PASS Final first half.docx

14 The Heart ============ highlighted = emphasized in lecture [History related to the heart] (not bolded = stuff he didn't list but were in the book) 1. **Chest pain \*most important symptom of cardiac disease\*** - Of course, it\'s not pathognomonic it - Can be in pulmonary, intestina...

14 The Heart ============ highlighted = emphasized in lecture [History related to the heart] (not bolded = stuff he didn't list but were in the book) 1. **Chest pain \*most important symptom of cardiac disease\*** - Of course, it\'s not pathognomonic it - Can be in pulmonary, intestinal, gallbladder, and musculoskeletal (*he included psychiatric during lecture*) diseases - True sign of CHD = **Angina Pectoris**, often caused by hypoxia of myocardium - Like "clenching a fist over the sternum" = ***Levine's sign* (EXCLUSIVE** to cardiac chest pain - May not be described as pain but "pressure or discomfort" or even nausea and vomiting; "An elephant sitting on chest" - Comes out with exercise, stress, cold weather, after sex, lessens as food is digested - Doesn't come out if they are just doing nothing - Most common causes of cardiac related chest pain = coronary atherosclerosis and aortic valvular disease 2. **Dyspnea** \*highlight = two main kinds associated with cardiac disease\* - Questions about how many level blocks - **Paroxysmal nocturnal dyspnea (PND)** = occurs at night or in supine position - Why? Because it increases intrathoracic blood volume, and a weakened heart may be unable to handle this increased load \--\> CHF - **Very specific for cardiac dysfunction and can be very life-threatening** - Patient wakes up from sleep and runs to the window "for more air" - *He also talks about how we should be careful about using abbreviations because PND could also mean postnasal drip. Both PNDs can be pulmonary-tracheal conditions except one is life-threatening and the other is a nuisance* - Often associated with **orthopnea** (difficulty breathing when lying down) - *How many pillows do you need to sleep? What about 4mos ago?* - **Dyspnea on exertion** = usually caused by chronic CHF and severe pulmonary disease; *"How many level blocks can you walk? What about 6 months ago?"* - **Uncommon types:** - **Trepopnea** -- rare; occurs when lying on one side as opposed to the other; like to lie on side opposite to diseased lung - Ex) pts with chronic congestive HF like to lie on their right side - **Platypnea** -- occurs when upright and relieved with recumbency; seen in COPD and was due to increased wasted ventilation ratio 3. **[Palpitations ]** - **Common and do not always indicate serious heart disease** - Can be caused by any condition that causes increased SV, like aortic regurgitation - May be associated with a "forceful contraction" - Patients may be able to tell you what it feels like: fluttering, skipped beats, pounding, jumping, stopping, irregularity - Has the patient had similar episodes? What made them go away? - Other causes of palpitations besides primary CVD - Thyrotoxicosis, hypoglycemia, fever, anemia, pheochromocytoma - Caffeine, tobacco, **drugs** *(in lecture, he mentions **St. John's wort**),* sympathomimetic amines (to treat bronchoconstriction) - May occur during periods of normal rate and rhythm in patients with anxiety states - **Hyperthyroidism** = important cause that originates outside the CV system 4. **Syncope** - Transient loss of consciousness from poor cerebral perfusion; may be noncardiac related; can be cardiovascular or neurologic - Must ask patients what they *mean* by "fainting" or "dizziness" - Whatever preceded the syncope is very important - Some cardiac related syncope is associated with exercise - If they had palpitations before syncope \--\> arrhythmogenic cause - Position of the patient just before syncope can help determine the cause - Ex) syncope after rising from bed may be due to ***orthostatic hypertension**,* which is a common form of postural syncope due to peripheral autonomic limitation where adaptive reflexes cannot compensate for erect position - May be caused by drugs; more common in older patients - **Micturition syncope** -- occurs when men strain during nocturnal urination, often after drinking lots of alcohol - **Most common type of fainting** & hard to manage = **vasovagal syncope** - During sudden, stressful, or painful experiences - Often preceded by pallor, nausea, weakness, blurred vision, lightheadedness, perspiring, yawning, diaphoresis, hyperventilation, epigastric discomfort, or a "sinking feeling" - Caused by **sudden fall in systemic vascular resistance w/o compensatory increase in cardiac output** - Have the patient sit or lie down for them to feel better - **Carotid sinus syncope** = associated with hypersensitive carotid sinus and is most common in the elderly; ex) wearing tight collar \--\> carotid sinus stimulated \--\> systemic pressure falls \--\> syncope - **Two types** - [Cardioinhibitory] (bradycardia) - [Vasodepressor] (hypotension without bradycardia) - **Posttussive syncope** = associated in patients with COPD; has several mechanisms but it is probably because coughiing produces increased intrathoracic pressure, which decreases both VR and cardiac output - May cause a rise in CSF pressure \--\> decreased brain perfusion 5. **Weakness -** nonspecific 6. **Cough -** nonspecific 7. **Edema** - nonspecific - Frequent complaint = swelling of the legs, which is a form of **dependent edema** - If they have CHF they will probably have **symmetric edema of** the legs that **worsens as the day progresses** & is less in the morning after sleeping with legs elevated - If accompanied with dyspnea \--\> determine which one came first! - Dyspnea before edema? = cardiac **causes** - Bedridden patients may have dependent edema in the sacral area 8. **Fatigue** - Common for decreased cardiac output. Ex) CHF and mitral valvular disease - BUT not specific for cardiac problems (duh); anemia and chronic diseases can cause it - Must differentiate organic fatigue from psychogenic fatigue - **Psychogenic fatigue** = tired all the time! But more at home and in the morning; they feel best at the end of the day UNLIKE people with **organic fatigue** 9. **Hemoptysis** - Pulmonary causes ofc but **mitral stenosis** is also an important cause - How does it occur? Mitral stenosis causes bronchial veins to rupture 10. Cyanosis - Cyanosis only in the lower extremities? **Differential cyanosis** - Related to right to left shunt through a patent ductus arteriosus (PDA) from pulmonary HTN, which is at the level of the carotid & left subclavian arteries - Deoxygenated blood is pumped to the lower extremity \--\> cyanosis in legs - **\*\*MUST KNOW\*\***  [Physical examination] 1. Inspection - Check for acute distress, if they have labored breathing, if accessory muscles are being used - Check the skin color and temperature - Warmer skin = severe anemia, beriberi, thyrotoxicosis - Cooler skin = intermittent claudication in the LE - Look for xanthomata's AKA stones of yellow masses most often on extensor tendons of the fingers but also common for Achilles tendon and plantar tendons; pathognomonic for **familial hypercholesterolemia (TC \> 450mg/dl)** A close-up of a hand with a wedding ring Description automatically generated - Xanthomata's are also involved in the palms, soles, knees, elbows, and hands of 15-20% of patients with **primary biliary cirrhosis,** - Causes very elevated TC (1000-1500 mg/dl) - Rare, progressive, often fatal liver disease mostly in women - Antimitochondrial ab in 90% of pts - Pruritic is a common