Cardiac, Pulmonary, and PV Exam Flashcards

Question

1. Discuss the following common or concerning symptoms, the etiology, presentation, as well as appropriate history questions to aid in the evaluation of patients presenting with such complaints. Discuss the significance of responses. Shortness of breath: dyspnea, orthopnea, paroxysmal nocturnal dyspnea

Answer 1

f the patient is short of breath, does this occur at rest, during exercise, or after climbing stairs? Dyspnea- uncomfortable awareness of breathing that is inappropriate to a given level of exertion complaint is common in patients with cardiac or pulmonary problems. Orthopnea- dyspnea that occurs when patient is supine and improves when patient sits up ask number of pillows and how they sleep. PND- episodes of sudden dyspnea and orthopnea awaken patient from sleep 1-2 hours forcing to stand up or get air. W/ associated wheezing and coughing subsides but usually reoccurs. Sudden dyspnea occurs in pulmonary embolus, spontaneous pneumothorax, and anxiety. Orthopnea and PND- occur in left ventricular HF and mitral stenosis, obstructive lung disease. PND mimicked by nocturnal asthma attacks.

Answer 2

)- Can absorb up to 5L of fluid before pitting occurs can be systemic or local. Have you had any swelling anywhere? Where (ankles)? When does it occur? Worse in morning or at night? Do your shoes get tight? Rings tight on fingers? Eyelids puffy or swollen in morning? Let out your belt? Clothes gotten tight? Associated symptoms (infection) Ask to record daily weight. Frequently cardiac causes (right or left ventricular dysfunction, pulmonary hypertension or pulmonary (obstructive lung disease). Can be nutritional (hypoalbuminemia), and/or positional. Dependent edema appears in lowest body parts: feet and lower legs when sitting or sacrum when bedridden. Anasarca severe generalized edema extending to sacrum and abdomen. Look for perioorbital puffiness and tight rings of nephrotic syndrome and an enlarged waistline from ascites and liver failure. right/left ventricular dysfunction, pulmonary hypertension, hypoalbuminemia (changing oncotic pressure from bad nutrition), allergic reaction, infection, liver/renal disease, lymphatic dysfunction (lympadema, damage to lymphatic tissue), dependent/positioning. 1+-4+. If immediately refills-1+, after 15-20seconds 2+, 3+ 1 minute, 4+ anything longer.

Answer 3

Most of anterior portion of heart is right ventricle. Listening for apical pulse at point of maximal intensity around 4ht-5th intercostal space midclavicular line. Braciocephalic vein (internal jugular becoming subclavian and external jugular vein). Aortic arch (brachiocephalic trunk (right common carotid right subclavian, common carotid left subclavian) PMI larger than 3cm indicated ventricular enlargement. young adults may have hyperkinetic impulse when excited or after exercise occur in hyperthyroidism, severe anemia, pressure overload of left ventricle from hypertension or aortic stenosis, or volume overload of left ventricle from aortic regurgitation. Sustained high-amplitude impulse increased LVH from pressure overload seen in hypertension. diffuse sustained low-amplitude hypokinetic impuslse seen in heart failure and dialted cardiomyopathy.

Answer 4

top of the heart located at the second intercostal interspace above the left atrium

Answer 5

try locating when patient lays supoine finding vertical location and distance from midclavicular at the 5thor 4thinterspace. ex. pregnancy or high left diaphragm may shift upward and to left. lateral displacement toward axillary from ventricular dilation in heart failure, cardiomyopathy, ischemic heart disease, thoracic deformities, and mediastinal shift. in left lateral decubitis diffuse diastole- period of ventricular relaxation where blood flows from atrium to ventricle, ventricular pressure rises late in this cycle due to atrial contraction. aortic valve closed preventing regurgitation of blood from aorta to LV, mitral open allowing blood from left atrium to LV. Pulmonic valve closes and tricuspid opens.

Answer 6

difficulty breathing caused by asthma attack, COPD, CHF etc.

Answer 7

efers to accumulation of excessive fluid in extravascular interstitial space can be caused by CHF, infection

Answer 8

-to blood vessels caused by hypertension, cardiac hypertrophy other degenerative cardiac ofr vascular disease

Answer 9

Heart murmurs are distinct heart sounds distinguished by their pitch and their longer duration. They are attributed to turbulent blood flow and are usually diagnostic of valvular heart disease.

Answer 10

difficulty breathing when laying down relived by sitting up ex. caused by edema

Answer 11

episodes of difficulty breathing particularly at nighttime that wake you up from sleep

Answer 12

- left ventricle tapered inferior tip, cardiac apex and is the point of maximal impulse. Locates left border of heart found in 5thintercostal space at or or just medial to left midclavicular line (7-9cm) not always palpable on a healthy patient w/ a normal heart. detection affected by pt’s habitus and position. diameter should be up to quarter or 1-2.5 cm,

Answer 13

valve that does not fully close letting blood flow back from where it came as seen in mitral and aortic regurgitation.

Answer 14

when valve narrows prevent valve from opening fully reducing or blocks blood flow from heart into body as seen in mitral and aortic stenosis

Answer 15

period of ventricular contraction, pressure in LV rises from 5mmhg to 120mmhg pressure falls. aortic valve open allowing ejection of blood from LV to aorta, mitral close preventing regurgitation. Pulmonic valve opens tricuspid closes.

Answer 16

- found in the jugular venous is found in children up to adulthood and has both systolic and diastolic components benign sound produced by trubulence of blood

Answer 17

found by PMI \>2.5 cm from hypertension or aortic stenosis if the PMI is displaced to midclavicular line or \>10cm lateral to midsternal line also an indicator as well as ventricular dilatation MI or CHF. COPD pt’s PMI in xiphoid or epigastric area also due to this phenomenon

Answer 18

aorta- curves upward from left ventricle to level of sternal angle, arching posteriorly to left and downward. aortic valve apical impulse- PMI inferior vena cava- medial border of sternum left ventricle mitral valve pulmonary artery pulmonary artery pulmonary veins pulmonic valve right atrium right ventricle superior vena cava- medial border of sternum tricuspid valve

Answer 19

Blood that has been through systemic circuit returns by superior & inferior venae cavae to right atrium through AV (tricuspid) valve into right ventricle. When right ventricle contracts, ejects blood through pulmonary valve into pulmonary trunk or artery (only arteries in body carrying deoxygenated blood to lungs) exchanging CO2 and O2 at lungs. Blood returns from lungs by two pulmonary veins (only veins carrying oxygenated blood) on left and two on right where they empty into left atrium. Blood flows through left AV (mitral valve) to left ventricle w/ contraction ejecting blood through aortic valve into ascending aorta and through systemic circuit.

Answer 20

During diastole, pressure in the blood- filled left atrium slightly exceeds that in the relaxed left ventricle, and blood flows from left atrium to left ventricle across the open mitral valve. Just before the onset of ventricular systole, atrial con- traction produces a slight pressure rise in both chambers. During systole, the left ventricle starts to contract and ventricular pressure rapidly exceeds left atrial pressure, closing the mitral valve. Closure of the mitral valve produces the first heart sound, S1. As left ventricular pressure continues to rise, it quickly exceeds the pressure in the aorta and forces the aortic valve open. In some pathologic conditions, an early systolic ejection sound (Ej) accompanies the opening of the aortic valve. Normally, maximal left ventricular pressure corresponds to systolic blood pressure. As the left ventricle ejects most of its blood, ventricular pressure begins to fall. When left ventricular pressure drops below aortic pressure, the aortic valve closes. Aortic valve closure produces the second heart sound, S2, and another diastole begins. Semilunar valves- semilunar valves open when ventricular pressure higher than aortic pressure close when aortic pressure higher than ventricle as blood is pumped out beginning S2 ventricular lower than atrial pressure AV valves open for relaxation.

