction- blocks air from getting distal
decreased nitrogen-naturally in air, helps keep alveoli open
decreased surfactant - to much surface tension, requires more energy and force to open, invovled in infant respiratory distress syndrome (no surfactant)
compression-tumor penumothroax
hyperventilation- too fast to fully open
hypoventilation-breath to shallow and not enough air to fully exapnd
clinical presentation of atelectasis
I: dyspnea, cyanosis, increased RR shallow breathing
P:ipsilateral tracheal deveiation, decreased chest wall expansino on affected side, decreased tactile fremitus (no voice vibrations where air is not folded up tissue increased distance from chest wall open space does not transmit well)
P: dull directly over compressed tisssue
A: decreased or absent breath sounds, fine crackles
ABG’s: decrease PAO2
CXR: ipsilaeral shift of mediastinum to area of low pressure, increased density/whitness in area of atelectasis, elevated hemidiapahragm on side with atelectasis
treatment for atelectasis
remove obstruction: mobilize secretions, chest tube for pleural effusion
positioning, mobility, breathing exercises
What is acute respiratory distress syndrom (ARDS)
an acute lung injury which is characterized by respiratory distress, sever hypoxemua and increase permeability of the alveloar capilarry memebrane
Pathophysiology of Acute repiratory distress syndrome
increased capillary permiability due to injury leads to edema and inflammation in interstitual space and then into alveoli
decreased surfacant production leading to increased surface tension and decreased lung compliance
V/Q mismatch right to left shunt-blood passes through without picking up oxygen (arterial hypoxemia)
rapid fbrosis later in disease progression-persistant even after ards clears up
etiology of ARds
shock any type
sever pnemonia
sever trauma
sepsis
aspiration
post infection
Clinical presentation of ARDS
I: severe dyspnea, often require mechanical ventilation with high PEEP-
keep lungs inflated and avoid lung collapse, cyanosis, increase RR and shallow breath
P: increased tactile fremitus due to fibrosis and edema
P: dull precussion
A: inspiratory crackles, diffuse wheezes
ABG: severe decrease in PAO2, increase in PaCO2-hyperventilation
CXR patchy infiltrate in periphery of lungs, white out
treatment for ARDS
PEEP to keep airways open
tackle underlying cuase
prone position
intubation and ventilator assist
secretion clerance if needed
what is pnemothoracx
an abnormal collection of air in the pleural space leading to collpased lung
pathophysiology of pneuomthroax
loss of negative pressure in the pleural sapce- cuases an expsnded rib cage and/or a collapsed lung, in large pneumothroax air can be reomved via chest tube
etiology of pneumo throax
trauma to chest wall (puncture), complication of invasive procedure, idopathic, rupture of respiratory strucuture (bleb), complucation from mechanical ventilation, infection of the pleura can also led to rupture
spontaneous pneumothroax
develops suddenly dur to rupture in air containing structure, most common in young tall men
primiary =bleb ruputure
secondar to another disease
truamatic pneuomothorax
due to penetrating or non penetrating injury to chest wall
tension pneumothroax
tear in the pleura that acts as a one way valve, air enters during inhalation but air does not leave during exhalation, medical emoergency-acute lif threatening situation
clinical presentation of pneumothroax
I: signs of respiratory distress, dyspnea, incerased resp rate, chest pain, dry cough due to irritation of pleural receptors
P: air trapping in space leads to decreased tacitile fremitus
P: resonant due to air
A: decreased or absent air is not moving
on xray will see blackened area around lung and flattented hemi-diaphragm, medistinum shift away from side of pneomothorac
flail chest
multiple rib fractures with a free floating rib section
on inspiration flail segment sucks in reducinng air entry
on expiration pushes out
ineffecient ventilation and poor oxygenation
Tx pain control, airway clearance, oxygen, intubation and ventilation if needed
what is pleural effusion and pathophysiology
and cuases
abnormal collection of fluid in the pleural + space
increased production or decreased clearace of fluids
Cuases: CHF, liver disease, kidney disease, CA, pneumonia, pulmonary emoblism, tuberculosis, trauma
exudative pleural effusion
increased permability of the pleural surface leading to increased fluid, protiens, WBC and immune cells into the plerual space, fluid cloudy, cuased by inflammtation infection or cancer
transudative pleural effusion
increased hydrostatic pressure in pleural cappilarries like in CHF, fluid is clear and has very few proteins
clinical presentation of pleural effussion
I: may have dyspnea-compressive atelctasis, increased RR, chest pain, dry cough due to irritation
P: decresased tacitile frem over fluid increased ovver atlectasis,
decreased chest wall exursion on side of effusion
P: dull precussion
auscultation: decreased/ absent breath sounds over effusion, may hear pleural friction rub
decreased PaO2, PaCO2
white in areas with increased fluid on xray, contralateral tracheal shiftr
diapragm
primary muscle of ventilaion
innervated by the phrenic nerve C3/4/5
dependent on the intercostals and abdominal muscles- does not work well in isolation
intercostals
innervated by T1-T12, act to stabilize the rib cage. internal intercostals active exhale, external intercostals a primiary muscle of inhalation
abdominals
innervated by T6-L1, stabilize inferior border of rib cage, increase intratrhoacic pressure for strong and effective cough
accesory respiration muscles
errector spinae, pec +/-, serratus anterior, sclaesns, SCM, traps
what is cystic fibrosis? Pathophysiology?
