Auscultation Flashcards
Bronchial breath sound
air in the alveoli has been replaced by something that is capable of transmitting high frequencies better:
1. pus⇒ pneumonia
2. blood⇒ pulm. hemorrhage
3. serum⇒ pulm. edema
4. solid consolidation⇒ pleural effusion—occupies half of hemithorax
• top= vesicular sound at b/c no fluid here
• middle= bronchial sound
• bottom= no sound at b/c alveoli are totally collapsed here
• The airways are still open—obviously! Otherwise, you wouldn’t hear anything
Crackles:
3 major characteristics:
- Discontinuous (<250msec) explosive pops—so short that they don’t have any musical characteristic
- Can be cleared w/ coughing
- Inspiratory⇒ can figure out pathology based on when during inspiration the crackle occurs:
o Early-insp.= Bronchitis! Lg. central bronchi are coated w/ pus
o Mid-insp.= Bronchiectasis! Medium-sized airways are dilated & coated w/ pus
o Late-insp= Velcro crackles—high-pitched, d/t small peripheral airways being partially crushed then reopening w/ deep brth
- d/t scarring= Pulm. Fibrosis! ⇒ hear w/ vesicular sound
- d/t fluid in alveoli= Pus, blood, serum! ⇒ hear w/ bronchial/tubular sound
Wheezes:
• 1st, identify if vesicular or bronchial ⇒ it’s vesicular, but a little higher pitched than we heard before…sounds like a whale on exhalation
3 major characteristics:
- High pitched
- Expiratory (or both expiratory and inspiratory, but never inspiratory alone!) ⇒ this is Stridor: high pitched, purely inspiratory continuous adventitious sound (comes from larynx)
- Longer than 250 msec, hence their musical quality
• Asthmatic pts:
o Air rapidly flows thru narrowed airway and creates an inward sucking effect on the airway walls, causing the walls to flutter and generate a wheeze
• Thus, it is not the diameter of the airway but the FLOW of air thru it which is responsible for the production of the wheeze…
• This explains why asthmatics in impending resp. failure may not wheeze⇒ they’re too weak to generate airflow
• This explains why breathing too quickly in a forced expiratory flow in a nL pt. will appear to be asthma
o NOT all wheezes are asthma! ⇒ wheezes lack specificity and sensitivity
o Length of wheeze determines severity of asthma (e.g. it’s worse if you wheeze throughout both inspiration & expiration)
• Differential Dx:
o Expiratory wheezes produced by larynx: masquerade as wheezes; d/t adduction over the vocal cords; wheezes are louder over neck
o Cardiac asthma: Wheezing in presence of L ventricular failure (interstitial edema causes airway narrowing)
Vesicular breath sound: NORMAL
• 3 major characteristics:
- Low frequency & pitch, so are soft & muffled
- Short in exhalation (b/c high freq. components are concentrated in last 2/3 of exhalation, and alveolar air inhibits high freq. sounds—recall that air doesn’t transmit sound as well as solid or liquid)
- NO silent pause b/c insp. & exp.
- What should normally be heard over lungs (tubes muffled by overlying air)
Rhonchi
• Like wheeze, is imposed on an underlying vesicular breath sound
• 4 major characteristics:
1. Low pitched
2. Early expiratory
3. Snoring quality (or kinda like a woman having sex?!)
4. Longer than 250 msec, so qualify as continuous
- Generated like a wheeze⇒ are flows thru a narrow airway; in this case, narrowing is d/t inspissated secretions (so are present in obstructive lung diseases)
- coarser and lower pitched than a wheeze…Are often localized⇒ if this is persistent, you need to worry about an endobronchial neoplasm (should just go away when asthma subsides)
Pleural friction rub:
- Like rhoncus, is imposed on an underlying vesicular breath sound
- Short, explosive, and sounds like a series of crackles in both inspiration & expiration
- Sounds like driving on a rocky road
4 reasons why they are not crackles:
- ***Rubs are both insp. & exp. (crackles are usually just inspiratory!) ***
- Rubs don’t clear w/ coughing (crackles do!)
- Rubs are usually localized over the chest (crackles tend to be bilateral!)
- Rubs are palpable (crackles are NOT palpable!)