Answer 21

``` S1 lub (valvular closure of AV valves, blood flow): Left ventricular Systole- ventricular contraction blood pumped into pulmonary artery to get oxygenated. Right ventricular systole- ventricular contraction blood pumped to body, Mitral valves open. S2- diastole dub blood entering through AV valves through pulmonary veins into left atrium into ventricle. Right side comingin from superior and inferior vena cave semilunar not open. In diastole, left ventricular pressure con- tinues to drop and falls below left atrial pressure. The mitral valve opens. This event is usually silent, but may be audible as a pathologic opening snap (OS) if valve leaflet motion is restricted, as in mitral stenosis. After the mitral valve opens, there is a period of rapid ventricular filling as blood flows early in diastole from left atrium to left ventricle. In children and young adults, a third heart sound, S3, may arise from rapid deceleration of the col- umn of blood against the ventricular wall. In older adults, an S3, sometimes termed “an S3 gallop,” usually indicates a patho- logic change in ventricular compliance. Finally, although not often heard in nor- mal adults, a fourth heart sound, S4, marks atrial contraction. It immediately precedes S1 of the next beat and can also reflect a pathologic change in ventricular compliance. ```

Answer 22

Right ventricular and pulmonary arte- rial pressures are significantly lower than corresponding pressures on the left side. Mitral component: louder and earlier. Tricuspid component: softer and later. S1 splitting does not vary with respiration. Note that right-sided cardiac events usually occur slightly later than those on the left. Instead of a hearing a single heart sound for S2, you may hear two discernible components, the first from left-sided aortic valve closure, or A2, and the second from right-sided closure of the pulmonic valve, or P2. The second heart sound, S2, and its two components, A2 and P2, are caused pri- marily by closure of the aortic and pulmonic valves, respectively. During inspira- tion, the right heart filling time is increased, which increases right ventricular stroke volume and the duration of right ventricular ejection compared with the neighboring left ventricle. This delays the closure of the pulmonic valve, P2, splitting S2 into its two audible components. During expiration, these two com- ponents fuse into a single sound, S2. Note that because walls of veins contain less smooth muscle, the venous system has more capacitance than the arterial system and lower systemic pressure. Distensibility and impedance in the pulmonary vascular bed contribute to the “hangout time” that delays P2. Of the two components of the S2, A2 is normally louder, reflecting the high pressure in the aorta. It is heard throughout the precordium. In contrast, P2 is relatively soft, reflecting the lower pressure in the pulmonary artery. It is heard best in its own area, the 2nd and 3rd left interspaces close to the sternum. It is here that you should search for the splitting of S2. S1 also has two components, an earlier mitral and a later tricuspid sound. The mitral sound—the principal component of S1—is much louder, again reflecting the higher pressures on the left side of the heart. It can be heard throughout the precordium and is loudest at the cardiac apex. The softer tricuspid component is heard best at the lower left sternal border; it is here that you may hear a split S1. The earlier louder mitral component may mask the tricuspid sound, how- ever, and splitting is not always detectable. Splitting of S1 does not vary with respiration.

Answer 23

Jugular venous pressure ( JVP) reflects right atrial pressure, which in turn equals central venous pressure and right ventricular end-diastolic pres- sure. The JVP is best estimated from the right internal jugular vein, which has the most direct channel into the right atrium. Changing pressures in the right atrium during diastole and systole produce oscillations of fill- ing and emptying in the jugular veins, or jugular venous pulsations (Fig. 9-20). Atrial contraction produces an a wave in the jugular veins just before S1 and systole, followed by the x descent of atrial relaxation. As right atrial pressure begins to rise with inflow from the vena cava during right ventricular systole, there is a second eleva- tion, the v wave, followed by the y descent as blood passively empties into the RV during early and middiastole. With each contraction, the left ventricle ejects a volume of blood into the aorta that then perfuses the arterial tree. As the ensuing pressure wave moves rapidly through the arterial system it generates the arterial pulse. Internal jugular pulsations: rarely palpable, soft biphasic undulating quality, usually w/ two elevations and characteristic inward deflection, pulsations eliminated by light pressure on veins just above sternal end of clavicle, height of pulsations changes w/ position, normally dropping as patient becomes more upright, height of pulsations usually falls with inspiration. Carotid pulsations: palpable, more vigorous thrust w/ single outward component, pulsations not eliminated by pressure on veins at sternal end of clavicle, height of pulsations unchanged by position, height of pulsations not affected by inspiration. Look for carotid artery medially superior to sternal notch between sternocleidomastoid for the carotid artery pulsation vigorous thrust w/ visible outward component almost always palpable and doesn’t change w/ position. Lateral to that between sternocleidomastoid and clavicularhead should be the internal jugular venous pulsation are soft undulating pulsations with three elevations per heartbeat and 2 troughs per beat and is rarely palpable eliminated by light pressure above clavicle and change with position in euvolemicpatient level dropping as patient becomes more upright level falls w/ inspiration. Internal Jugular: Rarely palpable flicker wave Soft and eliminated with light pressure. Height changes with position and respiration. (when sit them up goes lower) Carotid: Palpable Vigorous and not eliminated with light pressure. Height unchanged with position or respiration. Carotidpulse asses valvularheart disease detects aortic stenosis and insufficiency. Palpation to asses amplitude and contour of carotid upstrakeand ausculatationfor the presence or absence of bruits from turbulent blood flow. Don’t press on both at once. Increase pressure until you feel maximal pulsation then decrease pressure until you sense the arterial pressure wave and contour asses amplitude of pulse (pulse pressure speed of upstroke brisk smooth and rapid following S1 immediately. Summit is smooth round and roughly at systolic, downstrokeis less abrupt than the upstroke) can detect bounding upstroke etc. Shouldn’t move,change w/ movement.

Answer 24

· Atrioventricular (AV) node- low in atrial septm · Bundle of His · Left bundle branch · Right bundle branch · Sinoatrial (SA) node-in RA near junction of vena cava

Answer 25

The small P wave of atrial depolarization (duration up to 80 milliseconds; PR interval 120 to 200 milliseconds) The larger QRS complex of ventricular depolarization (up to 100 milliseconds), consisting of one or more of the following the Q wave, a downward deflection from septal depolarization the R wave, an upward deflection from ventricular depolarization the S wave, a downward deflection following an R wave A T wave of ventricular repolarization, or recovery (duration relates to QRS)

Answer 26

JVP accurately predicts elevations in fluid volume in heart failure, prognostic value for heart failure outcomes and mortality is unclear. Parallels pressure in right atrium, or central venous pressure, relating to volume in venous system best assessed from pulsations in right internal jugular vein in line with superior vena cava and right atrium. Able to detect volume status, right and left ventricular function, patency of tricuspid and pulmonary valves, pressure in pericardium, and arrhythmias caused by junctional rhythms and AV blocks falling with loss of blood or decreased venous vascular tone increases with right or left heart failure, pulmonary hypertension, tricuspid stenosis, AV dissociation, increased venous vascular tone, and pericardial compression or tamponade. Find highest point of oscillation in internal jugular vein using tangential lighting or where external jugular vein collapsed measured in vertical distance above sternal angle. If patient hypovolemic JVP will be low causing you to lower head of bed to see it, if patient is volume-overloaded hypervolemic JVP will be high cuaisng you to raise it. Seen in tricuspid stenosis, chronic pulmonary hypertension, superior vena cava obstruction, cardiac tamponade, and constrictive pericarditis. First eleveation, presystolic a wave (abnormally prominent a waves in increased resistance to right atrial contract-tricuspid stenosis, 1st,2nd,3rddegree AV block, supraventricular tachycardia, junctional tachycardia, pulmonary hypertension, and pulmonic stenosis signal atrial fibrillation) is slight rise in atrial pressure accompanies atrial contraction prior to S1 before carotid upstroke, trough x descent, starts w/ atrial relaxation continues as RV, contracting during systole pulls floor of atrium downward, ends before S2. during ventricular systole, blood continues to flow into right atrium from venae cavae. tricuspid valve closed and chamber begins to fill and right atrial pressure begins to rise again, creating second elevation v wave (increased in tricuspid regurgitation, atrial septal defects, and constrictive pericarditis) when opens early in diastole blood in right atrium JVP parallels pressure in the right atrium or primary volume in the venous system. Measurement of pulsations in the right internal jugular vein provides best accuracy. Highest point of pulsation in the internal jugular or external jugular vein. Jugular Venous Distension (JVD): Visualization of jugular vein. Is a sign of increased central venous pressure which may commonly suggest right sided heart failure, pulmonary hypertension. flows passively into RV and right atrial pressure falls again creating second trough. Measurement of the highest oscillation point (“meniscus”) of jugular venous pulsations, reflects pressure in the right atrium (ventral venous pressure). Provides information about volume status and cardiac function. Pillow just above shoulders. Examine both sides of neck and turning to the left on right side. Patient is placed in supine position with head of examination table elevated to 30 degrees. Ruler placed in the vertical plane with zero at the sternal angle. Place additional straight edge at the top of the jugular pulsation. Normal is less than or equal to 3 cm or 7-8cm in total distance above right atrium. Vertical distance in centimeters above sternal angle where your card crosses ruler How much pressure is required to force a column of water x number of centimeters up. Force require to move column of water up the head. Use cardor something flat from meniscus highest point of pumping line up on sternal angle at right angle Important for us to test in euvolemic, hypervolemic(ex. CHF or renal failure) (as high as angle in jaw), or hypovolemic patients (ex. GI bleed, marked dehydration) below sternal angle.