systemic hereditary disease, abnormal Na/Cl ion pump (cl- excertion, Na absorption.
of the exocrine glands, copious amounts of thick secretions/scarrion/cysts in effected glands
most commonly manifests in kidneys, lungs, kideneys and intestines. ion transport dysfunction-increased electorylyte content in sweat. increasedd obstruction in ednocrine ducts by thick seceretions.
increased secretion retention in the lungs leads to secretion retention, reoccurent infections, fibrosis, scaring, cystic dialations of the bronchi, malaabsorbtion of nutrients
etiology of cystic fibrosis
autosomal recessisve gene that affects exocrine glands, diagnosed in child hood usually due to impaired growth and development (malabsorption), thick yellow secretions
Dx and clinical presentation of cystic firosis
Dx: genetic testing, chloride sweat test, obstructive lung disease
I: low weight, possbile, osteoporsis from not absorbing nutrients, increased RR, barrel chest, clubbing, chronic productive cough, copious amounts of purulent or mucopurelent mucus
CF may be obstructive. retrictive or mixed
auscultation: decreased breath sounds, inspiratory and expiratory crackles, wheezing,
x ray: thickened bronchial walls, opacities, consolidation
tx cystic fibrosis
bronchodialtors, antibiotics for infections, o2 supplmentation
PT: airway clearance (<5 years: aggresive bronchial clerance/ vibration/ presussion, 6+ years: accapella/flutter/PEP mask, active cylce of breathing, autogenic drainage), secretion removal 2-3 x per day!!!
exercise: posture, strengh, endurance with O2 monitoring and avoidance of overexertion
what is pneumonia?
an acute inflammation of the lungs assoiated with the alveolar filling with exudates–> consolidation, common complication and cuase of morbidity and mortality in hospitalized pateints
pathophysiology of pneumonia
infectious agent ( virus or bacteria) or irritant that reaches the lungs and triggers an inflammatory reaction.
Etiology on pneumonia
aspiration, contact trauma/chest tube), inhalation ( droplet), hematogenous (circulation). increased risk in infants and elederly, chronic caridac and respiratory disease, immunosuppressed patients
clinical presentation of pneumonia
I: dyspnea, cyanosis, increased RR and shallow breath, cough, fever (high in bacterial, low inviral)
P: tactile fremitus increases becuase of consolidation
P: dull on precussion
A: wet inspiratory crackles. bronchial and bronchialvesicular breath sounds
decreased PaO2, decreased PaCO2
what is tuberculosis, pathophysiology?
an infectious, systemic inflammatory disease that primarly affects the lungs and other organs
mycobacteriiu tuberculosis (ariborne)
most infections dont have symtpoms (latent, may lay dormant then reactivate when immune system weaknes (post primairy TB)
clinical presentation of TB
cough lasting greater then 2 weeks, early dry cough late wet cough ( mucus and blood),
fevere, fatigue, night sweats, weightloss, swollen lymph nodes, brnochial breath sounds
Dx of TB infection
TB skin test
TB blood test
Xray: indiltrates and cavitation
sputum sample
medical history -immunocompromised/ recent travel
physical examination
interventions for TB medical and PT
medications 6-12 months
prevent exposure to others: negative pressure room, universal precuastions and N95 respiratorr mask
sesecretion clearnace/deep breathing/coughing
pneumonia
acute inflammation of the lungs in which some or all alveoli are filled wirh fluid or cells, often hopsital aquired, normally from airborne pathogens ( bacterial, fungal, viral, toxic), increased occurence in the immunocompromised, common in patients with swallowing disorders-aspiration
productive cough/fever/fatgue/dyspnea/tachy cardia
infection controll procedures/mobility/keep lungs clear/manage aspiration risk hob up 30 degrees
acute cornoary syndrome
term used to decribe a spectrum of clinical presentations which results from impairments in the blood supply to the heart
mysocarioal ischemia and myocardial infarction
myocardial ischemia
insuffiencent blood flow to the myo cardium , typically presents with angina can be silent
Levine sign
fist over sternum–> angina
angina
diffuse retrosternal pressure, heaviness, tightness of constriction in the chest cuased by reduced blood flow to the myocardium, clutch chest fist over sternum
may radiate to the left jaw left arm and or upper back between sapula (visceral reffered pain)
allviated often by rest and nitro
stable vs unstable angina
stable: preciptated by activities that increas myocardial oxygen demand (PA, sex, emotional stress,, cold ,meals, lying supine (venous return heart needs to contact harder) relived by rest or nitro. once demand in met angina disapears, predictable
unstable: occurs at rest without any obvious preciptating factors or with minimal exertion- very ishcemic tissue can expereince angina anytime with little aggrevation, not releived by rest, may not be relived by nitro, requires immediate medical attento n as there is high risk for infarctionp, atherosclerosis
positioning to decrease O2 demand without increasein venous return
seated against the wall with knees bent up. pillows behind back and under knees to support.