symptom  - **Eruptive xanthomata**: seen in familial disturbances of fat metabolism, especially hyperlipidemia types I and IV; Result when TG \>1500 mg/dl; cholesterol deposits - Mostly affects chest, buttocks, abdomen, back, face, and arms Close-up of a person\'s stomach with red spots Description automatically generated  - Also check for rashes like ***erythemia marginatum*** (red, disc shaped with raised edges) which suggests **acute rheumatic fever** in a febrile patient - Check for **Osler's nodes** which are evanescent painful lesions in the tufts of fingers and toes of 10-25% of pts with **infective endocarditis** - Inspect the nails - Inspect the **face and head** - **Supravalvular aortic stenosis**, a congenital problem, often presents with wideset eyes, strabismus, low-set ears, upturned nose, and mandible hypoplasia - **Pulmonic stenosis**: associated with moon facies and widely spaced eyes - **Hypothyroidism**: expressionless, puffy eyelids, lose outer 1/3 of eyebrows - May have a cardiomyopathy - **Lichtstein's sign =** often bilateral earlobe crease seen in those over 50yrs with significant CHD or premature atherosclerotic disease; may have many false positives and false negatives - Inspect the **eyes** - **Xanthelasma**: yellow plaques on the eyelids associated with hyperlipoproteinemia even though its less specific than xanthoma Close-up of a person\'s eye Description automatically generated Pt with hypercholesterolemia - If **Arcus senilis** is seen in patients younger than 40yrs old may have **hypercholesterolemia** - **Corneal opacities** are associated with **sarcoidosis** that may cause **cor pulmonale** or **myocardial involvement** - **Lens displacement =** often in **Marfan's syndrome** which can cause aortic regurgitation - **Conjunctival hemorrhages & Roth spots** = common in **infective endocarditis** - **Hypertelorism** = wideset eyes; associated with congenital heart disease like pulmonic stenosis and supravalvular stenosis - **Retina** can give clues for diabetes, HTN, and atherosclerosis - Inspect the **mouth** - High arched palate is associated with congenital heart problems (ex. Mitral valve prolapse) - Petechiae on the palate is associated with infective endocarditis - Inspect the **neck** - **Neck webbing** in **Turner's syndrome** may have **aorta coarctation** - **Neck webbing** may also be seen in patients with **Noonan's syndrome** **pulmonic stenosis** - Inspect the **chest configuration** - Since the heart and chest develops at the same time in embryogenesis - **Pectus excavatum (also in Marfan's)** May have mitral valve prolapse - **Pectus carinatum or pigeon's breast (also in Marfan's)** - Assess visible cardiac motions - Inspect the **extremities** - **Atrial septal defects (ASDs)** may have extra phalanx, finger, or toe - Long slender fingers is in Marfan's (associated with aortic regurgitation) - Short stature, cubitus valgus, medial deviation of extended forearm **associated with Turner's syndrome** 2. Blood pressure - Measured directly with an intraarterial catheter or indirectly with a **sphygmomanometer** - **[Sphygmomanometer ]** - Auscultate the **Korotkoff sounds** or low-pitched sounds related to turbulence produced by occluding an artery - There are several phases as the occluding pressure drops - Phase 1: pressure falls to systolic BP; tapping sounds are clear and gradually increase in intensity as the pressure falls - Phase 2: occurs at a pressure 10-15mmHg lower than Phase 1 and consists of tapping sounds followed by murmurs - Phase 3: pressure falls low enough to allow a large amount of blood to go across the partially occluded artery - Only tapping sound is heard - Phase 4: abrupt muffling and decreased intensity of sounds as pressure approaches diastolic BP - Phase 5: sounds completely disappear; no more occlusion or turbulence - Norm for adults: less than 120/ less than 80 - Borderline/prehypertensive: 120-129/ less than 80 - Classification applies to most adults without short-term serious illness A chart of blood sugar levels Description automatically generated - If systolic and diastolic pressures fall into different categories, the higher category is used to classify the BP - For diastolic BP, when Korotkoff sounds disappear is more accurate than the point of muffling but if the point of muffling is 10mmHg more than it is probably more accurate; ex. 125/75 to 65, where 75 is the point of muffling and 65 is the point of disappearance (diastolic BP) - BP should be measured to the nearest **5mm Hg** since there is a +/-3 margin of error - **[Two types of hypertension]** - **White coat hypertension**: common (15-20% of all stage 1 hypertensives); have low cardiovascular risk - **Masked hypertension**: more serious because they have normal BP in medical settings but actually have higher BPs throughout the day - High risk of CVD; in 10% of population - Cuff should be snug, 20% wider than arm, and 1in above the antecubital fossa - The bladder should overlie the artery - Cuff size too small? erroneously high reading - Lack of support for patient\'s arm? increased BP - too much pressure on diaphragm of stethoscope? low **diastolic** BP reading - **[Auscultatory gap]**: present when there is decreased blood flow to extremities like in HTN or aortic stenosis; systolic BP may get mistaken for lower BP = point of reappearance - **[BP by palpation]** - Arm should be flexed slightly; used to rule out auscultatory gap - Systolic pressure = reappearance of brachial pulse; that's all you feel for rapidly deflate; remember, brachial artery is medial and you can use thumbs - **[BP by auscultation]** - Inflate cuff 20 mm Hg above systolic P measured by palpation deflate cuff slowly to point of disappearance (diastolic) - Point of tapping = systolic - If the BP is high, measure it again at the end of the exam when pt is calmer - **[Rule out orthostatic (postural) hypotension]** - Have patient recumbent (laying down) for at least 5 mins and measure BP and pulse. Then, have them stand and measure it again - Diagnosed when BP drops equal to or more than 10mm Hg within 3mis of standing compared to lying down - Often accompanied by dizziness and increased HR - Risk factors: older age, meds, cardiac conditions, heat, prolonged bed rest, pregnancy, alcohol - **[Rule out supravalvular aortic stenosis]** - If hypertension is detected in the right arm auscultate the left arm - Shows difference in BP in the arms (ex. HTN in right, hypotension in left) - **[Rule out coarctation of the aorta]** - Common; 5-8% of all congenital heart defects; diagnosis often missed - May occur as an isolated defect or with other lesions, most commonly **bicuspid aortic valve** and **ventricular septal defect** (VSD) - Surgically correctable form of HTN - **Why you must always check LE BP in a new patient with HTN!!