Answer 27

After examining the JVP and carotid pulse, inspect and palpate the precordium: the 2nd right and left interspaces; the RV; and the LV, including the apical impulse (diameter, location, amplitude, duration). Left sternal border in 3rd, 4th, and 5thinterspaces w/ patient supine and head elevated ask patient to exhale and briefly stop breathing, plcing fingers to palpate systolc impulse of RV assessing LAD may detect systolic tap in thin individuals or S3 and S4 right sided movements time against upstroke. sustained left parasternal movement beginning at S1 points to pressure overload from pulmonary hypertension and pulmonic stenosis or chronic ventricular volume overload of atrial septal defect sustained movement later in systole seen in mitral regurgitation. Palpation: Heaves/Lifts (can see heart pumping through chest wall- Use palm and or fingertips. Ventricular pulses heave and lift fingers suggesting ventricular delitation. Thrills (underlying turbulent blood flow change grading of heart) ball of hand revealing a loud murmur. Right Ventricular Area (systolic impulse)-Left sternal border. Epigastric Area. Should not be feeling impulses there could be because of an enlarged ventricle Pulmonic Area. Aortic Area. PMI- Left Mid-clavicular line, 4thand 5thinterspaces. Just below the nipple. 2.5 cm. Measure less than.Underneath nipple can feel PMI, can see movement underneath. Percuss for resonant should hear for lungs filling. Percuss medially until you get to border and you can feel and measure the border of the heart shouldn’t be larger than 2.5cm. Would be further right if they have hypertrophy Thrills-over the cardiac valve points.- 3, 4, and 5thintercostal spaces should not be feeling impulses at all. Feel for right ventricular impulse at lower left sternal border while keeping one finger in 3rdinterspace then feel for right ventricular impulse in subxiphoid area. If patient’s chest has increased anteroposterior diameter palpate for right ventricular impulse high in epigastric area where it is easier to feel found in COPD due to increased right ventricular pressure and hypertrophy from pulmonary hypertension.

Answer 28

All patients eventually trust me. Pulmonic (right intercostal space sternal border. Left atrium is posterior, right atrium is superior right netierh examined directly. Pulmonary artery arising from right ventricle quickly bifurcates into left and right branches aorta from left ventricle. Anterior surface of heart right ventricle. . Left ventricle behind and to the left of right ventricle producing tapping apical impulse in left 5th interface measures about size of quarter 1-2.5 cm in diameter. Enlarged right ventrical may produce more prominent impulse than the apical, apical impulse noting location, diameter, and amplitude.. Location from midsternal line if difficult ask patient to roll onto side measure diameter and amplitude. Diffuse apical impulse suggest left ventricualr dilatation found in heart failure. Sustained tapping impulse lifting finger off chest wall suggests left ventricular hypertrophy in hypertension and aortic stenosis. Note cardiac rate and rhythm, S2 louder than S1 in aortic area and pulmonic area. S2 diminishes and S1 gets louder through 3rd interspace becoming louder as you proceed down the chest into the tricuspid and mitral area. Switch to bell along sternal border of left 4th and 5th interspaces next to sternum and down laterally. S3, S4, and mitral sinus place patient in left lateral decubitis position. aortic valve- right 2ndintercostal space to apex pulmonic valve- left 2ndand 3rdintercostal space close to sternum, but at higher or lower levels tricuspid valve- at or near lower left sternal border mitral valve- at and around cardiac apex

Answer 29

Heart murmurs are distinct heart sounds distinguished by their pitch and their longer duration. They are attributed to turbulent blood flow and are usually diagnostic of valvular heart disease. A stenotic valve has an abnormally narrowed valvular orifice that obstructs blood flow, as in aortic stenosis, and causes a characteristic murmur. So does a valve that fails to fully close, as in aortic regurgitation. Such a valve allows blood to leak backward in a retrograde direction and produces a regurgitant murmur Distinct heart sounds attributed to turbulent blood flow. Pathologic (systolic and diastolic) vs Innocent (all systolic- functional like pregnancy, infection, anemia) (changes w/ movement) Distinguished by: Duration (how long it lasts for), Configuration (sound based on shape Crescendo-louder increasing intensity, decrescendo- quieter decreasing intensity over time, or crescendo-decresceno: increases then decreases. plaeteau-same throughout), Pitch (high, medium, low) and Quality (Quality- harsh, blowing (aortic regurgitation), musical (murmurs of mitral valve prolapse), dull, booming, scratchy and rumbling (mitral stenosis). Intensity- low hard to hear graded on six point scale, Grade 1- faint, not heard in all, Grade 2- quiet but heard immediately, Grade 3 (moderate w/ palpable thrill), 4 (loud w/ palpable thrill), 5 (loud w/ thrill w/ stethoscope off chest wall), 6 (loudest thrill heart w/ stethoscope off chest wall) increasingly loud and palpable thrim. Location, Respiration and positioning (right sided valves increase w/ inspiration increasing venous return putting more pressure on heart determined by site of origin, explore where murmur is loudest relative to sternum, apex, midsternal, midvlacivluar and axillary lines. If see diastolic pathological. systolic murmur- between S1 and S2 along with carotid upstroke. Early mid or late systolic, pansystolic Carotid upstroke right after S1 blood sent to aorta and throughout palpate while listening to chest. If happens at same time it is systolic, if after it is diastolic. For systolic murmurs must concur with carotid upstroke right after S in systole if after it is after diastolic. Ex. Midsystolic- phsyiologic flow crescendo-decrescnendo murmur of aortic stenosis after S1 before S2 brief gaps between beat and sound, Some systolic murmurs can last throughout systole which are referred to as holosystolic or pansystolic. Diastolic murmur- falling between S2 and S1 before or after carotid upstroke. Mitral regurgitation- starts w/ S1 and stops at S2 without a gap between murmur and heart sounds. Mitral stenosis- starts after S2 following opening snap. Shape of murmur depending upon intensity over time. Radiation based on transmission from point of maximal intensity, reflects site of origin, and intensity of murmur, and direction of blood flow determining where else you can here it. Diastolic- sitting up and leaning forward for aortic regurgitation moving it closer to left wall exhale completely holding breath out, diaphragm left second interspace and sternal border of apex listening for descrendo diastolic murmur of aortic regurgitation. Mitral stenosis- left lateral decubitis more subtle opening snap and diastolic rumble of stenosis. Have to move patient to hear it better

Answer 30

Diastolic Sound, Best heard with bell at the apex, Attributed to rapid ventricular filling or diminished ventricular compliance. Sounds like Ken-Tucky. May be physiologic in well conditioned athletes, children, 3rdtrimester of pregnancy. Older patients usually pathologic of heart failure. May suggest heart failure. Women pregnant, too much vlood already adding ventricle to what is already filled hearing sound after S2. If diffuse PMI + S3 suggests congestive heart failure look for elevated JVP and carotid pulse

Answer 31

Diastolic Sound: atrial diastolic gallop caused from hearing atria contract Best heard with bell at the apex. Abnormal and considered pathologic. Before S1 component Attributed to atrial contraction due to diminished left ventricular stretch. Sounds like Tenne-ssee. Left ventricular hypertrophy is present secondary to hypertension, aortic stenosis, hypertrophic cardiomyopathy (fibrotic tissue w/ deadly rhythm inverted t wave) (larger than it should be) can cause sudden death.

Answer 32

- Location: Right 2ndand 3rdintercostal spaces. Timing: Midsystolic murmur. Intensity: Often Loud. Pitch: Medium. Quality: Harsh. Configuration: Crescendo-Decrescendo. Positioning: Heard best with patient leaning forward. Most common valvular lesion in the elderly. May radiate to cartoids. Left sided heart stuff happens a bit before right. Pulmonary closes before aortic- stenosis where forward blood being impeded w/ restrictions of forward blood, turbal atherosclerosis thickening cholesterol or old and valves are worn out so thickened leaflet of valves. Mitral valve regurgitation goes from ventricle back to atria

Answer 33

Location: Left 2ndand 3rdintercostal spaces. Timing: Midsystolic murmur. Intensity: Soft to Loud. Pitch: Medium. Quality: Harsh. Configuration: Crescendo-Decrescendo. Commonly heard in congenital heart disease. Aortic valve closer prior to pulmonic cant hear pulmonic closure because of stenosis.

Answer 34

Location: Apex, Timing: Pansystolic murmur. Intensity: Soft to Loud. Pitch: Medium to high. Quality: Harsh. Configuration: Plateau . Radiation: Left Axilla. Unlike Tricuspid Regurgitation there is no change with respiration. Holo throughout systole continuous rectangular type of shape, soft to loud,pitch medium to high, variation of plateua radiate to left axilla.

Answer 35

from leaflets ballooning into left atria. Standing decreasing venous return to heart prolonging it, squatting increase to return of heart and with preload stretching to accomadate blood and pressure.

Answer 36

Location: Lower left sternal border (4thand 5thICS). Timing: Pansystolic murmur. Intensity: Variable. Pitch: Medium. Quality: Blowing. Configuration: Plateau. Radiation: Right sternum, xiphoid. Increases intensity with inspiration. Venous return more pressure to right side of heart

Answer 37

- Location: Left 2ndto 4thintercostal spaces. Timing: Diastolic. Intensity: Usually grade 1-3. Pitch: High. Quality: Blowing. Configuration: Decrescendo. Radiation: Apex or Right sternal border. Positioning: Lean forward. Respiration: Hold breath after exhalation. Diastolic murmur. Insufficneicy blood is refluxed back form area of high to low pressure. Hear on left side having them lean forward on left side of heart w/ radiation of sounds stenosis on right intercostal spaces. More severe it gets decrease in length due to incompetency of the valve.

