ABG, PFT, heart sounds Flashcards
List the normal values for the following:
- pH
- pO2
- pCO2
- HCO3
- BE
- saO2
- pH = 7.35-7.45
- pO2 = 80-100 mmHg
- pCO2 = 35-45 mmHg
- HCO3 = 22-26 mEq/L
- BE = -2 - +2 mEq/L
- saO2 = 95-100%
What is step one of interpreting ABG?
Determine if pH value reflects acidemia or alkalemia
- above or below 7.4
What is step two of interpreting ABG?
Classify the pathophysiologic state on the basis of the relationship between pH and PaCO2 values
- inverse relationship = respiratory
- direct relationship = metabolic
What is step three of interpreting ABG?
Determine the adequacy of alveolar ventilation on basis of PaCO2 value.
- < 30 mmHg= Alveolar hyperventilation
- 30-50 mmHg= Adequate alveolar ventilation
- > 50mmHg= Ventilatory failure
What is step four of interpreting ABG?
Determine the Extent of respiratory and metabolic components.
- absolute value of difference between reported PaCO2 and 40; Divide by 100
- Subtract half of this value from 7.4 if reported PCO2 is > 40; Add the entire value to 7.4 if the reported PaCO2 is < than 40.
- Classify problem as “ACUTE” if reported pH is the same as or farther from normal than expected pH; Classify as “CHRONIC” if the reported pH is closer to normal than expected pH
What is step five of interpreting ABG?
Classify if compensated, partially compensated, or uncompensated
- if pH is normal and PaCO2 and HCO3 are BOTH abnormal, then the patient is compensated
- If pH is abnormal and PaCO2 and HCO3– are BOTH abnormal, then the patient is partially compensated
- If pH is abnormal, and either PaCO2 OR HCO3– are abnormal, then the patient is uncompensated
What causes a right shift in the oxygen dissociation curve?
conditions that enhance release of oxygen
- increased CO2
- Increased DPG 2,3
- Increased exercise
- Decreased pH
- Increased altitude
- increased temperature
What causes a left shift in the oxygen dissociation curve?
conditions that keep oxygen tightly attached to Hb
- decreased CO2
- decreased body temp
- increased pH
What are the levels of oxygen that indicate hypoxemia?
60-80 mm Hg: Mild hypoxemia
40-60 mm Hg: Moderate hypoxemia
< 40 mm Hg: Severe hypoxemia
Normal range:
- adults 60-80 mmHg
- infants 40-70 mmHg
What is the first thing to do when evaluating PFTs?
Look at the time volume plot to determine acceptability
- check for variable effort, cough, early glottic closure
- 6s of smooth continuous exhalation and/or a plateau in the volume time curve of at least 1s
- should have normal early peak, no abrupt cessation of flow, no sharp sudden spikes
What are the lung auscultation sites on the R anterior side of the body?
- R upper lobe apical segment
- R upper lobe anterior segment
- R middle lobe medial segment
- R middle lobe lateral segment
- R lower lobe anterior basilar segment
What are the lung auscultation sites on the L anterior side of the body?
- L upper lobe apical segment
- L upper lobe anterior segment
- L lower lobe anterior basilar segment
What are the lung auscultation sites on the L posterior side of the body?
- L upper lobe posterior segment
- L lower lobe superior basilar segment
- L lower lobe posterior basilar segment
- L lower lobe lateral basilar segment
What are the lung auscultation sites on the R posterior side of the body?
- R upper lobe posterior segment
- R lower lobe superior basilar segment
- R lower lobe posterior basilar segment
- R lower lobe lateral basilar segment
- lingular segment under armpitish area
Values for FVC and FEV1 that are over ___ of predicted are defined as within the normal range
80%
The FEV1/FVC ratio is expressed as a percentage, and a normal young individual is able to forcibly expire at least ___ of his/her vital capacity in one second.
A ratio under ___ suggests underlying obstructive physiology; however, the FEV1/FVC ratio declines as a normal sequelae of aging.