** - Normally, LE BP is 10 mm Hg higher than upper extremity - Patient is asked to lie on abdomen and wear a thigh cuff on the posterior aspect of the midthigh that is 6cm wider than the arm cuff; hear in popfossa - If no thigh cuff? Use normal cuff at the distal malleoli and hear for posterior tibial (against medial malleolus) or dorsalis pedis artery (along EHL tendon) - Suspected when **leg systolic BP is lower than arm, especially if femoral pulse is delayed compared to radial pulse** which should peak at the same time - **[Rule out cardiac tamponade]** - Suspect: low arterial BP & rapid and feeble pulse - **Paradoxical pulse (pulsus paradoxus)** is often a sign of it and is an exaggerated normal inspiratory fall in systolic pressure - Normal paradoxical pulse is the **normal** fall (5 mm Hg) during inspiration, so it would be more than 5 if there was cardiac tamponade - **Magnitude** determines if paradoxical pulse is normal - Techniques: measure BP **heard at expiration** while patient breathes normal. Continue to deflate the cuff slowly until sounds are heard during inspiration - **Difference greater than 10 mm Hg** = abnormal - Cardiac tamponade is caused by an increase in intra-pericardial pressure that interferes with normal diastolic filling - Abnormal paradoxical pulse is NOT specific to cardiac tamponade but it is also seen in larger pericardial effusions, constrictive pericarditis, and conditions associated with increased ventilatory effort, like asthma and emphysema 3. Arterial pulse - Note rate and rhythm of heart, contour of pulse, and amplitude - **[Cardiac rate]** - Assessed using radial pulse; NEVER palpate with your thumb because then you can record your own HR - Count pulse for 30secs and multiply by 2 to obtain bpm - Accurate for most **regular** rhythms - **Afib**: irregularly irregular rhythm; may have a **pulse deficit** since many impulses are bombarding the AV nodes and ventricles - **Pulse deficit** = difference between apical (precordial) and radial pulses - Due to varying diastolic filling periods, contractions may be very weak & unable to make an adequate pulse wave despite ventricles contracting - **Only auscultating the heart gives an accurate cardiac rate NOT radial pulses** - **[Cardiac rhythm]** - Maybe regular, regularly irregular (definite pattern), or irregularly irregular (no pattern; ex. Afib) - Best determined by **ECG** but physical examination can give clues - **Premature beats**: isolated extra beats during regular rhythm - **Bigeminy**: coupled rhythm of beats in pairs - 1st beat is a **sinus beat**, followed by a premature usually ventricular beat - If the premature beat is missed very early in the diastolic period, you may miss the rhythm by palpation alone - Could be associated with paroxysmal tachycardia or frequent atrial premature contractions - **[Palpating the carotid artery]** - MUST AUSCULTATE FOR BRUITS (laminar turbulent flow) FIRST! - Place fingers between trachea and SCM to feel carotids medial to SCM - Should be performed low in the neck to avoid pressure on the carotid sinus, which can cause a reflex drop in BP and HR - NEVER PALPATE BOTH AT THE SAME TIME - **[Characteristics of the carotid artery pulse]** - **Contour** -- shape of the wave; speed of upward slope, downward slope, and duration of wave - Normal (smooth and upward stroke is steeper and faster), diminished, increased (large, strong, hyperkinetic; increased rate of rise of ascending limb of pulse and brisk tap at its peak), or double-peaked (prominent percussion and tidal wave with or without a dicrotic wave) - Palpating finger feels a gentle pressure rise with a distinct peal - **amplitude**  [Form of the carotid artery: percussion wave, tidal wave, dichrotic notch] - shorter than this and more delayed or **tardus parvus** = aortic stenosis - aortic insufficiency = bifid pulse - water hammer pulse (pulse goes real high and then drops)= aortic insufficiency  4. Jugular venous pulse - **[Visualize jugular venous pulse]** = assess neck veins - Direct monometer of right heart pressure, indirect monometer of left blood pressure (LV) - External jugular vein is easier to visualize than the internal one because it is under the SCM and can be seen through surrounding tissue - **Right internal jugular vein** is straighter than the left and is the only one evaluated usually - Have the patient lie flat, 25 degrees horizontal, make sure their neck is not flexed, and have their head towards the right to relax the right SCM - Remember, the more they are up the lower the veins - Higher the venous pressure, the greater the elevation needed **related to the sternal angle (Angle of Louis)** - Hold a light tangentially to see shadows of the "a", "c", and "v" waves - Increased "a" wave could be due to increased resistance to right atrial emptying at or beyond the tricuspid valve like in... - Pulmonary hypertension - Tricuspid stenosis - Right atrial mass or thrombus; less common - Cannon (giant) "a" wave occurs when an atrium contracts against a closed tricuspid valve during AV dissociation like in... - Premature atrial/junctional/ ventricular contractions - Atrial flutter - Complete AV block - Ventricular tachycardia - Absent "a" wave -- no atrial contraction; seen in afib - Giant "cv" wave -- tricuspid regurgitation - Descents of the waves are more obvious A diagram of a wave Description automatically generated - *Video from the textbook shows a man with Atrial septal defect (ASD) which causes the blood from the left atrium to pass directly into the right atrium. He developed **Eisenmenger syndrome -** pulmonary hypertension and cyanosis from reversal of his shunt; with time pressure increases so much in the right heart that now you have a right to left shunt very high neck waves* - *Causes increased pressure in pulmonary circuit and more volume in right heart Severe tricuspid regurgitation with a giant "cv" wave* - Big V wave is the filling of the atria as the ventricles contract (atria receives blood from great veins AND right ventricle because of tricuspid regurgitation!) - **[Estimate jugular venous pressure]** - Use the **manubriosternal angle** to measure the pressure in the jugular venous system and the right heart - Have the patient supine and upright to demonstrate top of the neck veins best - Draw an imaginary horizontal line from vein height to sternal angle & estimate how much above the neck veins are; heart is 5cm below the sternal angle so if the height of the column is 3cm above the sternal angle, the estimated venous pressure is 3 + 5cm or 8cm water - CVP is probably elevated - Specificity = 93% to 96% - If there is neck distention up to the jaw margin while patient is seated 90 degrees, RAP exceeds 15 mm Hg usually; they have HF  - **[Evaluate hepatojugular reflex AKA abdominal compression]** - Used to assess high jugular pressure - Apply pressure over liver for 10secs to assess right ventricular function while pt is lying in bed with their mouth open, breathing normally (prevents Valsalva maneuver) - Normal = transient increase in internal and external jugular vein distension - Dilated sinusoids in liver right ventricular failure - Pressure on liver pushes blood out sinuses which goes from IVC and right side of heart neck distension **for entire period of compression** (also seen with elevated pulmonary artery wedge pressure 15 mmHg or higher) & distension **diminishes rapidly** on sudden release - Signifies increased central blood volume 5. Percuss the heart - **[Percuss the heart's borders]** - 3^rd^, 4^th^, 5^th^ intercostal spaces from the anterior axillary line to the right anterior axillary line - Normally, it goes from resonance to dullness 6cm lateral to left of sternum because the heart is there - Percussion dullness distance more than 10.5 cm in the left 5^th^ intercostal space has a sensitivity of 91.3% and specificity of 30.3% for detecting **increased left ventricular end-diastolic volume (LVEDV) or left ventricular mass** and it has a 94.4% sensitivity and 67.2% specificity for **cardiomegaly** - Palpable apical impulse greater than 3cm in left decubitus position is 100% sensitive for increased LVEDV or left ventricular mass and 40% specific 6. Palpate the heart - Done to evaluate apical impulse, right ventricle, pulmonary artery, and left ventricular motions for **thrills** - **[Point of Maximum