Answer 38

- Location: Apex. Timing: Diastolic. Intensity: Usually grade 1-4. Pitch: Low. Quality: Rumble. Configuration: Decrescendo. Radiation: None. Positioning: Left lateral decubitus. Respiration: Exhalation. Left lateral decubital position bring chest closer to wall. Hear opening snap. Shouldn’t hear valve trying to move. Can cause the atria to become hypertrophied resulting in atrial fibrillation.

Answer 39

crackles (rales)

Answer 40

hemoptysis

Answer 41

Bronchial breath sounds

Answer 42

Vesicular Breath sounds

Answer 43

Questions to ask: Provoke/Palliates: Anything that you do make the pain better or worse? What were you doing when it started? Quality: What kind of pain is it? Can you describe it to me? Region: Where is the pain located? Radiation: Does the pain go anywhere or are there other symptoms associated with it? Severity: How bad is the pain? 0-10, does it prevent you from doing things? Timing: Did it come on suddenly or gradually, intermittently? Does it change with respiration or movement? History of trauma or procedures to the chest? Think of your DDx while asking. A clenched fist over the sternum suggests angina pectoris; a finger pointing to a tender spot on the chest wall suggests musculoskeletal pain; a hand moving from the neck to the epigastrium suggests heartburn. Lung tissue has no pain fibers. Pain in conditions such as pneumonia or pulmo- nary infarction usually arises from inflammation of the adjacent parietal pleura. Muscle strain from prolonged recurrent coughing or costochondral inflamma- tion may also be responsible. The pericardium also has few pain fibers. The pain of pericarditis stems from inflammation of the adjacent parietal pleura

Answer 44

hortness of breath, is a painless but uncomfortable awareness of breathing that is inappropriate to the level of exertion. symptoms include Tachypnea, Pursed lip breathing (increases pressure) , Speaks short sentences, tripoding (makes airway a straighter shot to allow more in) Prolonged expiratory phase, Accessory muscle use recruiting other muscles to expand chest wall,(SCM, Nasal Flaring, Tripod position, Abdominal muscle use), Retractions, Cyanosis. “Have you had any difficulty breathing?” Find out if the symptom occurs at rest or with exertion, and how much exertion produces onset. Because of varia- tions in age, body weight, and physical fitness.. How many steps or flights of stairs can the patient climb before pausing for breath? What about carrying bags of groceries, vacuuming, or making the bed? Has shortness of breath altered the patient’s lifestyle and daily activities? How? Carefully elicit the timing and set- ting, any associated symptoms, and relieving or aggravating factors.

Answer 45

Most patients relate shortness of breath to their level of activity. Anxious patients present a different picture. They may describe difficulty taking a deep enough breath, a smothering sensation with inability to get enough air, and paresthesias,which are sensations of tingling or “pins and needles” around the lips or in the extremities. Most patients relate shortness of breath to their level of activity. Anxious patients present a different picture. They may describe difficulty taking a deep enough breath, a smothering sensation with inability to get enough air, and paresthesias,which are sensations of tingling or “pins and needles” around the lips or in the extremities.

Answer 46

Caused by emphysema, which is characterized by damage to alveoli, alveolar attachments; low cardiac output, tissue hypoxia/cachexia; patients maintain blood gases but have reduced FEV1. Also caused by chronic bronchitis, which looks like excess mucus secretion, cough and bronchitis; damage to pulmonary endothelium, patients develop hypoxemia and CO2 retention (air trapping) heavier fluid filled COPD- most patients w/ COPD have a combination of these pathologic changes and symptoms, woman may be more likely to develop a chronic bronchitis-type pattern of disease presentation. there may be distinct phenotypes of COPD based on genetic or inflammatory patterns that better describe pathophysiologic process in COPD. Barrel chest usually.

Answer 47

common symptom that ranges in significance from trivial to ominous. Typically, cough is a reflex response to stimuli that irritate receptors in the larynx, trachea, or large bronchi. These stimuli include mucus, pus, blood, as well as external agents such as allergens, dust, foreign bodies, or even extremely hot or cold air. Other causes include inflammation of the respiratory mucosa, pneumonia, pulmonary edema, and compression of the bronchi or bronchioles from a tumor or enlarged peribronchial lymph nodes. Cough may also be car- diovascular in origin such as signalling left-sided heart failure.

Answer 48

Duration: cough acute-less than three weeks, subacute- lasting 3-8 weeks, or chronic more than 8 weeks. Whether cough is dry or produces sputum, or phlegm. Ask to describe volume of sputum and its color, odor, and consistency.

Answer 49

The most common cause of acute cough is viral upper respiratory infec- tions. Also consider acute bronchitis, pneumonia, left-sided heart failure, asthma, foreign body, smoking, and ace-inhibitor therapy. Postinfectious cough, pertussis, acid reflux, bacterial sinusitis, and asthma can cause sub- acute cough. Chronic cough is seen in postnasal drip, asthma, gastroesopha- geal reflux, chronic bronchitis, and bronchiectasis. Diagnostically helpful symptoms include fever and productive cough inpneumonia; wheezing in asthma; and chest pain, dyspnea, and orthopnea in acute coronary syndromes.

Answer 50

Mucoid sputum is translucent, white, or gray and seen in viral infections and cystic fibrosis; purulent sputum— yellow or green—often accompaniesbacterial pneumonia. Foul-smelling sputum is present in anaerobic lung abscess, thick tena- cious sputum in cystic fibrosis. Large volumes of purulent sputum are present in bronchiectasis and lung abscess.

Answer 51

musical respiratory sounds that may be audible to the patient and to others. Tightness, difficulty getting a full breath and doesn’t feel she can exhale fully. high pitched sounds mostly respiratory, not all things that wheeze are COPD and CHF

Answer 52

refers to blood coughed up from lower respiratory tract. may vary from blood-streaked sputum to frank blood. For patients reporting hemoptysis, quantify the volume of blood produced, the setting and activity, and any associated symptoms. Hemoptysis is rare in infants, children, and adolescent. Cough and Hemoptysis, the causes include bronchitis;malignancy; and cystic fibrosis and, less commonly, bronchiectasis, mitral stenosis, Goodpasture syndrome, and Wegener granulomatosis. Massive hemoptysis (\>200 cm3) may be life-threatening.

Answer 53

small fluid filled sacs in the lung that Examples include: lobar pneumonia, in which the alveoli are filled with fluid and blood cells;

Answer 54

These symptoms, especially daytime sleepiness and snoring, are hallmarks of obstructive sleep apnea, commonly seen in patients with obesity, posterior malocclusion of the jaw (retrognathia), treatment-resistant hypertension, heart failure, atrial fibrillation, stroke, and type 2 diabetes. Mechanisms include instability of the brainstem respiratory center, disordered sleep arousal, disordered contraction of upper airway muscles (genioglossus malfunction), and anatomic changes contributing to airway collapse such as obesity, among others

Answer 55

(collapse of alveoli), more defined on xray, sufficient amount of air enters pleural cavity, surface tension adhering visceral to parietal pleura (lung to wall) is broken causing lung to collapse because of inherent elastciity (elastic recoil) when collapses (atelectasis) pleural cavity normall potential space becomes full of air. one can collapse w/out the other. can be caused following surgery ex. air in but not out. Infection or mass blocking out lungs causing it to shrink (atelctasis spirometry to expand lung and not let patients get pneumonia prone.

Answer 56

ask patient to say 99 normally sounds transmitted are muffled and indistict but in bronchophony louder sounds reflecting transmission through airless tissue

Answer 57

change occurs in lobar pneumonia when the alveoli get filled with fluid and cellular debris dyspnea- difficulty breathing can be seen w/ someone who is tripodding, using accessory muscle use, cyanotic, pale can be caused by MI, Pulmonary edema, pleural effusion, CHF, COPD, asthma, foreign object insertion, pulmonary embolism

Answer 58

Place stethoscope on the thorax and have patient say “ee” as in bee. (Normal will sound like “ee,” Consolidated lung tissue produces “a” like hay). Occurs in lobar consolidation from pneumonia

Answer 59

Feeling vibrations transmitted through the bronchopulmonary tree to the chest wall see below answers

Answer 60

coughing up blood from lower respiratory tract try to find where it originates from before assuming from lung. if vomited from stomach would be darker and have food particles in it.

Answer 61

caused by accumulation of pleural fluid and may be transudates seen in ehart failure, cirrhosis, and nephrotic syndrome, or exudates as seen in numerous conditions including pneumonia, malignancy, pulmonary embolism, tuberculosis, and pancreatistis

Answer 62

difficulty breathing when laying supine frequently described as pillows usually related to CHF because of fluid buildup taking up more space horizontal

Answer 63

Gets SOB when supine awakens from sleep takes up more space when sleeping.. Frequently seen in CHF

Answer 64

air in the chest cavity between the pleural layers due to a disconnect of visceral from pleura layer with no lung sliding (tension- deviated to the patient’s right one way valve going to die compressing heart, aorta, vena cava, decreased BP, and HR

Answer 65

aka crackles from abnormalities of lung parenchyma (pneumonia interstitial lung disease, pulmonary fibrosis, atelectasis, heart failure) or airways (bronchitis, bronchiectasis). intermittent, non-musical and brief. fluid in alveoli pop, bubbles in ginger ale. can arise from abnormalities of the lung parenchyma (pneumonia, interstitial lung disease, pulmonary fibrosis, atelectasis, heart failure) or of the airways (bronchitis, bronchiectasis. If you hear crackles, especially those that do not clear after coughing, listen care- fully for the following characteristics: Loudness, pitch, and duration, summarized as fine or coarse crackles (louder, lower-pitched, and longer), Fine late inspiratory crackles that per- sist from breath to breath suggest abnormal lung tissue soft high-pitched very breath accompany CHF.), Number, few to many, Timing in the respiratory cycle, Location on the chest wall (The crackles of heart failure are usu- ally best heard in the posterior inferior lung fields.), Persistence of their pattern from breath to breath, Any change after a cough or change in the patient’s position (Clearing of crackles, wheezes, or rhon- chi after coughing or position change suggests inspissated secretions, seen in bronchitis or atelectasis.)