80% ; 70%
- reduced ratio is the primary criteria for diagnosing obstructive lung disease
What would the FEV1 values be to indicate normal, mild, moderate, and severe obstruction?
normal = >80% mild = 65-80% moderate = 50-65% severe = <50%
What shape do flow volume curves make when there is an obstruction
there is a rapid peak then curve descends more quickly than normal and takes on a concave shape, reflected by a marked decrease in FEF 25-75
What values are reduced proportionately with restrictive lung disease?
FEV1 and FVC
- note, FEV1/FVC ratio will be normal or even elevated; can’t get air in but can get it out
What differences will you see on flow volume loop for restrictive disease?
the shape will be the same, but the curve will be much smaller
How do you interpret PFT values?
- look if FEV1 is normal (>80%), or abnormal (<80%)
- look at FEV1/FVC ratio (<80% = obstruction, >80% = possible restriction)
- Look at FVC (>80% = pure obstruction, <80% = can’t r/o concurrent restriction)
What does a thrill on the R base of the heart indicate?
- Aortic stenosis
2. Systemic hypertension
What does a thrill on the L of the heart indicate?
- pulmonic stenosis
2. pulmonic hypertension
What does a heave on the L lower sternal border indicate?
- ventricular hypertrophy
2. chronic lung disease
What could an increase PMI indicate?
- volume overload - L ventricular hypertrophy; displaced lateral and wide spread
- Pressure overload - increase in force and duration but not displaced
When is S1 intensified?
- complete heart block is present (book says this, schulte says this diminishes S1)
- gross disruption of rhythm occurs, such as during fibrillation
- when AV valves wide open with no time to drift together (hyperkinetic state like exercise, fever, hyperthyroidism)
- Calcified valve structure where leaflets still mobile (mitral stenosis)
When is S1 intensity decreased?
- increased overlying tissue, fat, or fluid
- systemic or pulmonary HTN, which contributes to more forceful atria contraction; if ventricle is noncompliant, the contraction may be delayed or dominated, esp if the valve is partially closed when contraction begins
- fibrosis and calcification of diseased mitral valve can result from rheumatic heart disease; calcification diminishes valve flexibility so that it closes with less force (mitral insufficiency)
When is S2 intensity increased?
- systemic HTN, syphillis of the aortic valve, exercise, or excitement
- pulmonary HTN, mitral stenosis, and CHF accentuate pulmonary closure
- if valves are diseased but still mobile; the component of S2 affected depends on which valve is compromised
When is S2 intensity decreased?
- a shock like state which arterial hypotension causes loss of valvular vigor
- The valves are immobile, thickened, or calcified; the component effected depends on involved valve
- aortic stenosis vs pulmonic stenosis - overlying tissue, fat or fluid
Wide splitting occurs when delayed activation of contraction or R ventricle emptying slows pulmonic closure. What condition is this seen in?
- R BBB
- stenosis delays closure of pulmonic valve
- pulmonary HTN delays ventricular emptying
- mitral regurgitation induces early closure of aortic valve
- Aortic valve closes before pulmonic
When does a paradoxical split occur?
- L BBB
- Aortic stenosis
- PDA
- pulmonic closes before aortic
When does a fixed split occur?
- atrial septal defect
- ventricular septal defects with L to R shunting
- R ventricular failure
- occurs with delayed closure of the pulmonic valve when output of the R ventricle > L ventricle
Where is S3 aka “ventricular gallup” heard? what causes it?
heard at apex in L lateral position, L lower sternal border (low pitch)
- Caused by volume overload
1. Mitral, aortic, or tricuspid regurgitation (valve damage)
2. Decreased compliance in ventricles/ CHF
3. BBB - can be normal in young children with thin chest wall
Where is S4 aka “atrial kick” heard? what causes it?
heard at apex, low pitch
- caused by decreased compliance of ventricle
1. CAD, scar tissue after MI or infection
2. Aortic, pulmonic stenosis
3. HTN
4. ventricular hypertrophy
How do you determine the grades of murmurs 1-6?