Impuse]** - = outward motion of cardiac apex as it rotates counterclockwise and strikes the anterior chest wall during isovolumetric contraction; usually 10cm within midsternal line & no larger than 2-3cm in diameter (between size of a nickel and quarter) - Is felt in 70% of normal individuals - Changes position in COPD or if pregnant - Usually corresponds to the left ventricular apex but if there is an enlarged right ventricle the heart is rotated clockwise PMI made by right ventricle (more diffuse) - Only apply fingertips to patient's chest at the 5^th^ intercoastal space and midclavicular line since they are most sensitive at feeling localized motion - Not felt? Move fingertips in area of the cardiac apex - if laterally displaced or is felt in two interspaces during the same phase of respiration **cardiomegaly** - In a patient without risk factors to left ventricular hypertrophy, PMI felt in left lateral decubitus that is greater than 3cm is said to be 91% specific and 92% sensitive for left ventricular enlargement - Apical diameter greater than 3cm is 86% predictive for increased LVEDV - Apical diameter less than 3cm & a normal LVEDV negative predictive value = 95% - In COPD over inflation of lungs causes PMI to move down and to the right - Felt in epigastric area and lower end of sternum - If it\'s in the normal location cardiomegaly A drawing of a human chest Description automatically generated - **[Palpate for localized motion]** - In 4 main cardiac areas to auscultate: 2^nd^ intercostal space right of sternum = aortic area; left of sternum = pulmonic area; left lower sternal border = tricuspid; 5^th^ intercostal space midclavicular line = mitral; **areas DON'T overlie valves (except tricuspid);** Erb's point = 3^rd^ intercostal space left of sternum that may be the best place to listen for aortic insufficiency - Systolic impulse in pulmonic area pulmonary HTN - Caused by pulmonic valve closing under increased pressure - Suggestive of dilated pulmonary artery but it may be felt in thin individuals without pulmonary HTN - **[Palpate for generalized motion]** - Palpate for any large area of sustained outward motion called a **heave** or **lift** - **Right ventricular rock** = sustained left parasternal impulse associated with lateral retraction, suggesting a large right ventricle - Any condition that increases ventricular filling rate can produce a palpable impulse **after** main left ventricular impulse - 2^nd^ impulse in area of PMI is associated with S3, which is more easily felt than heard - Can use a tongue blade as a fulcrum to magnify movement - **[Palpate for thrills]** - = superficial vibratory sensations felt on skin overlying area of turbulence; indicates a loud murmur - Apply with gentle pressure using heads of metacarpal bones rather than fingertips - Not important because auscultation can detect loud murmurs from turbulence - Intensity grading scale from 1 to 6, with 6 being the loudest murmur; 4 or higher = thrill; very subjective 7. Auscultate the heart - Depends on stethoscope, environment, patient, listener, and their knowledge - **[The technique]** - Put on the earpieces of the stethoscope anteriorly or else the intensity of sound will be dampened and do not put them in too tight that it excludes external noise - More useful to hear with your eyes closed - Eyes \> auditory \> tactile so if you eliminate visual stimuli, the brain concentrates more on auditory stimuli - Bell = applied lightly; diaphragm = applied firmly - High pitched sounds like valve closure, systolic events, and regurgitant murmurs are better heard with the diaphragm - Always inspect and palpate before auscultating - **[Auscultating cardiac areas]** - Aortic, pulmonic, tricuspid, mitral areas but don't limit to these areas alone - While at the apex and LLSB with the bell, determine whether there is an S3 or S4 - Cardiac murmurs may radiate widely but it is typically heard at the apex with radiation to the axilla or in the neck if loud enough - There are no acoustic walls in the chest - Patient may be in supine, left lateral decubitus, upright, or upright leaning forward position - All precordial areas are examined while **supine**; Start at aortic or apex - Then have patient turn onto left side to hear for the low-pitched diastolic murmur of **mitral stenosis**, best heard with the bell - Then, with the patient upright, examine all areas of the diaphragm - Then, have them sit up and lean forward to listen for the high-pitched diastolic murmur of **aortic regurgitation** at the right and left 2^nd^ and 3^rd^ intercostal spaces which starts immediately with S2  - **[Influence of breathing]** - most murmurs or sounds from the right heart are best heard during inspiration due to increased return of blood and resultant increased right ventricular output - also S3 & S4 originate in the right heart so they are also heard best during inspiration - Always inspect and palpate before auscultating - **[Timing (is key!) of cardiac events]** - Most reliable way of identifying S1 and S2 is to time sounds by palpating the carotid at the same time of listening to the heart - Examiner uses right hand for stethoscope and left hand for carotid NOT radial because the delay from S2 to radial pulse is significant - **[Describe any murmurs present]** - Murmurs throughout systole are **holosystolic or pansystolic** - They begin with S1 and end - **Systolic ejection** murmur begins after S1 and **before S2** - **Holodiastolic** murmurs occur throughout entire diastolic period - **Location**, **radiation, duration, relationship to respiration and body position** - **Intensity** is graded from I to VI, in increasing loudness - I -- lowest; often not heard by inexperienced listener - II -- low; usually heard by inexperienced listeners - III -- medium intensity without a thrill - IV -- medium intensity with a thrill - V -- loudest murmur that is audible with stethoscope; associated with a thrill - VI -- loudest; can hear when stethoscope is removed from chest; with a thrill - Any murmur with a thrill must be at least grade IV/VI which is louder than grade II/VI because there is more turbulence; both or neither may have clinical significance - "/IV" is used cuz there is a less popular grading system involving only 4 categories - An important axim to remember is: - *Intensity of a murmur tells nothing about severity of clinical state* - **Quality** of murmur can be rumbling, blowing, harsh, musical, machinery, scratchy - **[Describe any pericardial rubs]** - Sounds like sandpaper - Results from pleural or pericardial irritation - Pericardial rubs usually have 3 components: one systolic and two diastolic - Systolic part occurs during ejection - Diastolic parts occur during rapid filling and atrial contraction - These rubs are best heard when sitting and holding breath in expiration - Sitting forward lessens chest pain in patients with pericardial rubs - A rub that disappears while the patient holds their breath = pleural - **[Goals of auscultation]** - Describe intensity of S1 and S2 in all areas & characterize systolic or diastolic sounds - S1 is loudest at the apex, S2 is loudest at the base - Splitting of S2 and A2 and P2 during inspiration is best heard at pulmonic area with patient lying on their back to increase VR and widen A2-P2 split 8. Examine for dependent edema - Transudation occurs when peripheral venous pressure is high like in CHF - Dependent edema is common in patients with heart, kidney, and liver failure & patients receiving excess IV fluids - Press on patients shin for 2 to 3 seconds and see if it