Answer 66

mucus and coarse. describe sounds from secretions in large airways that may change with coughing. describe sounds from secretions in large airways that may change with coughing. last lot longer lower-pitched, snoring quality,

Answer 67

high pitched whistling sound associated w/ an upper airway obstruction by a foreign body or anaphylaxis. ominous sign of upper airway obstruction in the larynx or trachea that requires urgent airway evaluation. Wheezing is either expira- tory or continuous. Dry cough some wheezing and squeaking. occurs in partial lower air- way obstruction from secretions and tissue inflammation in asthma, or from a foreign body

Answer 68

fast breathing usually associated w/ dyspnea or anxiety increases the likelihood of pneumonia and cardiac disease

Answer 69

musical respiratory sounds that may be audible to the patient and to others. High-pitched, hissing or shrill quality usually asthma. Tightness, difficulty getting a full breath and doesn’t feel she can exhale fully. high pitched sounds mostly respiratory, not all things that wheeze are COPD and CHF. beware of silent chest where air movement is minimal.

Answer 70

-Place stethoscope on thorax. Have patient whisper “ninety-nine,” (Normally faintly heard, Consolidation much more clear and audible)

Answer 71

Apex of the lung each lung rises approximately 2- 4 cm above the inner third of the clavicle. Body of the sternum- sternum bone midline between clavicles inferior to manubrium superior to xiphoid process Costochondral junctions- cartilaginous joint connecting rib to sternum Fissures of the lungs- oblique, horizontal the things seperating lobes of lung Lobes of the lungs- 5 three on the right (upper, middle, and lower) , 2 on the left. Lower border of right lung of upper lobe ends at the 6th rib and lower lobe of lung ends at the 8th rib at midaxillary line. Lung ends at T10 spinous process descindg 3-5 cm when expiring. Manubrium- top bone of sternum where the sternal angle and suprasternal notch is located Ribs and interspaces- 12 ribs and 12 interspaces below the ribs dont count on anterior count on posterior Sternal angle- 5 cm below suprasternal notch until feeling bony ridge where manubrium meets the sternum Suprasternal notch- notch in between clavicles above sternum Xyphoid process- bottomest of sternum

Answer 72

Parietal pleural covers the inside of the chest wall along rib cage and diaphragm richly innervated by intercostal and phrenic nerves. Visceral pleural covers outside lungs lacks sensory nerves. 10-20ml pleural fluid normally present to facilitate movement. Potential space between parietal and visceral contains pleural fluid w/ surface tension of this keeping lungs in contact w/ thoracic wall, allowing lung to expand and contract during respiration. Irritation of the parietal pleura pro- duces pleuritic pain with deep inspira- tion in viral pleurisy, pneumonia, pulmonary embolism, pericarditis, and collagen vascular diseases.

Answer 73

Autonomic primarily controlled in brainstem. Diaphragm principle muscle: Inspiration Contracts and descends, Chest expands, compressing the abdominal contents and pushing out the abdominal wall Decreased intrathoracic pressure, The muscles in the rib cage also expand the thorax, especially the scalenes, which run from the cervical vertebrae to the first two ribs, and the parasternal intercostal muscles, or parasternals, which cross obliquely from the sternum to the ribs. As the thorax expands, intrathoracic pressure decreases, drawing air through the tracheobronchial tree into the alveoli, or distal air sacs, filling the expanding lungs. Oxygen diffuses into the adjacent pulmonary capillaries as carbon dioxide exchanges from the blood into the alveoli.Expiration chest wall lungs recoil passively diaphragm relaxed Accessory muscle use- SCM, Nasal Flaring, Tripod position (makes airway straighter to let more air in Abdominal muscle use recruiting extra muscles to expand chest wall, intercostal Retractions. Accessory muscle use signals difficulty breathing from COPD or respiratory muscle fatigue. Lateral displacement of the trachea occurs in pneumotho- rax, pleural effusion, and atelectasis.

Answer 74

Signs of difficulty breathing include: tachypnea, Pursed lip breathing (increasing pressure), Speaks short sentences (Prolonged expiratory phase), Accessory muscle use (SCM, Nasal Flaring, Tripod position (makes airway straighter to let , Abdominal muscle use recruiting extra muscles to expand chest wall), Retractions, Cyanosis emphysema presentation- damage to alveoli, alveolar attachments w/ low cardiac output w/ tissue hypoxia/cachexia, patients maintain blood gases but have reduced FEV1. chornic bronchitis presentation- excess mucus secretion, cough, and “bronchitis” presentation. damage to pulmonary endothelium, patients develop hypoxemia and CO2 retention (air trapping) COPD presentation- most patients w/ COPD have combination of pathological changes and symptoms. Women more likely to develop chronic-bronchitis type pattern of disease presentation. There may be distinct phenotypes of COPD based on genetic or inflammatory patterns.

Answer 75

Skin for Rash, scars, injuries (DCAPBLS), cyanosis or pallor (Peripheral and central), bruises from rib fracture shape and color of fingernails (pink). Listen for and watch work of breathing: Nasal flaring, accessory muscle use, number of words used, expiratory time (If excessively prolonged), Watch the rate, rhythm, effort, and depth of breathing, Regular, irregular, shallow, deep, variable. Listen for sounds audible without a stethoscope

Answer 76

Begin by looking at shape of thorax should be wider than it is deep, contour, symmetry, and deformities. Asymmetric expansion occurs in large pleural effusions. retraction occurs in severe asthma, COPD, or upper airway obstruction look for in intercostal spaces during inspiration. Unilateral impairment or lagging sug- gests pleural disease from asbestosisor silicosis; it is also seen in phrenic nerve damage or trauma. can appear as a Barrel chest AP \> Lateral commonly found in COPD funnel chest (pectus excavatum)- excavator cuts. note depression in lower portion of sternum. compression of heart and great vessels may cause murmurs. pigeon chest (pectus carinatum)- sternum is displaced anteriorly, increasing AP diameter. Costal cartilages adjacent to protruding sternum are depressed. thoracic kyphoscoliosis-abnormal spinal curvatures and vertebral rotation deform ches.t distortion of underlying lungs may make interpreatation of lung findings caused by genetic scoliotic or arthritis. Traumatic flail chest segment- two or more ribs fractures in two or more segments multiple rib fractures may result in paradoxical movements in the thorax. as descent of diaphragm decreases intrathoracic pressure, on inspiration, injured area caves inward; on expiration, it moves outward causing paradoxical mo tion..

Answer 77

Place your thumbs at about the level of the 10th ribs, with your fingers loosely grasping and parallel to the lateral rib cage. As you position your hands, slide them medially just enough to raise a loose fold of skin between your thumbs over the spine. Ask the patient to inhale deeply. Watch the distance between your thumbs as they move apart during inspiration, and feel for the range and symmetry of the rib cage as it expands and contracts. This movement is sometimes called lung excursion, decrease indicative of lung disease. Unilateral decrease or delay in chest expansion occurs in chronic fibrosis of the underlying lung or pleura, pleural effusion, lobar pneumonia, pleural pain with associated splinting, unilat- eral bronchial obstruction, and paral- ysis of the hemidiaphragm. Trachea bifurcates at the level of the sternal angle (angle of Louis) anteriorly and at T4 spinous process posteriorly. CXR carina should be at T4 R mainstem bronchus is at a more acute angle. Trachea sits in middle underneath sternum trachea bifurcates at T4.

Answer 78

Gently palpate the entire chest identifying areas of tenderness, Note crepitus (cracking or grinding sound over bones, joints, or skin w/ or w/out pain due to air in subcutaneous tissue can be subcutaneous emphysema feels like rice krispies indicative of a broken trachea), Crepitus may be palpable in overt fractures and arthritic joints; crepitus and chest wall edema are seen inmediastinitis. Step off (fractures), masses, chest wall/lung expansion (Posteriorly, place thumbs at about 10th ICS in the midline (noting breathing pattern for abnormalities ex. Phrenic nerve diaphragm problem or pneumothorax) Anteriorly place thumbs along costal margin, Bring hands together to form a loose skin fold, Have patient take a deep breath Observe the distance that the fingers move apart during deep inspiration) IPPA (inspect palpate percuss auscultation). Palpate for symmetrical tactile fremitus

Answer 79

helps you establish whether the underlying tissues are air-filled, fluid-filled, or consolidated. Penetrates only 5-7 cm, Stand somewhat off to the side to percuss, Strike one finger twith one finger at opposte hand wice at each location, Sounds should be resonant over the chest except, Area of cardiac dullness just left of sternum about the size of a fist, Dullness of liver: 5th ICS R MCL, 7th ICS R MAL 9th ICS R scapular line. imprecise assessment, but may direct your attention to possible asymmetries. resonance of lung changes to tympany of gastric air bubble. Confirm by listening for breath sounds, voice sounds, and whispered voice sounds. All these attributes should increase or decrease together. Dullness replaces resonance when fluid or solid tissue replaces air-containing lung or occupies the pleural space beneath your percussing fingers. Examples include: lobar pneumonia, in which the alveoli are filled with fluid and blood cells; and pleural accumula- tions of serous fluid (pleural effusion), blood (hemothorax), pus (empyema), fibrous tissue, or tumor. Dullness makes pneumonic and pleural effusion three to four times more likely, respectively. Generalized hyperresonance is com- mon over the hyperinflated lungs of COPD or asthma. Unilateral hyperreso- nance suggests a large pneumothorax or an air-filled bulla, COPD from alveolar air trapping and delayed expiration. This technique tends to overestimate actual movements of the diaphragm. Identify the descent of the diaphragm, or diaphragmatic excursion. First, deter- mine the level of diaphragmatic dullness during quiet respiration. Holding the pleximeter finger above and parallel to the expected level of dullness, percuss downward in progressive steps until dullness clearly replaces resonance. Confirm this level of change by percussing downward from adjacent areas both medially and laterally. An abnormally high level suggests a pleural effusion or an elevated hemidi- aphragm from atelectasis or phrenic nerve paralysis