Seen in 3 diseases:
- Bacterial pneumonias *rarely seen in TB, lung ca., or pleural effusions*
- Collagen vascular diseases
- Pulmonary infarcts
Whispered pectoriloquy:
- Can hear whispered or spoken words b/c all the alveolar air has been removed (lung is consolidated!!!) (usually, high pitched vowels are filtered out and only soft and low pitched sounds get thru)
- Testing for ergophony: loss of alveolar air makes “eee” sound like “aaa”
Opening snap:
Auscultation
- Heard with bell in left lateral decubitus
- Opening snap
- Loud S1 (thickened leaflets)
- Mid-to-late diastolic rumble (pushing against stenotic mitral valve)
- Crescendo–> decrescendo–> crescendo (presystolic accentuation)
Physical symptoms
- Dyspnea
- Hemoptysis
Physical signs
- Atrial fibrillation
- Mitral facies – purple nose/cheeks
- JVP: giant V wave of regurgitation
Cause
- Rheumatic disease
Aortic Regurgitation with Systolic flow murmur
Auscultation
- Blowing, diastolic, heard at right 2nd intercostal space or Erb’s point
- Soft S1, tambour S2 (if due to dilation of aortic root)
- May have murmur of functional mitral stenosis (Austin Flint)
- May have systolic ejection sound (indicates severe insufficiency)
Physical symptoms
- Left-sided heart failure = dyspnea on exertion, orthopnea, PND
- Palpitations, chest pain, pounding in chest
Physical signs
- Water hammer pulse; bisferiens pulse
- Wide pulse pressure
- Inferolaterally displaced PMI (indicates volume overload)
- Everyone’s sign: deMusset, Traube, Quincke pulse, Mueller, Duroziez, etc.
Causes
- Rheumatic fever
- Bicuspid aortic valve
- Infective endocarditis
- Dilated aortic root (Marfan syndrome, tertiary syphilis, dissecting aorta)
Pericardial friction rub:
- Crackling of leather, scratching, scraping, squeaking, grating, and fleeting
- Gallop-like lilt; sounds like S3 (Kentucky)→ doesn’t qualify as a gallop, though, b/c it’s too loud
- SOUND Increases on exhalation, decreases on inhalation
JVP: **Kussmaul’s sign:
- Increase in JVP with inspiration
- Decrease in JVP with exhalation**
Has up to 3 components: 1 systolic, 2 diastolic
- Ventricular contraction= mid-systolic
- Ventricular filling= early-diastolic (equiv. to S3—gives the gallop-like lilt)
- Atrial contraction= late-diastolic
Heard all over, but are loudest along L parasternal area & lower L sternal border
• Can be palpable, just like pleural friction rubs
Associated w/ diseases characterized by inflammation of pericardium:
o Pericarditis
o Acute MI
o Dressler’s Syndrome (post-MI syndrome)
o Pulmonary Embolism (rare)
o Metastatic involvement of pericardium (rare)
o 10-20% of tamponades / pericardial effusions have rubs (b/c the effusion is localized—some areas aren’t coated in fluid so can still rub)
Differentials:
o 3-component rub may sound like a ventricular gallop (S3 Kentucky)
o 1-component rub may sound like a systolic ejection murmur
S3 Gallop- seen in volume overloaded states
- Low-pitched, soft, early diastolic sound that is best heard over apex in LL decubitus w/bell
- Is most impt. extra sound, but is really hard to hear so you have to aggressively seek it out ⇒ higher pitched, louder, & not as long as S4
- Is more palpable than audible in pts. w/ LV hypertrophy
Produced by sudden deceleration in LV flow at the end of rapid filling; 3 major causes:
1. **Bradycardic athlete (physiologic S3): ** blood just flows into ventricles quickly / inc. LV preload
2. Diastolic Overload:
• AV valve regurg. (esp. mitral—so will be accompanied by systolic murmur)
• VSD or PDA (NOT ASD)
• Aortic valve regurg (bad news—indicates LV dysfxn, unlike mitral regurg)
3. abnL LV compliance/floppy heart (heart failure, early in MI, dilated cardiomyopathy—accompanied by low-pitched diastolic murmur d/t sudden rush of blood across AV valve)
• Can see from algorithm that it’s in early diastole→ this is when ventricle starts filling
• Can have a physiologic S3 (like athlete), but if it’s a gallop (Kentucky: Ken=S1, Tuc=S2, Ky=S3) it’s pathologic (or if hear S3 above age 40)
Other physiologic S3’s:
• hyperkinetic heart syndrome (catecholamines, inc. sympathetic tone)
• pregnancy *these may also have venous hum at neck*
• Hemodynamics:
o Dec. ejection fraction (<30%– indicates poor systolic fxn)
o Inc. atrial filling pressure (>25mmHg)
• Right Ventricular S3:
o d/t tricuspid regurg, inc. impedance to RV emptying (cor pulmonale, massive PE)
o best heard over L lower sternal border, NOT apex like L-sided
o louder w/ inspiration, not expiration like L-sided (Carvallo maneuver)
Mid-systolic click due to MVP:
• Short, high-pitched,
• Not a gallop b/c too loud and not lilty
• Is Mitral Valve Prolapse (MVP)!!!!