pits - Pitting edema is quantified from 1+ to 4+ depending on **depth** and **duration** - 1+ is 2mm in depth and disappears rapidly - 2+ is 4mm in depth and disappears in 10-15secs - 3+ is 6mm in depth and may last more than 1min = **dependent extremity swollen** - 4+ is 8mm in depth or deeper; lasts 2-5mins = extremity grossly distorted - Bedridden patients can have dependent area at the sacrum [Clinicopathologic correlations] **[Abnormalities of the first heart sound S1]** Dependent on factors: - Rate of rise of ventricular pressure - Faster louder mitral component of S1 - Increased contractility increased intensity of S1 - Valve condition - Stiff valve from mitral stenosis louder - Valve unable to move from calcification softer - Valve position - Affects S1 intensity - **Arc of coaptation** is the angle the valve closes - If the valve is in mid-position, it travels less than when closes from widely opened position. More open louder the closure (S1) - Directly related to pressure in left atrium when the LVP exceeds it and closes the valve. This occurs when there is a shortened PR interval - Mitral valve is opened normally during diastole during ventricular filling - P wave corresponds to atrial contraction, which elevates left atrial pressure ("a" wave), further opening mitral valve in late diastole - Short PR interval? ventricular contraction is so quick after atrial contraction that the atrial pressure is still high when the LVP exceeds it mitral valve stays open longer and closes later than normal, accentuating S1 - Longer the PR interval, the softer the S1. Ex) **Wenckebach's phenomenon** produces an S1 that softens until the dropped beat occurs - Distance of heart from chest wall - Obese, have COPD, or large pericardial effusion S1 is softer in intensity **[Abnormalities of S2]** - Factors: changes in systolic pressure & valve condition - Increased systolic pressure increases S2 intensity (ex. HTN) - Calcification/fibrosis of semilunar valves softer S2 unlike a fibrotic AV valve - [**Splitting of S2** is normal ] - Any condition that delays right ventricular systole, delays P2 and produces a widened splitting of S2 - Right ventricular emptying is delayed by a right bundle branch block or pulmonic stenosis; pulmonic component of S2 is delayed during both inspiration and expiration, and **wide splitting** of S2 occurs - Any condition that shortens left ventricular systole allows A2 to occur earlier than normal **wide splitting** of S2 - Mitral regurgitation, VSD, and PDA shorten left ventricular systole and S1 to A2 interval is shorter than normal **double outlet** to the left ventricle occurs and systole is shorter - In VSD, there is a left to right shunt so right ventricular systole is also slow - **[Paradoxical splitting of S2]** - Caused by delaying left ventricular emptying process through the closure of the aortic valve after right ventricular systole and P2 have occurred, like from left bundle branch block or aortic stenosis - Can also be caused by delay is left ventricular ejection from left ventricular failure and severe HTN - **Normal sequence of A2 and P2 are reversed** - During inspiration, P2 moves normally away from S2 toward A2 = **narrowed split** - With expiration, P2 moves normally and approaches S1; P2 and A2 split widens = **paradoxical** - **Fixed splitting** = auscultatory hallmark of ASD; wide and does not change with respiration because inspiratory increases in VR to the right atrium normally raise its pressure - During expiration, the RAP is lower, but the left to right atrial shunt keeps the volume in the RA constant during respiration no normal splitting A diagram of a variety of colors Description automatically generated with medium confidence **[Systolic clicks]** - **ECs** (ejection clicks) are high-pitched short sounds that occur early in systole at the onset of ejection and are produced by deformed semilunar valves opening - may be produced by pulmonic or aortic stenosis - more calcification less mobility ECs disappear - **midsystolic clicks** are not ECs; they may be single or multiple and change in position during the cardiac cycle - most common condition associated with them = mitral or tricuspid valve prolapse **[Diastolic opening snaps]** - AV valve is silent & occurs 100ms after S2 (time it takes to say mama quickly) - **Opening snap** occur with a deformed AV valve; sharp and high-pitched - Mitral OS (opening snap) of mitral stenosis occurs after A2 - Worse mitral stenosis increased pressure in left atrium gradient across mitral valve increases mitral valve opens earlier than normal when LVP falls below left atrial pressure - Tricuspid OS of tricuspid stenosis occurs after P2 - **OS interval** = between S2 and OS; shortens as stenosis worsens - Severe OS interval = 50-60msec **[Murmurs ]** - Caused by turbulent energy (often caused by obstruction or large volume of blood through stenotic normal opening) in heart and BV walls - **Blowing murmurs** = produced by large gradients with variable flow volumes - **Rumbling murmurs** = from areas of small gradients - **Harsh murmurs** = from large gradients and high-flow - **Ejection murmur** = medium pitched murmur from turbulence across a semilunar valve during systole, such as in aortic stenosis or pulmonic stenosis - Diamond-shaped and crescendo-decrescendo - Begin slightly after S1 and end before S2 - EC from stenosis may precede the murmur - Best heard with diaphragm - Intensity does not indicate severity because they are based on flow - Change in flow or volume can produce ejection murmur even in normal valve - Highly sensitive but not very specific sign of aortic stenosis - Increased flow across minimally narrowed aortic valve loud murmur - Decreased flow across severely stenotic aortic valve barely audible  - **Regurgitant systolic murmurs** are from retrograde flow from high pressure to low pressure, like in mitral or tricuspid regurgitation - Holosystolic or pansystolic; begin with S1 & end after S2 cuz the ventricular pressure is higher than atrial pressure, even after semilunar valve closes - S3 indicates volume overload - High pitched and best heard with diaphragm - Regurgitation = incompetence = insufficiency but the preferred term is regurgitation because it implies retrograde flow - Highly sensitive for valve regurgitation A diagram of a normal heart rate Description automatically generated - **Diastolic AV murmurs** begin after S2 with AV valve opening - Ex. Mitral and tricuspid stenosis - There is a pause between S2 and beginning of murmur - Isovolumetric relaxation occurs during this period - Decrescendo, beginning with an OS if the valve is mobile, and low pitched - Best heard with **bell** and patient in left lateral decubitus position - Rapid filling does not occur because AV valve is stenotic and a gradient persists throughout diastole - Atrial contraction increases the gradient at the end of diastole or presystole and there is an increase in the murmur then during normal sinus rhythm - = **presystolic accentuation** - Diastolic AV murmur is sensitive [and] specific for AV valve stenosis - 1^st^ heart sound is the loudest sound. Cadence and emphasis of sounds are best heard by saying this mnemonic:  - OS is mitral OS and DM is diastolic murmur - "aaaalve" is presystolic accentuation in mitral stenosis with normal sinus rhythm - **Diastolic semilunar murmurs** begin immediately after S2 - Heard in aortic or pulmonic regurgitation - Unlike diastolic murmurs, there is no delay after S2 - High pitched, decrescendo best heard with diaphragm while sitting up and leaning forward - Low sensitivity by **high specificity** A diagram of a normal pulse Description automatically generated  15 Peripheral Vascular System ============================= highlighted = emphasized in lecture; **he barely went over this chapter :/** Two most important diseases of the peripheral vascular system = **atherosclerosis** of the larger arteries & Microvascular disease - Peripheral vascular disease (PVD) is a nearly **pandemic** condition that usually affects **men over 50** - Risk factors: - Abnormal cholesterol - Diabetes - Coronary artery disease - HTN - Kidney disease involving hemodialysis - Smoking - Strokes - Classic symptoms of PVD: pain, heaviness, fatigue, burning, or discomfort in feet, calves, or thighs that usually appear only when walking uphill, faster, or long distances; eventually come on more quickly with less exercise needed - Legs or feet may feel numb at rest, cool to the touch, or pale - Severe PVD may present as: - Erectile dysfunction - Pain and cramps at night - Pain or tingling in feet or toes, which can be so severe that any weight (clothes, sheets) is painful - Pain is worse when raising leg and improves when dangling legs - Skin that looks dark and blue - Sores that do not heal Most common cause of peripheral arterial occlusive disease is **atherosclerosis**, affecting medium and large vessels of the extremities - May manifest by aneurysmal dilatation - Abdominal aorta commonly affected - **Abdominal aortic aneurysm** (AAA) -- focal dilation 50% greater than normal diameter of aorta; often below renal arteries and may extend to external iliac - Risk factors: advanced age, male, Caucasian, family history, smoking, presence of other large vessel aneurysm, atherosclerosis - 5x more common in men than women - 3.5x more common in white men than Black men - Top 15 causes of mortality in 85-89 age range - Produces few, if any symptoms; may be a **pulsatile mass**; 1^st^ finding is often a **catastrophic rupture of the aneurysm** - AAA larger than 5cm 20% risk of rupture in 1 yr & 50% in 5yrs **Microvascular arterial disease** is in patients with diabetes - Peripheral neuropathy of the sensory, motor, or ANS = common sequelae - Diabetic patients -- [tragic "Rule of 15"] - 15% of all diabetics will have a foot ulcer in their life - 15% will lead to osteomyelitis - 15% will lead to amputation - Diabetic patients also have a "Rule of 50" - 50% of amputations are transfemoral/transtibial - 50% of patients have a 2^nd^ amputation in 5yrs or less - 50% of patients die in 5yrs or less PVD often progresses to **venous stasis** and **thrombotic disorders** pulmonary embolism **[Structure and Physiology]** - PVD causes ischemia of the extremities, especially when muscles are actively contracting - *Venous system* = low-pressure capacitance vessels that contain 70% of blood volume; little resistance; controlled by valves & neural and humoral stimuli - When upright, venous pressure in the legs is the highest - Over many years, veins dilate due to their walls weakening causes veins to not be able to close adequately blood refluxes and venous pump is less sufficient in returning blood to heart - Leads to chronic venous insufficiency **venous stasis** - **Complications of venous stasis**: - Pigmentation, dermatitis, cellulitis, ulceration, thrombus - *Lymphatic system **= extensive vascular network responsible for returning tissue fluid (lymph) back to the venous system*** - Most important clinical symptoms of lymphatic obstruction = *lymphedema* and *lymphangitis* **[Review of symptoms]** Remember, most PVD pts are asymptomatic but when they are symptomatic these symptoms result 1. Pain = principal symptom of atherosclerosis, especially while walking a. *Intermittent claudication* = pain in the LE during exercise relieved by rest i. **Pain is always distal to occlusive disease** ii. **Supply does not equal demand** -- as disease progresses, pain at rest occurs; often severe; aggravated by cold and elevation especially when sleeping b. *Venous claudication* = pain from **deep vein thrombosis** that is caused by venous valvular incompetence, outflow obstruction, and calf muscle pump dysfunction iii. Motionless standing is more painful!! Because contraction of the leg muscles while walking pumps blood through veins back to the heart c. *Neurogenic claudication* = common for lumbar spinal stenosis or spinal cord nerve inflammation; often related to posture iv. Certain postures like arching puts pressure on lumbosacral nerve roots and cauda equina d. If a male patient complains about LE pain while walking, the examiner should inquire about [erectile dysfunction]; leg numbness or weakness may also occur e. *Leriche syndrome **= chronic aortoiliac obstruction*** with intermittent claudication and erectile dysfunction; severe atherosclerosis of the terminal aorta and iliac arteries at the aortic bifurcation f. *Pseudoclaudication* = musculoskeletal disease in the lumbar region that involves bilateral leg pain or numbness that occurs during walking and resting 2. Skin changes g. Skin color changes are common in PVD h. Cool & pale extremities in chronic **arterial** insufficiency i. Warm extremities in chronic **venous** insufficiency v. Erythematous, erosions from excoriations, and edema also j. With chronic insufficiency, stasis changes produce **increased pigmentation**, swelling, aching, or heaviness in mostly **lower 1/3 of medial leg** k. Acute deep vein thrombosis secondary inflammation surrounding vein, leading to warmth redness and fever l. Most reliable symptom associated with deep venous obstruction = swelling m. LE Superficial veins only carry 20% of drainage, so are not associated w/ swelling 3. Edema n. Compare both extremities; **2cm circumference** difference at the ankle or midcalf is significant o. **Lymphedema** -- from primary abnormality in lymphatic system development or acquired obstruction to flow vi. *firm, nonpitting edema* regardless of cause vii. skin slowly becomes more rough like pigskin viii. painless; **only symptom is usually heaviness of extremity** 4. Ulceration p. Caused by persistent ischemia of limb; associated with gangrene q. Almost inevitable after skin has thickened and circulation is compromised r. Ulceration related to arterial insufficiency occurs due to **trauma** to heel and toes ix. Painful, have discrete edges/borders, "punched out" appearance, crust covered, erythematous x. Rapidly developing ulcers s. Ulceration due to venous insufficiency leads to stasis ulceration which is usually painless and appears as a diffusely red, thickened area over the medial malleolus xi. Cobblestone appearance of skin xii. Ulceration occurs with even slight trauma xiii. Slowly developing ulcers xiv. Poorly defined borders; shallow xv. **Stasis dermatitis** -- skin becomes firm and reddish brown xvi. Infection is a common complication [Stasis dermatitis and ulceration] Close-up of a person\'s legs with a rash on their feet Description automatically generated A close-up of a skin disease Description automatically generated 5. Emboli t. Thrombus formation is from stasis and hypercoagulability u. Venous stasis is the most important cause of thrombus formation v. Risk factors: bed rest, CHF, obesity, pregnancy, extended airplane travel, oral contraceptives w. Secondary symptoms: xvii. Shortness of breath from pulmonary emboli xviii. Abdominal pain from splenic, intestinal, or renal artery emboli xix. Neurologic symptoms from carotid or vertebrobasilar artery emboli xx. Pain and paresthesia from peripheral artery emboli 6. Neurologic symptoms \*mostly