Answer 80

Have patient cough one or two times Clear out throat so don’t sound like stuff in lungs, Have patient breathe in and out deeply through open mouth (higher lung volume), Listen for air movement, Listen through all of inspiration and expiration, Compare side to side to compare between lungslisten for one full rbeath at each location.

Answer 81

These include: Vesicular- majority of lung sounds heard most over everywhere louder in higher fields, Bronchovesicular- inspirations louder, exploratory softer, heard over large airways over right Bronchial- bigger and thicker short inspiratory longer expiratory (same volume and intensity high pitched over manubrium), Tracheal- almost equal between both. Note the intensity of the breath sounds, which reflects the air flow rate at the mouth, and may vary from one area to another. Breath sounds are usually louder in the lower posterior lung fields. If the breath sounds seem faint, ask the patient to breathe more deeply. Shallow breathing or a thick chest wall can both alter breath sound intensity. Breath sounds may be decreased when air flow is decreased (as in obstructive lung disease or respiratory muscle weakness) or when the transmission of sound is poor (as in pleural effusion, pneumothorax, or COPD). A gap suggests bronchial breath sounds. In cold or tense patients, watch for muscle contraction sounds—muffled, low-pitched rumbling, or roaring noises. Changing the patient’s posi- tion may eliminate this noise. If bronchovesicular or bronchial breath sounds are heard in locations distant from those listed, suspect replacement of air-filled lung by fluid- filled or consolidated lung tissue.

Answer 82

Vesicular, or soft and low pitched. They are heard throughout inspiration, continue without pause through expiration, and then fade away about one third of the way through expiration. ■ Bronchovesicular, with inspiratory and expiratory sounds about equal in length, at times separated by a silent interval. Detecting differences in pitch and intensity is often easier during expiration. 1st and 2nd interspaces anteriorly, posterior scalupae intermediate pitch and intensity ■ Bronchial, or louder, harsher and higher in pitch, with a short silence between inspiratory and expiratory sounds. Expiratory sounds last longer than inspiratory sounds. ■ Tracheal, or loud harsh sounds heard over the trachea in the neck.

Answer 83

Superimposed on normal breath sounds. Note that tracheal sounds originating in the neck such as stridor and vocal cord dysfunction can be transmitted to the chest and mistaken for wheezing, leading to inappropriate or delayed treatment. Stridor and laryngeal sounds are loudest over the neck, whereas true wheezes and rhonchi are faint or absent over the neck.

Answer 84

Note any pleural rubs, which are coarse, grating biphasic sounds heard primarily during expiration. Increased transmission of voice sounds suggests that embedded airways are blocked by inflammation or secre- tions

Answer 85

Diaphragmatic excursion- overestimates movement of diaphragm. Percuss each hemithorax individually from superior to inferior until resonance is replaced by dullness. Confirm this level by checking several adjacent starting points. Have patient inhale deeply then fully exhale and hold. Percuss and mark the level where dullness replaces resonance. Do this for each hemithorax. Have the patient inhale deeply and hold. Percuss and mark the level where dullness replaces resonance (Do this for each hemithorax, Expected distance 3-5.5 cm. A high diaphragm can indicate effusion or atelectasis (collapsed lung) or phrenic nerve paralysis

Answer 86

Add these special transmitted voice sounds to your exam when you hear abnormally located bronchovesicular or bronchial breath sounds

Answer 87

decreased or absent when the voice is higher pitched or soft or when the transmission of vibrations from the larynx to the surface of the chest is impeded by a thick chest wall, an obstructed bronchus, COPD, orpleural effusion, fibrosis, air (pneumo- thorax), or an infiltrating tumor. Asymmetric decreased fremitus raises the likelihood of unilateral pleural effusion, pneumothorax, or neoplasm, which decreases transmission of low- frequency sounds; asymmetricincreased fremitus occurs in unilateral pneumonia which increases transmis- sion through consolidated tissue. imprecise assessment but directs attention towards assymetris that can be confirmed by listening for breath sounds, voice sounds, and whispered voice sounds should increase or decrease together. Feeling vibrations transmitted through the bronchopulmonary tree to the chest wall (Should be symmetric, More prominent between scapulae). Place ulnar surface of the hands to the thorax symmetrically (Patient to say “ninety nine,” Note areas of absent, increased or decreased). Fremitus increased in pneumonia and consolidation. Fremitus decreased with soft/high pitched voice, thick chest wall, over precordium, COPD (Lung farther away from wall because of barrel chest), pleural effusion (water doesn’t transmit sound as much), fibrosis (doesn’t wiggle as much), pneumothorax. If one side more than the other there is probably a mass, fluid, or some other kind of consolidation.

Answer 88

The lower border of the lung crosses the 6th rib at the midclavicular line and the 8th rib at the midaxillary line. Posteriorly, the lower border of the lung lies at about the level of the T10 spinous process. On inspiration, it descends in the chest cavity during contraction and descent of the diaphragm. L oblique fissure divides the 2 lobes. Axilla is where you can assess all 3 lobes of the right lung. Remember posteriorly lung extends very caudally with inspiration and the diaphragm is very cephalad meaning back pain can be from thoracic structures, chest pain can be from abdominal structures. Oblique fissure approximated by a string that runs from the T3 spinous process obliquely down and around the chest to the 6th rib at the midclavicular line. Horizontal fissure runs close to the 4th rib and meets the oblique fissure in the midaxillary line near the 5th rib. trachea bifurcates into its mainstem bronchi at the levels of the sternal angle anteriorly and the T4 spinous process posteriorly. 2nd intercostal space for needle insertion for tension pneumothorax. 4th intercostal space for chest tube insertion.T4 for the lower margin of an endo- tracheal tube on a chest x-ray. T7-8 thoracentesis insertion superior to 8th rib.

Answer 89

- (Egophony) Place stethoscope on the thorax and have patient say “ee” as in bee. (Normal will sound like “ee,” Consolidated lung tissue produces “a” like hay). Bronchophony- Place stethoscope on thorax and have patient say, “ninety nine” (Normal will sound muffled, Consolidation sounds more clear and understandable sounds better through solid median). Whispered pectoriloquy-Place stethoscope on thorax. Have patient whisper “ninety-nine,” (Normally faintly heard, Consolidation much more clear and audible)

Answer 90

have you ever had pain or swelling in your legs that caused you to limit your activities? Where was the pain (what part of the legs)? Have you had problems with poorly healing or wounds that do not heal in your legs or feet? Can be due to atheroma or blockage of blood flow in legs by lipids or more generally PAD. Can be DVT or compartment syndrome.

Answer 91

pain upon exertion. Do you ever experience cramping in your legs during exercise or exertion? (Claudification) does it go away with rest? Pain in abdomen w/ eating (bates “food fear”) or intestinal angina symptom of mesenteric ischemia from arterial emboli occlusion of one of mesenteric arteries.

Answer 92

sign of a lack of oxygenation to those limbs may be due to blocking of the vessels or vasoconstriction with pressure not able to overcome those arteries. Usually due to compartment syndrome indicating a lack of blood flow as well as nerve receptor or stimulation. Brownish discoloration or ulcers just above the malleolus suggests chronic venous insufficiency. Thickened, brawny skin suggests lymphedema and advanced venous insufficiency. Posterior tibital pulse Acute arterial occlusion from embo- lism or thrombosis causes pain and numbness or tingling. The limb distal to the occlusion becomes cold, pale, and pulseless. Pursue emergency treatment. A painful, pale, swollen leg, together with tenderness in the groin over the femoral vein, suggests deep iliofemo- ral thrombosis. Risk of PE in proximal vein thrombosis is 50%. Only half of patients with DVT in the calf have tenderness or venous cords, and absence of calf tenderness does not rule out thrombosis. Note that Homan sign, discomfort behind the knee with forced dorsiflexion on the foot, is neither sensitive nor specific, and discredited by Homan himself.

Answer 93

can be due to compartment syndrome, edema, infection etc. Local swelling, redness, warmth, and a subcutaneous cord signal superficial thrombophlebitis, an emerging risk factor for DVT. Unilateral calf and ankle swelling and edema suggest venous thromboem- bolic disease (VTE) from DVT, chronic venous insufficiency from prior DVT, or incompetent venous valves; or it may be lymphedema. Calf asymmetry \>3 cm increases the LR for DVT to \>2.26 Also consider muscle tear or trauma, Baker cyst (posterior knee), and muscular atrophy. If you detect unilateral swelling or edema, measure the calves 10 cm below the tibial tuberosity. Normally, the difference in calf circumference is \<3 cm. Mea- sure and compare other areas of asymmetry, if needed, including the thighs and ankles. for legs Bilateral edema is present in heart fail- ure, cirrhosis, and nephrotic syndrome.Venous distention suggests a venous cause of edema. In DVT, the location of edema sug- gests the point of occlusion—the popliteal vein if the lower leg or ankle is swollen, the iliofemoral veins if the entire leg is swollen.

Answer 94