myocardial infarction
death of cardiac tissue due to lack of blodd flow, cuased by sudden complete occulsion od one or more of the coronary artiereis.
area of infarction is irreversible
describe the evaluation triad for myocardial infarction
symptoms: angina, anxiety, diaphroesis, sypneam dizziness fatigue, nausea
ECG changes
1) signs of ischemia- ST segment depression and inverted t wave
2) small acute MI- no ST segment change, NSTEMI-non ST segment elevation MI, no ECG changes
3) large acute MI: st segment elevation STEMI and pathological q-wave
Cardiac biomarkers: bloodwork–> troponin 1 an 11, myoglobin, creatine kinase-myocardial band
medical managment of MI
1) Surgery: percuaneous transluminal coronary angioplasty- stent placement, coronary artery bypass graft with donor vessels
2) medications
beta blockers
calcium channel blockers
angiotensinogen receptor blocker
supplmental oxygen
nitrates -vasodialtor
angio tensinogen converiting enzyme
goals of PT managment of MI
improve exercise capacity
iprove exercise effeiceincy-same work less cost
imporve exercise tolerance-same work less signs and symptoms
imporve qulity of life
differentiate arteriosclerosis and atherosclerosis
arteriosclerosis-thickening, hardening and stiffening of arterial walls, loss of elasticity, restricts blod flow to tissues, common in smaller sized arteries
atheriosclerosis-a form of arteriosclerosis, slow progressive condition, narrowing of srtiers due to a buikd up of plaque (cholestrol/lipids/Ca2+) gradual closure of lmen and prevention of blood flow down stream, rupture can result in blood clot formation local occulsion or further down stream thromboembolism
weakening of artery wall and rupture
medium to large sized arteries
herat attack/stroke/ aprtic anerusym, peripheral vascualr disease
what is cardiac rehabilitation
a comprehesnive exercise, education and lifestyle modification program designed to optimize physical psychological social and vocational functioning
pulmonary rehabilatation
indicators: dyspnea that interfers with lifestyle, reduced ability to perform exercise/ADL/selfcare
SPO2 should not fall belw 88%
BORG scale 5 and lower
no abnormal cardiac signs
no pain nausea dizziness headaches
4 phases of cardiac rehabilitation
I acute impatinet phase
II subacute conditioning phase
III intensive rehabiliation phase
IV maintenance phase
decribe the acute inpatient phase of cardiac rehab
begins in hospital setting
prepare for discharge, monitior activity tolerance, support risk factor modification techniques, provide emotional support, biuild self effeicacy, education on s/s with aciviy and collaborate
assess hemodynamic response to activity, I in functional mobility , monitoring vital signs before and after
low level intensisty
LEVEL 1: 1 MET, stable in ICU for 24hrs, bed rest gentle AROM upper and lower with breathing exercises
LEVEL 2: 2 METS, sitting for meals, perform ADLS, walking in room and to bathroom few times per day
LEVEL 3: ambulate up to 250 ft a few times a day
LEVEL 4: 4 METS perform adls independently and ambulate up to 1000 ftfew times a day, climb 1 flight of stairs
desbribe phase 2 sub acute conditioning phase of cardiac rehabilitation
begins after hospital discharge in outpatient setting
conditioning exerises are doine with close cardiac monitoring
phase 3 cardiac rehab : intensice rehan phase
exercise in lare groups
resistance training typically intiated in this phaseph
phase IV of cardiac rehab: maintence
patient is encouraged to continue exercise training in a group setting or self monitored program
education on self monitoring for patients with heart disease
-self monitor intensity of activities (pulse, HR, RPE)
awareness of S/S that suggest exercise intolereance
heart disease symptoms recognition and response
should be able to recognize symptoms and know how to respond
call doctor, go to emeregency etc.
written information should be provided
what is congestive heart failure?
a syndrome charcterized by impairment in the hearts pump function. leading cuase of cardiac deaths in north america, most frequent cardiac diagnosis for hospital admissions, insuffient pump to meet metabolic demands of the body both at rest and during activity, m>F
left sided failure, right sided failure/ cor pumonale , bivnetricular failure
pathophysiology of Lsided heart failure
L heart pump is failing- decreased stroke volume, increased L end systolic volume, increased pressure in L ventricle pressures increased L atrial pressure, increased pressure in the pulmonary viens, fluid movment from veins to intersitial space of the lung leading to pulmonary edema
to compensate for decreased SV leads to increase in symapthetic activty to increase HR and maitaine arterial pressure.
left ventircle does not relax completely-stiffenens, weak L ventricle, increased resistance downstream
pulmonary edema, dyspnea, increased WOB, orthopnea, SOb when sleeping, pink frothy sputum, tachypnea, crackles on auscultation
the myocardium may veucome fatigued an worsen failure. eventual decrease in CO decreasing arterial blood flow and decreased perfusion to kidneys–> renal failure.