from cerebrovascular occusion\* x. Strokes, dizziness, changes in consciousness y. Internal carotid artery occlusion produces contralateral hemiplegia, contralateral sensory deficits, and dysphasia z. Vertebrobasilar disease causes diplopia, cerebellar dysfunction, changes in consciousness, and facial paresis **[Physical examination]** - Stethoscope, tourniquet, tape measurer - Inspect, palpate, auscultate, and some additional tests if diseases is present i. General inspection a. Examine extremities for erythema, cyanosis, swelling, asymmetry, deformities, edema, hair loss, surgical scars, venous patterns and skin color changes  A close-up of a person\'s legs Description automatically generated b. Assess skin temperature using the back of your hand & comparing each extremity i. Coolness is common with arterial insufficiency c. Inspect for varicosities especially in the proximal femoral ring and distal leg because those area may not be visible when patients are lying down ii. *Long saphenous vein* varicosities = medial, anterior to medial malleolus & drains into femoral vein in femoral triangle iii. *Short saphenous vein* = posterior, posterior to lateral malleolus & drains in popliteal vein between two gastrocnemius heads  Close-up of a person\'s legs with varicose veins Description automatically generated ii. Palpation d. Venous palpation iv. At the saphenofemoral junction (SFJ) that is 3-4cm inferolateral to the pubic tubercle, near the inguinal ligament v. Ask pt to cough and see if there are any impulses or thrills vi. Palpable thrill results from turbulent retrograde flow at the SFJ vii. *Saphena varix* -- varicosity where the saphenous vein meets the femoral vein in the SFJ; often a bluish swelling that may be mistaken as a hernia viii. *Saphenopopliteal reflux* may be in 25% of pts with primary varicose veins 1. Associated with; 98% palpable short saphenous vein in popfossa sensitivity and 75% specificity for saphenopopliteal incompetence ix. **Delay i** e. Arterial palpation x. Most important finding = decreased or absent pulse xi. Always record amplitude, rate, tenderness, tortuosity, nodularity xii. Best to do it in a warm place because cold temps may cause peripheral vasoconstriction reduces peripheral pulse intensity xiii. Socks or stockings must be removed to evaluate LE pulses xiv. If you think you are confusing your pulse for the patient's pulse, palpate their pulse with your right hand and your own pulse with your left hand 2. Easy to confuse if you use your thumb to palpate radial pulse, which has a lower amplitude xv. At the corners of the pubic triangle; also evaluate symmetry and timing with radial artery pulse since the peak at the same time xvi. Arterial pulse examination may miss PVD up to 50% of the time f. Grading of Pulse amplitude -- 4 point scale xvii. 0 No palpable pulse; absent xviii. 1+ faint, but detectable pulse; easily obliterated with pressure xix. 2+ normal easily identified; not easily obliterated with pressure xx. 3+ increased pulse; obliterated with moderate pressure xxi. 4+ strong, bounding pulse; can't be obliterated with pressure g. Palpate radial pulse xxii. Stand in front of pt and palpate both wrists with your index, middle, and 4^th^ fingers of the opposite hand xxiii. Evaluate for symmetry of timing and strength h. Palpate brachial pulse xxiv. Can use thumbs because its stronger than digital pulses xxv. Medial, under the belly of the biceps muscle xxvi. Stand in front of patient and palpate both arms xxvii. Once you feel brachial pulsation, apply progressive pressure until maximal systolic force is felt i. Palpate carotid artery AFTER auscultating it xxviii. Supine position w pts head elevated & turned away from carotid artery being evaluated; helpful for pts to hold their breath during auscultation xxix. Listen for murmurs which may be a bruit from atherosclerosis or it may be from the heart j. Palpate abdominal aorta xxx. Important because once AAA is identified mortality is less than 5% if it's non-ruptured but climbs to 90% once it ruptures xxxi. Patient should be supine xxxii. Palpate deeply but gently into the midabdomen xxxiii. Pulsatile mass indicates AAA (60% sensitive) 3. But only 50% of pts with diagnosed aortic ruptures have it xxxiv. Caution! Thin pts may have a normal pulsatile aorta xxxv. Other findings associated with AAA: abdominal bruit, femoral bruit, femoral pulse deficit xxxvi. Bruit w/ severe pain in abdomen or back, with absent or diminished distal pulse that later returns suggests acute rupture of an AAA k. Rule out abdominal bruits xxxvii. Pt should be supine xxxviii. Place diaphragm in midline 2inches above umbilicus xxxix. Listen for *aortic bruit*s, especially if heard in systole & diastole which raises suspicion for renovascular HTN (39% sensitivity, 99% specificity) 4. If it is only heard during systole, it holds little value because they are found in normal individuals & those with essential HTN xl. *Renal bruit* may be the only clue to renal artery stenosis, which is a surgically correctable form of hypertension 5. Listen 2in above umbilicus and 1-2inches to the left and right l. Palpate femoral pulse and rule out coarctation of aorta xli. Pt should be supine; At the corners of the pubic triangle; also evaluate symmetry and timing with radial artery pulse since the peak at the same time xlii. Femoral artery runs obliquely through the pubic hair triangle inferior to the inguinal ligament at a point midway between the pubic tubercle and ASIS xliii. Auscultate for a bruit if one of the femoral pulses are diminished xliv. Compare the timing of the femoral and radial pulses 6. Delay in the femoral pulse relative to the radial pulse suspicious of coarctation of aorta, especially in a pt with HTN a. These pts have UE HTN and LE hypotension m. Palpate popliteal pulse xlv. Difficult to assess xlvi. Must assess each popliteal artery separately xlvii. Place thumbs on the patella and remaining fingers in the popfossa medial to the lateral biceps femoris tendon using firm pressure xlviii. Hold patient\'s leg in flexion n. Palpate dorsalis pedis pulse xlix. Best palpated when foot is dorsiflexed; can feel both sides at same time l. DP artery passes along the extensor retinaculum lateral to the extensor tendon of the great toe li. Usually easily palpated in the groove between EDL and EHL o. Palpate posterior tibial pulse lii. Can be palpated posterior to the medial malleoli between the tibialis posterior tendon and FDL tendon; both can be felt simultaneously liii. Absent in 15% of normal subjects but most sensitive sign of occlusive peripheral arterial disease if older than 60 = absent posterior tibial pulse iii. Examine lymphatics p. Physical signs of lymphatic system disease = liv. **Palpable lymph nodes** lv. **Lymphangitis** lvi. **Lymphedema** q. Lymph nodes are either *painless* or ***tender***, *single* or ***matted***, and *mobile* or ***fixed*** lvii. Bolded = most likely pathological r. *Generalized lymphadenopathy* -- palpable LNs in 3 or more chains lviii. May indicate lymphoma, leukemia, collagen vascular disorders, systemic bacterial, viral, and protozoal infections s. *Localized lymphadenopathy* -- often from local infection or neoplasm t. *Lymphangitis* -- inflamed lymphatic channels from infection distal to it lix. Hallmark = red streaks on the skin! lx. Infection ca rapidly spread to regional LNs lxi. Associated with fever, chills, malaise and sometimes headache, loss of appetite, and muscle aches lxii. **B-hemolytic streptococci** -- most common cause lxiii. Those with diabetes, immunodeficiency, varicella, chronic