commonly found in conditions like Raynaud’s phenomenon, thromboangitis obliterates. In the cold the fingers get white from a lack of circulation and when warming up turn blue from hypoxia and then become red and painful when blood flow rushes to the fingers and triggers the pain receptors.

Answer 95

Refers to an Atherosclerotic disease that is distal to aortic bifurcation w/ stenosis, occlusive, and aneurysm disease of abdominal aorta, its mesenteric and renal branches, and arteries of lower extremes ties, exclusive of coronary arteries. Risk factors include increasing age, can cause MI or stroke, is a marker for CV mortality and functional decline resulting invarious heart condition problems as well as AAA. Is worse w/ exertion- requires more blood flow through tiny arteries, cold worsens pain and heat improves it, worse w/ elevation blood has to push up, worse with compression stockings creating more resistance. An expanding hematoma from an abdominal aortic aneurysm (AAA) may cause symptoms by compressing the bowel, aortic branch arteries, or the ureters. Persisting food fear, weight loss, or dark stool symptoms suggest mesenteric ischemia from arterial embolism, arterial or venous thrombosis, bowel volvulus or strangulation, or hypoper- fusion. Failure to detect acute symp- toms can result in bowel necrosis and even death. Symptomatic limb ischemia associated w/ pain or cramping in legs with exertion is atherosclerotic PAD. Pain with walking or prolonged standing, radiating from the spinal area into the buttocks, thighs, lower legs, or feet, is neurogenic claudication. Usually calf muscles, but also occurs in the buttock, hip, thigh, or foot, depending on the level of obstruction; rest pain may be distal in the toes or forefoot. The positive likelihood ratio (LR) of spinal stenosis is \>6 if the pain is relieved by sitting and bending forward, or if there is bilateral buttock or leg pain. Hair loss over the anterior tibiae points to decreased arterial perfusion. “Dry” or brown–black ulcers fromgangrene may ensue. Ask about warning signs such as leg pain on exertion and rest and leg/pain that does not stop patient from from walking especially those who smoke, diabetes, hypertension, African American, CAD, poorly healing or nonhealing wounds, and high cholesterol. Initial treatment includes supervised exercise programs.

Answer 96

occurs when major vessel is obstructed connects between branching networks of smaller arteries increasing size over time to create collateral circulation perfuming structures distal to occlusion most common one is connect two saphenous veins w/ perforating/bridging veins connect superficial to deep system. Readily visible when dilated.

Answer 97

intima: surrounds lumen, continuous lining of endothelium modulating blood flow/vascular reactivity, regulating immune and inflammatory reactions. Media: smooth muscle dilates/constricts to accommodate blood pressure w/ bad injury the media clamps down. Adventitia: connective tissue.

Answer 98

ankle brachial index allows providers to screen for PAD where you measure BP with Doppler in each arm and leg X2 combining average of both sides in equation of ABI=Ankle/arm 0.9-1.3,

Answer 99

lipid macrophages of connective tissue and calcium form in along the intima lining. Begins in intima, where circulating lipoproteins, especially LDL, exposed to proteoglycans from extracellular matrix, undergo oxidative modification, and trigger a local inflammatory response that attracts mononuclear phagocytes. Once in intima, phagocytes mature into macrophages, ingest lipids, and become foam cells that develop into fatty steaks.

Answer 100

atheroma builds up leading to aherosclerosis which are confluent plaques of atheroma. Chronic inflammatory disease initiated by injury to vascular endothelial cells, provoking atheroma toys plaque formation and vascular lesions of hypertension. These can go from soft to hard as they become brittle due to calcification

Answer 101

small branches located between arterioles and venues that innervate all parts of the body width of single RBC allowing for perfusion of oxygen out into the interstitial spaces. At arteriolar end outward filtration due to hydrostatic and interstitial colloid oncotic pressure and inward resorption at venous end of capillary (due to colloid osmotic reassure from plasma proteins.) When burst capillary can appear reddened or bruised depending upon location

Answer 102

compartment syndrome

Answer 103

one-way valves of deep, superficial, and perforating veins propel blood toward heart, preventing pooling, venous stasis, and backward flow contraction of calf muscles during walking serves as venous pump propelling blood upward against gravity. can become incompetent and weak leaking. have media that change vein caliber and valves in response to minor changes of venous pressure.

Answer 104

ulnar, radial, and interiors us veins in forearm brachial veins of upper arm axillary vein w/ the axillary vein becoming subclavian. Drap into superior vena cava

Answer 105

carry 90% venous return from legs. Ex. External iliac, deep femoral, superficial femoral, popliteal, anterior tibial, perineal, posterior tibial. Because of their weaker wall structure, the leg veins are susceptible to irregular dilatation, compression, ulceration, and invasion by tumors, and warrant special attention.

Answer 106

veins from legs and lower trunk drain upward into inferior vena cava into right atrium

Answer 107

connect superficial to deep system

Answer 108

veins are thin-walled and highly distensible and can contain up to ⅔ of blood volume. Venous intima consists of nonthrombogenic endothelium, unidirectional valves that promote venous return to heart pause between systole and diastole closer. Media contains circumferential rings of elastic tissue and smooth muscle that change vein caliber from change in venous pressure w/ venues draining capillary beds and form interconnecting venous plexuses.

Answer 109

small (lateral side of foot upward along posterior calf joints in popliteal) and great saphenous (originates on dorsal of foot, just anterior to medial malleolus up medial aspect of legs joining femoral vein of deep venous system below inguinal ligament) subcutaneous relatively poor tissue support

Answer 110

veins from arms, upper trunk, head, and neck drain into superior vein cava, which empties into right atrium

Answer 111

commonly occur in the lower limb deep veins aka DVT. Causes sudden onset pain, pale cold left leg below the knee no palpable pulse or doppler at popliteal, posterior tibial, or dorsal is pedis can be noted. Commonly has atrial fibrillation required to get an arteriogram.

Answer 112

considered a large artery is the aorta and comes directly off of the heart vessel or arches w/in hand interconnect radial and ulnar arteries, doubly protecting circulation to the hand and gainers against possible arterial occlusion

Answer 113

located on most of the upper arm into the armpit drain most of arm

Answer 114

at end of elbow just medial to biceps tendon

Answer 115

dorsum of foot; lateral to extensor tendon of big toe.

Answer 116

drain little, ring fingers, ulnar hand and forearm located up to elbow. located on medial surface of arm 3cm above elbow.

Answer 117

below inguinal ligament, midway between anterior superior iliac spine and symphysis pubis

Answer 118

alongisde artery

Answer 119

superficial vein found in leg. originates dorsum of foot, passes anterior to medial malleolus and joins femoral vein of deep venous system below inguinal ligament.

Answer 120

draining some fluid from arm located above the clavicle

Answer 121

follows deep venous system

Answer 122

passes medically behind femur; palpable behind knee. extension of femoral artery that passes medially behind femure, palpable just behind knee. popliteal artery divides into two arteries perfusing lower leg and foot.

Answer 123

behind knee mdeial malleolus of ankle. interconnecting arch between two chief arterial branches protects circulation of foot.

Answer 124

lateral flexor surface at wrist

Answer 125

superficial vein lymphatics from portion of leg drained by this (heel and outer aspect of foot) join deep system at level of popliteal space. Lesions in this space are not usually associated w/ palpable inguinal lymph nodes. begins on lateral side of foot, passes upward along posterior calf, joins deep venous system in popliteal fossa.

Answer 126

only inguinal nodes that are palpable. Superficial lower abdomen and buttock, external genitalia (not testes), anal canal, perinatal area, and lower vagina. Vertical group: upper part of saphenous vein drains same region of leg. Horizontal group- high anterior thigh below inguinal ligament draining superficial portions of Lowe abdomen and buttock, external genitalia (not testes), anal canal, perinatal area, and lower vagina.

Answer 127

medial flexor surface (overlying tissues may obscure)

Answer 128

For the arms inspect the size, symmetry, swelling, color of skin and nail beds, and note vascular pattern and any prominent veins. Palpate the arms palpating the radial and brachial pulses (if you suspect arterial insufficency) (0-3 grading), BP epitrohclear nodes (local or distal infection, lymphadenopathy, or HIV) with elbow flexed palpate medically between muscles with capillary refill in fingers (press on nail and color should return in less than 2 seconds). Measure blood pressure in both arms, palpating carotid upstroke and auscultate for bruits w/ assymetrical blood pressure found in coarctation of aorta and dissecting aortic aneursm measuring aorta. Bounding carotid, radial, and femoral pulses are present in aortic regurgita- tion; asymmetric diminished pulses point to arterial occlusion from ath- erosclerosis or embolism. Swelling from lymphedema of the arm and hand may follow axillary node dissection and radiation therapy. Visible venous collaterals, swelling, edema, and discoloration signal upper extremity DVT.

Answer 129

For the legs- inspect size, symmetry, swelling, color of skin and nail beds, distribution of hair on lower legs and feet, check for varicosities (standing) or bulging distended veins looking for pigmentation, rashes, scars, ulcers (toes and soles). Palpate legs for femoral, popliteal, posterior tibial and dorsal is pedis pulses, superficial inguinal nodes, capillary refill in toes, check pitting edema if edema present (thumb over each dorsal foot, posterior of each malleolus, over each anterior tibia). Individual findings of calf, leg, or ankle swelling or asymmetry; venous dilatation; erythema; or superficial thrombophlebitis have low diagnostic value for DVT compared to combined scoring systems and ultrasound. Ulcers or sores on the feet raise the LR of peripheral vascular disease to 7. Warmth and redness over the calf signal cellulitis. Atrophic and hairless skin is commonly present but not diagnostic of PAD. Varicose veins are dilated and tortu- ous. Their walls may feel somewhat thickened. If the femoral pulse is absent, the LR of PAD is \>6.26 If the occlusion is at the aortic or iliac level, all pulses distal to the occlusion are typically affected and may cause postural color changes. An exaggerated, widened femoral pulse suggests the pathological dila- tation of a femoral aneurysm. An exaggerated, widened popliteal pulse suggests a popliteal artery aneu- rysm. Popliteal and femoral aneurysms are uncommon. They are usually from atherosclerosis and occur primarily in men age ≥50 years.