Sound is d/t “Chordal Snap”- tension of chordal apparatus as leaflets snap back
o Not all mid-late systolic clicks are assoc. w/ murmur, although murmur is common in MVP
o NOTE: 5-15% of MVP pts. get a diastolic click, which is d/t ballooning of the valves in the opposite direction
• Bedside maneuvers are impt b/c they inc. or dec. LV size:
Inc. LV size pulls down on ballooning valve, thus delaying prolapse, decreasing murmur:
• Exhalation
• Bradycardia
• Passive leg raising
• Squatting
o Dec. LV size decreases preload, so murmur is made louder:
• Inspiration
• Tachycardia
• Straining in Valsalva
• Standing
Treatment: Beta-blockers to increase pre-systolic load, prevent prolapse
Patent Ductus Arteriosis:
Auscultation:
- Continuous, machinery-like, train-in-tunnel, to-and-fro
Physical symptoms
- Dyspnea, easy fatigability
- Tachycardia
Physical signs
- Differential cyanosis (i.e. “half a smurf”) – cyanosis of lower extremities but not the upper
- Clubbing (can also be differential)
- Cyanosis + clubbing = signs of Eisenmenger’s syndrome (pulmonary hypertension and reversal of shunt)
Cause
- Congenital rubella infection
- Genetic factors
Early systolic ejection sound:
Auscultation
- Heard at apex
- No murmurs
- Extra sound closest to S1
Physical symptoms
- None
Physical signs
- None
Cause
- Congenital bicuspid aortic valve
Complications
- Early-onset aortic stenosis/regurgitation
- Predisposed to endocarditis
Aortic stenosis:
Auscultation:
- Crescendo-decrescendo, mid-systolic, harsh, heard at right 2nd intercostal space, radiates to carotids
- Soft/absent S2
- May have S4
- May have Gallavardin phenomenon (sounds like MR at apex)
Physical symptoms
- Dyspnea, dizziness, and angina on exertion
- Physical signs
- Pulsus parvus et tardus and brachio-radial delay
- May have prominent A-wave (Bernheim phenomenon)
- Sustained and mildly-displaced PMI with apical thrill
Cause
- Bicuspid aortic valve
- Rheumatic fever
- Degenerative changes
S4 Gallop:
o More common than S3
o Soft, but not as soft as S3 (although it kinda just sounds like a salt shaker)
o Easier to palpate than S3 (a palpable S4 should always be considered pathologic!)
Clinical implications are more benign than S3
- Sometimes considered a nL sound of aging, caused by the reduction in ventricular compliance d/t hypertrophy (HTN) or fibrosis (ischemia) (STIFF HEART!).
Other examples of stiff heart / thick ventricle:
- Aortic stenosis
- Coarctation of aorta
- Hypertrophic cardiomyopathy (almost always has audible, palpable S4: triple ripple) *once ventricular hypertrophy becomes failure (flaccid) S4 softens, disappears, and you’re just left w/ S3*
- Coronary Artery Disease / MI (v. common in MI!)