increased inactivity and bed rest leads to muscle wasting/myopathies osteoporosis. can be compensated by increased HR or uncompensated and worsening
Pathophys of R sided heart failure
failure of the R ventricle. decreased SV, increased end systoloic volume, back up of blood in RA and systemic venous system. systemic hypertension peripheral pitting edema, jv distension, ascites, kidney and brain issues becuase of decreased perfusion
cor pulmonale- enlargement and failure of the right side of the heart due to chronic severe pulmonary hypertension. Right heart is working too hard to pump blood into pulmonary circulation
signs and symptoms of L sided vs R sided heart failure
L: dyspnea, fatigue, weakness, pulmonary edema, paraoxysmal nocturnal dyspnea, orthopnea ( fluid all over lung in supinne affecting gas exahnge)
R: dyspnea, fatigue, weakness, jugular vien distension, peripheral edmema, pitting edema, fluid weight gain, ascities - fluird in belly
intercentions for congestive heart failure
positioning to reduce orthopnea
relaxed breathing exercises
supplmental oxygen
graded increase in ambukation
graded exercise
cardiac rehabiliation program
what is pulmonary edema and pathophys
abnormala acumlatation of fluid in the lungs (often due to LHF)
fluid moves from high pressure pulmonary capillaries into intersitsial space and then into the alveolar space.
P: increased capillary membrane permeability
increased capillary hydrostatic pressure
decreased capillary osmotic pressure
lymphatic insuffiency
Cardiogenic pulmonary edema
high pressure (increased pulmonary capillary hydrostatic pressure), backflow of blodd in the system due to kideny/heartmuscle/valve damage leading to blodd accumlation in pulmonary capilliers which increases pressure
LHF
non cardiogenic pulmonary edema
low pressure, increased permeability of the pulmonary capilaries and alveolar endothelium due to truama or roxins
ARDS
clinical presentaton of pulmonary edema
I: dyspnea, increased work of breathing, cyanoitc, orthopenea, cough with PINK FROTHY sputum
Palpation: tactile fremitus normal to increaseed
P: dull on precussion
A: decreased breath sounds, fine inspiratory crackles/course crackles
decreased PAO2
cadiomelgaly ( increased size of heart), enlarged pulmonary vessles, white fluffy/hazy airspace
what is a pulmonary embolism?
a blood clot that has been lodged in a pulmonary artery, commonly associated with DVT in the lower estremities, life threatening
pathophysiology of PE
pulmonary embolus obstructs bloddflow to an area of the lung, if compltely blocked can lead to infarction and necrosis of lung tissue, very large can lead to increased pulmonary artery resitance and will increase the work load of the R ventricle leading to RHF
Risk factors for PE
immobilization, secondary to increased coagulation, CHF, Hx od DVT, obestiy, pregnancy, stroke, trauma, varcoise veins
clinical presentation of PE
Acute onset of dyspnea, increased RR, chest pain, may have cough with bloddy sputu hemoptysis
decreased PA O2, decreased PaCO2 , increased PH repiratory alkalosis
infarcted area of lung apperars white
diagnosed using CT or V/Q scan
prophalactic post op PE prevention
anticoagulant medication, bed exercises, erarly mobilization, compression stockings- contraindicated in DVT
intervention for suspected or confrimed PE
discontinue exercise and movilization untill further notice, notify nurse or sx, document, increase anticoagulant medication, thrombolytic medication- medications break down clot
what is peripheral vascular disease
refers to disorders of blood vessels of the body, primarly due to artherosclerosis, significant occulsion of vessels must occur before symptoms
S/S of peripheral vascular disease
s/s distal to occulsion
leg pain-intermittent cluadication, coldness in limb, decrease pulses in limb, decreased mobility and fucntion of limb due to pain, possible numbness, pain palness with elevation-BUergers test, decreased heair growth, skiin break down, ulceration (arterial and venous insuffiency ulcers), gangrene in very severe cases-debride clean amputation, delayed healing, shiny/thin/hairless skin
what is intermittent claudication
pain or cramping that occurs in the buttocks or legs (primiarly calves) as a result of poor circulation to affected area
pain increases with activity due to increased metabolic demands of the tissue and not enough blood flow to accomadate
pain decreases with rest
interventions for intermittent claudication
progressive increase in aerobic exercise-may be painful but will stimulate colateral blood flow, education on risk factors and selfmanagment, self assessment of skin and education on skin care. walk into pain, rest untill symptoms decreased and continue
neurogenic claudication
Valvular heart diesase
1) stenosis-failure of valves to open suffienctly and therby impeding flow foward
2) regurigitation- failure of valve to close, thus allows back flow during contraction
tricuspid
pulmonary
bicuspid/mitral-stenosis secondary to rhumatic fever/calcification
aortic-stenosis due to calcification (age, lipd accumlation)/ most common/ can cause LHF, insuffiency/regurgitationback flow can lead to pulmonary edema
5 moments of hand hygeine.