Answer 130

checks for perfusion of hand and compares latency of radial and ulnar artery. Have the hand facing up, have patient make tight fist multiple times or enough till skin blanches then make fist and compress both radial and ulnar artery and have patient open hand slightly, but not fully extended. Release ulnar artery; hand should flush 3-5 seconds and then repeat for radial artery w/ persisting pallor indicates occlusion of tested artery. Persisting pallor indicates occlusion of the ulnar artery or its distal branches, Arterial occlusive disease is much less common in the arms than in the legs. Absent or diminished pulses at the wrist occur in acute embolic occlusion and in Buerger disease, or thromboan- giitis obliterans.

Answer 131

raise both legs to 90 degrees, hold for 2 minutes until maximal pallor of feet, have patient sit up w/ legs down on table and the pinkness should return in 10 seconds and the veins should refill in 15 seconds and a normal response also has a decreased pulse, which indicated good collateral formation- new blood vessels formed because of poor current of blood vessels. If it doesn’t pink in time they have decreased arterial flow. Persisting dependent rubor suggests arterial insufficiency (see p. 538). If the patient’s veins are incompetent, dependent rubor and the timing of color return and venous filling are not reliable tests of arterial insufficiency.

Answer 132

fibrous cap break off leading to clotting from release of semi-liquid material containing thromboplastin from the deeper layers of plaque leads to acute arterial occlusioin.

Answer 133

categorized by swollen les, skin color and texture changes, and non-healing wounds.

Answer 134

Pressure builds from trauma or bleeding into one of the four major muscle compartments between the knee and ankle; each compartment is enclosed by fascia that limits expansion to accommodate increasing pressure. Tight, bursting pain in calf muscles, usually in the anterior tibial compartment, sometimes with overlying dusky red skin. 5 P’s not sensitive or specific have a high index of suspicion if any of them and is caused by increased pressure within a muscular compartment of an area that prevents venous drainage and thus proper arterial perfusion of the muscles and nervous structure they are in. If left untreated will result in ischemia, infarction, and subsequent contracture (volkmann’s). common in long bone fracture particularly in legs. 5 P’s parenthesia (tingling) is the first sign loss of 2-point discrimination vibratory sensations, associated pain w/ passive stretch or that is out or proportion to the injury, pallor (late sign poor prognostic indicator), pulselessness or pulse deficit (early sign)-swelling pressing arterial system with no blood flow past injury, paralysis if \>6 hours after symptom onset can be permanent if it remains long in this fashion. Measure w/ manometer.

Answer 135

common in people who are somewhat active for a period then sit for a very long period directly after periods of activity causing pooling of blood in veins that form a clot resulting in swelling of one leg versus the other, soreness, discoloration, warm slightly red swollen, and tender no pitting edema should measure size of calves, check pulses, see how far up it goes. DVT and PE are disorders of venous thromboembolic disease (VTE); DVTs are distal, limited to the deep calf veins, or proximal, in the popliteal, femoral, or iliac veins. Classically, painful calf swelling with erythema, but can be painless; signs correlate poorly with site of thrombosis.

Answer 136

acute infection, usually from strep. Progenies or staph aureus spreading up lymphatic channels from distal portal of entry. blood poisoning reddened line w/ infection entering body spreading through lymph system due to bacterial spreading from portal of entry can be legs or abdomen .

Answer 137

see berger test

Answer 138

hard edema, non-pitting, non-tender, thickened skin w/ interstitial accumulation of fluid high in protein when lymphatic channels are blocked or absent leading to fluid retention and swelling in extremities and is frequently seen in patients w/ tumors, fibrosis, lymph node dissection from surgery. Edema is initially soft and pitting, then becomes indurated, hard, and nonpitting. Skin is markedly thickened; ulceration is rare. There is no pigmentation. Edema often occurs bilaterally in the feet and toes. Lymphedema arises from interstitial accumulation of protein-rich fluid when lymph channels are infiltrated or obstructed by tumor, fibrosis, or inflammation, or disrupted by axillary node dissection and/or radiation. Appears as Peau d’orange skina nd woody edema

Answer 139

caused by diabetes, trauma, prolonged pressure located on planter aspects of foot, tip of toe, lateral tot fifth metatarsal, characterized by deep surrounded by calculus and insensate w/ condition of food being dry, cracked insensate calluses.

Answer 140

vasoconstriction of fingers and toes, usually triggered by cold. Primarily found in younger people with no clear cause but can resolve in middle age and is secondarily related to autoimmune disorders (scleroderma, systemic lupus erythematosus, mixed connective tissue disease; cryo- globulinemia; also to occupational vascular injury; drug) affecting distal fingers and toes. In the cold the fingers get white from a lack of circulation and when warming up turn blue from hypoxia and then become red and painful when blood flow rushes to the fingers and triggers the pain receptors

Answer 141

uncommon disease, usually seen in adults greater than 45 years of age caused by inflammation of the small and medium blood vessels that is non-atherosclerotic, occlusive thrombus and is strongly associated w/ tobacco use. Clinically appears to have cold sensitivity/Raynaud’s phenomen, digit ischemia or dead tissue past obstruction, abnormal Allen’s test especially common in Mideast and Asia and leads to progressive amputation as blood doesn’t flow through.

Answer 142

distended and enlarged veins that that are tortuous, dilated, thickened that are not red or swollen due to incompetent valves leading to pooling and increased pressure leads to swelling of the vein and surrounding tissue with turbulent blood flow allowing pallets to remain in sinus causing thrombus

Answer 143

Inflammatory nonatherosclerotic occlusive disease of small- to medium-sized arteries and veins, especially in smokers; occluding thrombus spares the blood vessel wall most common peripheral vascular system disease due to weak vein walls that dilate under normal to high pressure, valve failure ensues, high pressure leakage eventually occurs between deep and superficial veins w/ them becoming incompetent causing dilation recognized as varicose veins leading to swelling and increased pressure then leading to leakage then pooling and is cyclical. Commonly found in people who stand for long periods of time, hemorrhoids in people who sit for a long time are also varicose veins. better with exertion as there is more blood going through and not stopped by anything, cold improves pain w/ heat worsening it, better with elevation- blood gets to flow out, better with compression stockings. Stages and progression of venous insufficiency: telangiectasia- visible veins, venues and capillaries in the surface of the skin; varicose veins- distended and enlarged veins that arise to the surface. Pigmentation changes in the skin as a result of lack of oxygenation to skin causing death and sloughing of skin. Later stage causing active ulceration or the sloughing of frying looking skin.Edema is soft, with pitting on pressure, and occasionally bilateral. Look for brawny changes and skin thickening, especially near the ankle. Ulceration, brownish pigmentation, and edema in the feet are common. It arises from chronic obstruction and incompetent valves in the deep venous system.Often digit or toe pain progressing to ischemic ulcerations

Answer 144

Ask is it bilateral or unilateral if bilateral indicative of venous insufficiency if unilateral can be a result of infection, compartment syndrome etc. how far up the leg does it go? Is it colored red-brown as a result of hemocitarin deposits that are being pushed out from veins and can result in ulcers. Is it pitting edema? If so is it soft, frequently bilateral, press in for 1-2 seconds and graded 1-4. 1-2mm or less slightly pitting, no visible distortion, disappears rapidly. 2 2-4mm indent somewhat deeper pit, no readable detectable distortion, disappears in 10-25 sec. 3 4-6mm pit is noticeably deep may last ore than a minute with dependent extremity looks swollen and fuller. 4 6-8mm pit is very deep lasts for 2-5 min. Dependent extremity is grossly distorted commonly caused by right sided heart failure. As a result of increased plasma volume from sodium retention, altered capillary dynamics resulting in net filtration, inadequate removal of filtered lymph fluid, lymphatic or venous obstruction, and increased capillary permeability. Mechanisms for the development of edema include increased plasma volume from sodium retention, altered capillary dynamics resulting in net filtration, inadequate removal of filtered lymph fluid, lymphatic or venous obstruction and increased capillary permeability. Edema is a soft, bilateral palpable swelling from increased interstitial fluid volume and retention of salt and water, demonstrated by pitting after 1 to 2 seconds of thumb pressure on the anterior tibiae and feet. Pitting edema occurs in several conditions: when legs are dependent from prolonged standing or sitting, which leads to increased hydrostatic pressure in the veins and capillaries; heart failure leading to decreased cardiac output; nephrotic syndrome, cirrhosis, or malnutrition leading to low albumin and decreased intravascular colloid oncotic pressure; and with selected medications.

Answer 145

erythema edema along the vein and is tender along vein w/ a palpable, thickened vein using NSAIDS and compression unless it is a deep vein system also involved.