- Prolonged PR interval
- In order for it to be a gallop, it must have the characteristic “**Tennessee” lilt and tachycardia ** (Ten= S4 nee= S1 See= S2)
- NOT generated by atrial contraction per se, but by resulting forceful tension of the ventricle/AV valve apparatus
R vs. L:
- R sided S4= lower L sternal border or subxyphoid + distended neck vv. w/ lg. A or V waves (booming A from R Atrium!), loud P2, louder on inspiration
• Differentials:
o Split S1 *both of these differentials use diaphragm (not bell), do not change w/ sitting/standing, and can be heard all over chest*
o S1-ejection click complex
Mitral regurgitation:
Auscultation:
- Blowing, holosystolic, heard at apex, radiates to axilla
- May have diastolic flow murmur (indicates severe insufficiency)
- Soft S1
- Widely split S2 (early closure of aortic valve)
- S3 is common
Physical symptoms
- Left-sided heart failure = dyspnea on exertion, orthopnea, PND
Physical signs
- May have bounding pulse but NORMAL pulse pressure
- Inferolaterally displaced PMI (indicates volume overload)- Double PMI, single carotid
Cause
- Dilated cardiomyopathy
- Rheumatic heart disease
- Mxyomatous valve degeneration (will also hear mid-systolic click)
- Papillary muscle/chordae tendineae rupture (MI, endocarditis, etc.)
Mitral stenosis with opening snap:
Auscultation
- Heard with bell in left lateral decubitus
- Opening snap
- Loud S1
- Mid-to-late diastolic rumble
- Crescendo–> decrescendo–> crescendo (presystolic accentuation)
Physical symptoms
- Dyspnea
- Hemoptysis
Physical signs
- Atrial fibrillation
- Mitral facies – purple nose/cheeks
Cause
- Rheumatic disease
Amphoteric breath sounds
- Late inspiratory crackles
- Early expiratory wheeze
- Funky breath sound!!! ⇒ is like blowing air into jug (really, air is blowing into a cavity, like in TB!)
Aortic regurgitation with tambour
Auscultation
- Blowing, diastolic, heard at right 2nd intercostal space or Erb’s point
- Soft S1, tambour S2 (if due to dilation of aortic root)
- May have murmur of functional mitral stenosis (Austin Flint)
- May have systolic ejection sound (indicates severe insufficiency)
Physical symptoms
- Left-sided heart failure = dyspnea on exertion, orthopnea, PND
- Palpitations, chest pain, pounding in chest
Physical signs
- Water hammer pulse; bisferiens pulse
- Wide pulse pressure
- Inferolaterally displaced PMI (indicates volume overload)
- Everyone’s sign: deMusset, Traube, Quincke pulse, Mueller, Duroziez, etc.
Causes
- Rheumatic fever
- Bicuspid aortic valve
- Infective endocarditis
- Dilated aortic root (Marfan syndrome, tertiary syphilis, dissecting aorta)
Bronchial sounds with late inspiratory crackles:
Presumably due to alveolar infection/pus/fluid in alveoli conducting bronchial sounds, causing late inspiratory crackles
Bronchial sounds:
• If you hear this, it means that the air in the alveoli has been replaced by something that is capable of transmitting high frequencies better:
1. pus⇒ pneumonia
2. blood⇒ pulm. hemorrhage
3. serum⇒ pulm. edema
4. solid consolidation⇒ pleural effusion—occupies half of hemithorax
• top= vesicular sound at b/c no fluid here
• middle= bronchial sound
• bottom= no sound at b/c alveoli are totally collapsed here
• The airways are still open—obviously! Otherwise, you wouldn’t hear anything at all!
Crackles:
3 major characteristics:
1. Discontinuous (<250msec) explosive pops—so short that they don’t have any musical characteristic
2. Can be cleared w/ coughing
3. Inspiratory⇒ can figure out pathology based on when during inspiration the crackle occurs:
o Early-insp.= Bronchitis! Lg. central bronchi are coated w/ pus
o Mid-insp.= Bronchiectasis! Medium-sized airways are dilated & coated w/ pus
o Late-insp= Velcro crackles—high-pitched, d/t small peripheral airways being partially crushed then reopening w/ deep brth
• d/t scarring= Pulm. Fibrosis! ⇒ hear w/ vesicular sound *see algorithm*
• d/t fluid in alveoli= Pus, blood, serum! ⇒ hear w/ bronchial/tubular sound
late inspiratory squeak and crackles: probably due to pulmonary interstitial fibrosis
Squeak=
- Pulmonary fibrosis
- Bronchiolitis obliterans
- Allergic alveolitis
Late crackles=
- pus/fluid/blood in alveoli- bronchial sound
- Interstitial scarring (fibrosis- silicosis, asbestosis)- vesicular sound