before touching a patient
before clean aseptic procedures
after body fluid exposure or risk of
after touching a patient
adter touching patient surroundings
at least 15 sec
alcohol based hand rub
must use soap and water if hands are visbly soiled
when to use gloves
when contact with blood or body gluids may occur
cahnge between pateints and sites
be aware of touching self clothing and environment
wash hands after removing gloves and when task is complete
when to wear gown
if your clothing may get soliled
wash hands after removing
when to wear mask and eye protection
for all couging patients, procedures whre spalshing may occur
order of donning PPE
sanitze, gown, mask, eye protection, gloveso
order of doffing PPE
gloves, gown, snaitize, goggles, mask, sanitize
contact transmission
transmissionof organisms via skin to skin contact or indireect physical contact with infected environmental surface
MRSA/VRE/ESBL/C-Diff/norovirus/ diarhea
hand hygiene
gloves
gown if contact to patient or their enviro
dedicated equiptment or disinfect before use with other patients
hand hygine after
droplet transmission
transimission of organisms through droplets generated from the respiratory tract. ie. coughing sneezing, talking or respiratory procedure
travel short distances and settle on surfaces
deposit on the nasal or oral mucus of new hosts
mumps, rubella, pertusis, influenza, pneuomnia, meningitis, Acute resp illness
hand hygine, patient wears mask outside the rooom, mask and eye protection within 2m of patient, hand hygine after encounter, clean and disinfect equpitment and surfaces
Airborne transmission
trnasmission of organissms which have become aerosolized and remain suspended in air, are inhaled by a suscpetible host, special ventilation systems are requried to control airborne transmission of icroorganisms
TB/ shingles/ measles/ SARS/ Varcellia
isolation room, negative pressure room, mask on patient outside room, fit tested N95 repiratora dn eye proteection for all health care workers
only imune staff to have contact with patients with measkles or varcella
thoracic surgery
performed in order to remove an irreversibly damage area of the lung
medain sternotomy/ throacotomy
pneumonectomy-removal of a lung
lobectomy- removal of a lobe
segmetal resection- removal of a segment
wedge resection- removal of a portion of a lung
lung voume reduction surgery/bullectomy-removal of large emphysematous tissue
Thoracotomy
commonly performed for lung resections or to remove an irrversibly damage area of the lung
posterior lateral throactomy is the most comon through 4th intercostal space
chest tubes are replaced to evacute air and fluid from pleural space
muscles incised: lats, SA, external intercostoals, internal intercostsalsm, traps, rhomboids
can lye on chest tube as long as it is not kinked or pulled. important to change positions. pneumonectomy-avoid lying with surgical side up untill further ntoice- saline fluid sac-may comprimise.
education to provide the patient in thorocotomy
deep breathing, supportive coughing manequvars, lines, scar managment, relaxation, bed mobility, positioning, transfers, early mobilizationpotential
complications of pulmonary surgery
aspiration, pain, phereic nerve impairment, atlectasis, ulcers, DVT
what is a DVT?
a thrombus/blood clot that forms in a deep vein of the body, most comon in the legs, may partially or completely block blodd flow
can dislodge and travel to lungs/ heart or brain.
venous stasis due to immobility post op can increase risk of DVT along wiht hypercoagulation and changes to blood vessel wall
S/S of DVT?
leg painm tenderness, ankle edema, calf swelling, dialated veins, postive homans sign
how to prevent DVT
early mobilization
ankle pumps
anticoagulants
graded compression stockings
what to do if patient has or DVt is suspected
stop treatment wich may be contrainindcated untill further notice, alert surgeon/ doctor/nurse, document
cardiovascular surgery
often a median strenotomy
a specialized type of surgery invovling the heart and the great vessesl, patient placed on extracorpal memebrane oxygenator or by pass machine due to interupted blood floww during procedure-takes over lung and heart function.
CABG
valve replacment
heart transplant
aortic anersym repair
sternal precuations
strum takes 6- 8 weeks to heal
1. no pushing
2. no pulling
3. no lifting one arm above 90 degrees
4. no hand behind back (toilet, shirt tucking)
5. no driving 4 weeks
6. no lifting greater then 10 lbs
” move within the tube”, gently hug pillow to avoid arm use
benefits of early mobility in cardiac surgery
improves breathing, chest mobility, secretino clearnace, assists in Gi function and bowel mobility, imporves conditioning and activity tolerance, allows increaed independence, improves mood, prevents aspiration/ thrombus/muscle atrophy/contractures/ pressure sores/ neropathy
difference between positive and negative ventilation
negative pressure ventilation sucks air in by increasing space available eg// iron lung, not used as much anymore
postive pressure ventiliation: pushes air in, air is forced in, used when inspiratory muscles are not working effectively or are becoming too fatigued.