- Barely audible in quite room
- quiet, but clearly audible
- moderately loud
- loud, associated with a thrill
- very loud, thrill easily palpable
- very loud, audible with stethoscope not in contact with chest, thrill palpable and visible
Timing and description of murmur: early diastole briefly, before S3; high pitch, sharp snap or click; not affected by respiration; easily confused with S2
mitral valve opening snap
Timing and description of murmur: early systole, intense, high pitch; radiates; not affected by respiration
aortic valve ejection click
Timing and description of murmur: early systole, less intense than aortic click; intensifies on expiration, decreased on inspiration
pulmonary valve ejection click
- Low-frequency diastolic robe, more intense in early and late diastole, does not radiate; systole usually quiet; palpable thrill at apex in late diastole common; S1 incr and often palpable at L sternal border; S2 split often with accentuated P2; opening snap follows P2 closely
- visible lift in R parasternal area if R ventricle hypertrophied
- arterial pulse amplitude decr
mitral stenosis
- caused by rhuematic fever or cardiac infection
mid systolic ejection murmur, medium pitch, coarse, diamond shaped crescendo-decrescendo; radiates along L sternal border and to carotid with palpable thrill; S1 often heard best at apex, disappearing when stenosis is severe, often followed bu ejection click; S2 soft or absent and may not be split; S4 palpable; ejection sound muted in calcified valves; the more severe stenosis, the later the peak of the murmurs in systole
- aplica thrust shifts down and left and is prolonged if L vent hypertrophy is present
aortic stenosis
murmur fills systole, diamond shaped, medium pitch, coarse; thrill often palpable during systole at apex and R sternal border; multiple waves in apical impulse; S2 usually split; S3 and S4 often present
- arterial pulse brisk, double wave in carotid common; jugular venous pulse prominent
sub aortic stenosis
- fibrous ring below aortic valve found in septal defect
systolic ejection murmur, diamond shaped, medium pitch, coarse; usually with thrilll S1 often followed quickly by ejection click; S2 often diminished, usually wide split; P2 soft or absent; S4 common in R vent hypertrophy; murmur may be prolonged and confused with that of vent septal defect
pulmonic stenosis
- almost always congenital
diastolic rumble accentuated early and late in diastole, reselling mitral stenosis but louder on inspiration;diastolic thrill palpable over R ventricle; S2 may be split during inspiration
- arterial pulse amplitude decr; jugular venous pulse prominent, esp a wave
tricuspid stenosis
- seen with mitral stenosis
- caused by rheumatic heart disease, congenital defect, endocardial fibroelastosis, R atrial myxoma
holosystolic, plateau-shaped intensity, high pitch, harsh blowing quality, often quite loud and may obliterate S2; radiates from apex to base or to left axilla; thrill may be palpable at apex during systole; S1 intensity diminished; S2 more intense with P2 often accentuated; S3 often present; S3-S4 gallup common in late disease
- apical thrust more to left and down
mitral regurgitation
- caused by rheumatic fever, MI, myxoma, rupture of chordae
typically late systolic murmur preceded by mid systolic clicks, but both murmur and clicks highly variable in intensity and timing
mitral valve prolapse
early diastolic, high pitch, blowing, often with diamond-shaped mid systolic murmur; sounds often not prominent; duration varies with BP; low-pitched, rumbling murmur at apex common; early ejection click sometimes present; S1 soft; S3 split may have drum like quality; M1 and A2 often intensified, S3-S4 gallup common
- in LVH, prominent prolonged apical impulse down and to left
- pulse pressure wide; water-hammer or corrigan pulse common in carotid, brachial and femoral arteries
aortic regurgitation
- rheumatic heart disease, endocarditis, aortic diseases (Marfan syndrome, medial necrosis), syphilis, ankylosing spondylitis, dissection, cardiac trauma
difficult to distinguish from aortic regurgitation on physical examination
pulmonic regurgitation
- secondary to pulmonary HTN or bacterial endocarditis
holosystolic murmur over R ventricle, blowing, increased on inspiration; S3 and thrill over tricuspid area common
- in pulmonary HTN, pulm a. impulse palpable over 2nd L intercostal space and P2 accented; in RVH, visible lift to R of stermun
- jugular v pulse hase large v waves
tricuspid regurgitation
- congenital defects, bacterial endocarditis (esp in IV drug users), pulmonary HTN, cardiac trauma