indications for mechanical ventilation
1.severe hypventilation, hypoxia, hypoxemia
( apnea, acute hypercarbia, PaCO2 < 50 mm Hg with sup o2, respiratory rate greater then 30 bpm, vital capcity less then 10 litres/ minute, inpiratory force < 25 cm H2 O
2. central depression- decreased LOC, ansetheia or sedation, head injury, drug overdose
3. decreas wirk of breathing and respiratory muscle fatigue
4. poor pulmonary hygeine- secretion clearnace
some complicatinos of mechanical respiration
barotruama-alveolar rupture
volotruama- alveolar over distension
ventilator aquried pneumonia- micro aspiration of gastric or oral secretions
diaphargm atrophy due to disue, causes difficulty with weaning
hemodynamic compromise- over inflation compression of great vessesl decreased venous return therefore decreased cardiac output
3 types of mechanical ventilation
mandatory- intiated and controlled and ended by ventilator
Assisted- intiated by patient but controlled and ended by ventilator
spontaneous-intiated, controlled and ended by patient but volume and pressure deleivered is based on patient demand
3 types of invasive ventilation
continuous mandatory ventilation
assist control ventilation
synchronized intermittent mandatory ventilation
types of non invasive ventilation
CPAP- continuous postive airway pressure
continuous mandatory ventilation
tidala volume and preset respiratory rate deliverd by the ventilator, ventilator provides total support.
when people can not breath at all on their owm, completely sedated, possibly no diaphragm innervation ( High SCI)
Assist control ventilation
tidal volume and minimal number of mandatory breaths per minute delivered by ventilator- will deliver a minimum minute ventilation.
patient is able to intiate inspiration but still reiveces preset tidal voume
if patient does not intiate within a specific time period the ventilator will deliver a breath to maintian the resp rate
synchronized intermittent mandatory ventilation
preset mandatory tiral volume and respiratory rate delivered by ventilator, patient is able to breath spontenously between ventilator breaths
spontaneous patient intiated breathas are synchronized with ventilator breaths
Coninuous positive airway pressure
CPAP.
patients spontaneous breaths are augmented with predetermined level of positive pressure delivered throughout the entire repiratory cycle. keeps airways open continuously in patients who can breath on their own but who require assitance in keeping airways unobstructed. commonly used as a weaning modes for those who are intubated or attempt to postpone intubation.
sleep apnea, neuromucular diseases, acute/chronic resp failure, children with actue resp failure
Positive end expiratory pressure
a positive pressure is applied to the lung at the end of expiratory phase of ventilation, helps to keep alveoli open during expiration and reduces pulmonary shunting
complications: increase in dead space, decreased cardiac output, ventilator associated pneumonia, increased risk of barotrauma
high lelvels can cause excessive alveolar distension or pulmonary baro truama
pressure support ventialtion
patient intiated breaths are augmented by the ventilator to maintain a constand preset inspiratoroy pressure, patiente intiates all breaths and controls respiratory rate and inspiratory time. helps to decrease the work of breathing
weaning from mechanical ventilation
the process of decreasing mechanical ventilation, a spontaneous breathing trial while being closely monitored is typicaly performed to assess readiness to begin weaning process.
are maximal exercise tests within PT scope?
breif description
no!!
administterd by a physician
also known as a stress test
to complete exhaustion
graded
bruce protocol
may use metabolic cart for direct VO2 measure
pre exercise testing
Ax risk for adverse reactions to exercise
prescreen patients s to identofy whether patient is at risk of adverse respone to exercise
screen for those who may require further assessment prior to starting an exercise program
hx, physical examination, lab tests, ris stratification, test selection
risk stratification
- known cardio/metabolic/ or pulmonary disease = high risk ( CVD, stroke. diabetes, renal, copd, asthma, Cf, intistial lung disease)
- have s/s of cardio/metabolic or pulmonary disease= moderate risk
(angina, dizzy, syncope, orhtopneam nocturnal dysna, perpipheral edema, palatiation, hihg HR, intermittent claudication, heart mumor, faitgue, SOB - number of risk factors, <2 =low risk, > or = 2 is moderate risk (age, family hx, smoking, lacohol, sedentary, obestity, HTn, predibetes, dislipedema)
low risk exercise individuals
do not require medical screen prior to exercise program, do not require exercise testingm
moderate risk individuals and exercise
do not rieuiwre medical screeen for light to mod xercise but should be screened before vigourus exercise. do not require exercise testing
high risk individuals and exercise
require medical screen. requie maximal exercise test with MD supervision
CV risk factors (11)
- age men above 45 and women above 55
- family Hx: sudden death, MI or coronary revascularization before 55 in father/brother or before 65 in mother or sister
- PA level: not engaging in at least 30 min 3 x per week
- obesity: high BMI > 30. high waist circumference male > 102, female> 88 high
- pre diabetes: had tests looking into sugars, any history of diabetes
- dyslipedimia: on statins, ldl> 130, HDL<40 , total serum> 200
- HTNsystolic greater then 140, diastolic greater then 90
- stress pshycosocial- high
- smoker: current, quit within last 6 months, second hadn exposure
- alcohol consumption: male > 14 / week, female> 9/week
- diet:
indications for exercise testing
1) diagnostic: work capcity ,movement edurance, onset of s/s, endurance, effect of medicationm evualate progress
2) prognostic-determine liklehood of adverse events, determine surgical risk
3)prescription- what medications might be needed, what exercise programing is appropriate
submaximal exercise testing
may be administered by a PT- not to complete exhasution, are evualative, used as a measure of endurance or exercise capacity, can be used to predict VO2 max
6MWT, modifide Bruce protocol
S/S when to stop an exercise test or to stop exercise
fatigue, SOB, wheezing, poor perfusion: cyanosis/pallar/ lightheaded/confused/ataxia/ cold clammy/ nausea, angina, claudicatin/leg cramps, drop in SBP below resting or greater then 10 mmHG with increasing work rate, SBP > 250 DBP> 115, failure of HR to increase with increasing intensity, noticeable change in heart rhythm, requests to stop, failure of exercise equiptment
goal for respiratory interventions
optimize gas exhange at all levels, which will imporve patients condition, decrease thier symptoms and optimize their function.
positioning for V/Q matching
often the first step in any treatment procedure, optimal gas exhange dependes on ventilation and perfusion. Perfusion however is dependednt on gravity. shunting-good perfusion but poor ventilation/blood passes without gas exhange. dead space-ventilation good but no gas exhange due to no perfusion.
in unilateral lung diseases place the good lung down. bilateral lung disease lie in prone (ARDS) “proning”. pneumonectomy- removeal of lung DO NOT LIE WITH AFFECTED SIDE UP.
positioning to decrease dsypnea
places muscles in mechanically advantageous position, allows postural muscles to relax to decrease energy expenditure.
often a variation of the tripod positioing
diaphragmatic breathing
GOAL: increased ventilation, prevent atelectasis, decrease WOB, assist with secretion removoal
used: post op, resp failure and chronic diseases
deep breaths contraindiacted in overinflated individuals (COPD- can breath with diapragm but not deeply). teaches technique: patient to use diaphagm for breath and decrease use of accessory muscles. belly breathing. diaphragmatice breathing is more energy effient. long slow breaths. additionally promotes relaxation. hands on bellly to guide. 3- 4 breaths a cycle 10 reps per hour
-can add 3- 5 sec breath hold to prevnet atlectasis and increae perfusion time
pursed lip breathing
take breath in through nose and exhale through pursed lips, smell the roses and blow out the candle, exhale should be 3x as long as inhale, creates positive back pressure that stents airways open for longer, increases effeceincy of lung emptying, helps control and reduce resp rate, improve gas exage and promote relaxation
COPD!!
inspiratory muscle training
lifting wieghts for inspiration, aim is to increase strength and endurance of respiratory muscles
uses an inspiratory muscle trainer/ incentive spiraometer with alterable resistance in cm/H2O
strength: 2-4 x per week 60-80% 8-12 reps 1-3 sets
endurance: 4-6x per week, 40-85> 15 min or as tolerated
segmental breathing
localized breathing towards a segement of lung that requires greater expansion or ventilation. uses tactile cues to increase expansion to specific areas
sustained maximal inspiration
mx inspiration sustained for 3-5 sec-breath hold prevents atectasis and increases perfusion time.
incentive spiratormeter uses a device to measure flow or volume
volume: inhale deeply with constant flow kekeeping flow within prescribed ranges
flow: keep ball up and level when inhaling
may be used post up to prevent atlectasis or airway closure
provides visual feed back provides incentive or goal for patient which may imporve patient compliance
inflating lungs to prevent atelectasis
breath stacking
stacking little breaths on top of one anthoer untill maximal capcity is reached followed by relaxed exhale
used when a single deep breath is too pain full or there is weakness in the inspiratory muscles
postural drainage
patient is placed in a position that allows draingage of secretions from bronchial airways via gravity
position is maintained for 5- 10 min or longer if tolerated
face and SpO2 should be monitiored
s/s of intolerance: increased SOB, anxiety, dizziness, hpertension, bronchospasm.
positions can be modified
contraindications for postural drainaige
-inceased ICP > 20 mmHG
-head and neck injury-spinal instability
-active hemmorrhage with hemodynamic instability
-recent spinal surgery or acute spinal injury
-active hemoptysis
-empyema
-bronchial pleural fistula
- pulmonary edema associated with heart failure
- large pleural effusion
-elder, confused or anxious patients
-rib fratures
-surgical woulnd or healing tissues
-pumonary emobolism
-untreted pnsumothroax
contraindications in adults for trendelnburg
-patients who increased ICP needs to be avoidied (TBI, etc)
-uncontrolled hypertension
-distended abdomene
-espophageal X
-recent gross hemoptysis related to lung carcinoma
- uncontroled airway at risk of aspiration
precussions and vibrationss
secretion mobiliation technique, to loosen and dislodge secretions
precussion: hand in cupped position over specific lung segmet, thin towel or gown should cover area, hollow sound, rhytmic, avoid bony promineces, faace and SpO2 should be monitored,
vibrations: only on exhale!!, enhance mucocillary transport, strech of resp muscles, course large amplitude low frequency, fine low amplitude high frequency generally better tolerated,
mechanical vibraition and percussion machines avaialble
use secretion clearnce techniques post
check skin before and after
contraindications for precussions and vibrations
sever osteoporosis
-rib fracture
- pulmonary embolus
-pneumothorax
-anticoagulation therapy
-malignancy
-burns, skin grafts
- open wounds
- increased ICP
- suncutaneous emphysems
-GI bleedding
PEP device gneral
positive expiratory flow device- hand held devices that create back pressure to splint airways while exhaling through device. this back presure allows air to pass through interalveolar connections with rpessure to dislodge or move mucus. can be used with aerosoled medications.
performed > 15 min 2- 3 x per day
low pressure PEP
10-20 cm H2O, more commonly used, equal effectivness to high pressuer but with less risk
high pressure PEP
50-150 cm H2O, PEP mask is used, less used then low presure becuase of risk of pneumothorax
non oscillated PEP devices
theraPEP, thershold PEP
smooth flow, creates back pressure similarly to pursed lip breathing
oscilatting PEP
accapella, flutter- position dependent ball end up increases presure ball end down decreases pressure, cornet, quake, bubbe PEP (kids)
provides accelrated expiratory flow rates and interupts airflow through oscilation/vibration of airways which loosens secretions and helps move them centrally
Active cycle o breathing technique
helps to clear broncial secretions using three ventilatory phases breathing controlled, thoracic expansion, forced expiration techniques
repeated cycles: 1. breathi controled 20 -30 secs, 2. 3-4 deep thoracic expansions to loose secretions can be accompanied by vibrations/precussions/ breath holds . 3. forced expirations 1- 2 huffs to mobilize or a cough to expell
perfomred 10 min /segment, or 3- 4 cycles/ untill secretions are cleared
-can be done in postural drainage positions or sitting
-independent
Autogenic Drainage
varying expiratory flow at various lung volumes to help mobilize secretions from peripheral airways into central airways to be expelled through hiffin gor coughing. 3 phases
1.unstick- exhale to low volumes will mobilize mcus- 5- 6 reps with 3 sec hold on exhale
2.collect- breathing at mid lung volumes 5-6 reps with 3 sec hold on exhalation. taking slightly deeper breaths then normal and exhaling normally
3.evacuate- breathing into larger volumes 5 -6 reps with 3 sec hold.
may perform huff or cough to expell at the end.
-breath through nose diapharmatically
30-45 min session per day
But time consuming, concentration, cognitive capacity, prpropception, skilled PT, active participation
Suctioning
a procedure used to remove secretions through insertion of a cathetor via nasopharynx, oropharync, artifical airway.
to reovme secretions or stimulate a cough when patient is unable to do so independently
when there is visible secretions, ausultations of cracles, tactile fremitus detects, SOB, increased work of breathing, suspected aspiration, hypoxemia, hypercapnia, chest radiographs
- assess outcome after procedure through method that indicated necessity
-a controlled act that requires adequte training, can be delegated
contraindications to suctioning
severe O2 deaturations, increased ICP, hemoptysis, malignant arhythmia, huperinflation post CABG/head injury
nasopharnxy: nasal bleeding, croup, basal skull fracture, actue head/facial injury, CSF leak, nasal stenosis, nasal pathology
potential complications to suctioning
infecton, mucosal truama, hypocia/hypoxemia, heymodynamic instability, laryngo/broncho spasm, atelectasis, pnemothroax, increased ICP, pain, anxeity
minimizing complications with suctinoing
infection control measures (sterile/ wash hands, PPE), hyper oxygenation before can decrease desat, hyperinflation to decrease increase in ICP, limit suction time to 10 - 15 sec per pass, medication and sedation prior to limit pain and anxiety
Huff
forced expiratory technique with an open glottis that may assist to mobilizze and clear secretions from airways
-fog up window
mid to low lung volumes helps to clear peripheral airways
huff from high lung vlumes for clearing procimal airways
huffing perferred to coughing in obstructive lung diseases to decrease air way collapse (cough pressure can collapase small airways
better tolerated in those with coughing pain or weak cough, fatigue due to coughing
cough assist
abdominal thrust, j stroke, quick presure up and in during cough or thoracic asssit through rib cage
helps incrase expiratory flow, indicated in those with neuro or muscular weakness or lots of secretions
contraindicated in those with GERD and recent abdominal surgery, preganancy, abdomina aneruisym, fragile rib cage, elevated ICP, post surgical, thorax spine truama
long sit cough
in parapelegics, deep breath with thrust foward with cough, sudden torso flexion to increase effectiveness
rib springing
chest compression followed by over pressure at end expration
thought to deepedn subsequnet inspiration
usually only a few reps performed
sniff
hypoxemic respiratory failure
gas exhange failure
arterial hypoxemia-low blood O2, no increase in CO2
due to: pneumonia, ARDS, obstructive lung disease, pulmonary embolism
hypercapnic respiratory failure
ventilation issue
too much CO2 in the blood eads to decreased O2 in the blood
depression of resp center by drugs/ acute upper or lower airway obstruction, weak impaired respiratory muscles
DVT
deep vien thrombosis
risk: venous stasis/damage, hypercoagubility, turama, sx, pregancy obestiy, cancer, smoking, genetics
S/S dull ache, tightness/pain in calf, tenderness on plpation, fever, pain with dorsifelxion-HOMANS sign
doppler ultrasonagraphy
anticoagulants
heperin-acute immediate response, warfarin long term
no mobilizaton is halted untill anticoagulation is acheived.
prevent ankle pumps