steroid use, and other systemic illness have increased ris for serious or rapidly spreading lymphangitis u. *Lymphedema* -- caused by lymphatic flow obstruction; hard to distinguish from other types of edema iv. Palpate for epitrochlear nodes v. Have the patient flex the elbow 90 degrees w. Feel 3cm proximal to medial epicondyle of humerus in the groove between the biceps and triceps x. Rarely palpable but if they are present, note their size, consistency and tenderness y. Acute infections of the ulnar side of the forearm and hand may cause epitrochlear adenopathy lxiv. Also in non-hodgkin lymphoma! v. Other special techniques used in conjunction with other testing z. Evaluate arterial supply in LE lxv. Most important sign of arterial insufficiency is decreased pulse lxvi. **Elevation test** = pallor that develops after elevation & dependency of ischemic extremity provides a guide to the extent of decreased circulation 7. have patients lie on their back and elevate their legs 60 degrees above the bed; inspect feet for pallor after 60secs 8. normally no pallor is present (grade 0); definite pallor in 60 secs (grade 1); pallor in 30 to 60secs (grade 2); pallor in less than 30secs (grade 3); pallor without elevation is grade 4 9. then have the patient sit with their feet dangling off the side of the bed to assess the time for color to return (**rubor dependency test**) b. normally it takes 10-15secs for color to return and 15secs for superficial veins to fill; if it takes longer then moderate occlusive disease is present with adequate collateral blood supply but if it takes more than 40 secs = severe ischemia is present (may be accompanied with dusky or cyanotic color) 10. **only useful if valves of superficial veins are competent** lxvii. Ankle-brachial index (ABI) or Ankle brachial pressure index (ABPI) 11. Quick noninvasive test & cornerstone of LE vascular evaluation 12. Ratio of systolic BP in the legs over systolic BP in the arms using ultrasound 13. Each foot's posterior tibial artery and dorsalis pedis artery is used, with the higher of the two used for the ratio 14. Use the highest of the left and right arm brachial systolic BP 15. 16. Normal ration = 0.90-1.30 17. Lower BP in legs indicates PVD (less than 0.90) 18. Greater than 1.30 = abnormal due to calcification & noncompressible vessels 19. 90% sensitive and 98% specific for hemodynamically significant stenosis of more than 50% a. Evaluate capillary refill time lxviii. Put pressure on the nail bed to blanche/whiten it time how long it takes for blood to flow back; usually less than 2secs lxix. If it takes a long time, it indicates arterial vascular insufficiency, dehydration, hypothermia, and most types of shock lxx. Should do it in room temperature area b. Evaluate arterial supply in the upper extremity lxxi. Much less common than in LE lxxii. Allen test -- Determines patency of radial and ulnar arteries in order to assess if arterial insufficiency is present in the UE; takes advantage of the radial-ulnar loop 20. Occlude radial artery with one hand and ulnar artery with the other 21. Ask pt to clench fist tightly 22. Observe palm color which should be pale at this point 23. Release pressure on the radial artery while maintaining pressure on ulnar artery 24. Color of palm should return within seconds 25. If it takes a long time to return = radial artery insufficiency 26. Repeat test but this time occluding ulnar artery 27. If color doesn\'t return within secs = ulnar artery insufficiency c. Test for incompetent saphenous veins lxxiii. Easy; ask pt to stan and dilated varicose veins become obvious lxxiv. Compress proximal end of varicose vein with one hand while placing other hand 15-20cm below distal end of vein lxxv. When saphenous valves are incompetent, an impulse is transmitted to the examiners distal fingers d. Test for retrograde filling lxxvi. *Trendelenburg maneuver* -- assesses venous valvular competency in communicating veins, as well as in the saphenous system 28. Pt is supine and affected leg is raised 45 degrees for 15-20secs to drain venous blood from it 29. While leg is elevated, place a tourniquet around the proximal thigh to compress superficial veins 30. Have the pt stand and look for varicose veins to reappear 31. Rapid filling below SFJ = incompetent perforators; can determine their location by moving tourniquet position 32. 91% sensitive, 15% specific for superficial reflux **[Clinicopathologic correlations]** [Signs of acute arterial occlusion] = **5 Ps** - Pain - Pallor - Paresthesia - Paralysis - Pulselessness [Chronic progressive small-vessel disease] - Characteristic of diabetes mellitus - Commonly observed when arterial pulses are present despite gangrene in extremity  - **Necrobiosis lipoidica diabeticorum =** Cutaneous hallmark of diabetes - Waxy, yellow, or reddish brown, sharply demarcated, plaquelike lesions - Often on anterior surface of lower legs - Shiny and atrophic with marked telangiectasia over surface - Tend to ulcerate and when they do, they heal slowly - Often **predates** development of frank diabetes - Severity of lesion does NOT relate to severity of disease [Deep vein thrombosis (DVT)] - Unilateral marked swelling, venous distention, erythema, pain, increased warmth, and tenderness - Calf swelling is most associated iliofemoral thrombosis - Calf pain (*Homans sign*) is present in 50% of DVT pts with femoral vein thrombosis after squeezing affected calf or slow dorsiflexion - Low sensitivity and may have lots of false positives - Often associated with inflammation and **thrombophlebitis** - In many cases, indurated veins in grown or medial thigh is palpable = **cord** - Often associated with symptomatic **pulmonary embolism** in 10% of pts - If thrombi is too big maybe pulmonary artery obstruction - 45& of DVT pts have asymptomatic, pulmonary embolism, or both - *Raynaud's disease/phenomenon* -- whilte (pallor), blue (**cyanosis**), and red (rubor) of the distal fingers or toes - *Decreased blood supply* pallor because of arteriospasm - Can be primary (idiopathic) or secondary - *Gangrene* **-- deep tissue necrosis from a decreased blood supply** - Commonly affects extremities, including toes, fingers and limbs - Affected by anything that affects blood flow 16 The Breast - 1 in every 8 women will develop breast cancer - Most common disease to develop in women and 2^nd^ most common cause of death in women after lung cancer - Higher incidence in US compared to Europe, Asia, and underdeveloped countries - There was a dramatic decline in breast cancer incidence in 2000 thanks to reducing hormone replacement therapy - Estrogen & progesterone therapy increases risk for breast cancer and CAD - [Risk factors for breast cancer] - Age, genetics, family & personal history of breast cancer, early menarche (before 12), late menopause, excessive alcohol, obesity, nulliparity (never gave birth to a viable baby), hormone replacement therapy, chest radiation - Affected 1^st^ degree relative doubles risk for breast cancer - 2 affected 1^st^ degree relatives or if the relative was diagnosed prior to menopause it triples the risk - If you had cancer in one breast, you have 4% increased incidence of getting it in the contralateral breast - Women who had their 1^st^ child at 30 or older - Breast cancers are painless masses best screened by a breast self-examination (BSE) and mammography (72.4% sensitive, 46.4% specific) **[Structure and Physiology]** - *Mammary glands* -- in all mammals; conical and often unequal in humans - Breast extends from the level of the 2^nd^ or 3^rd^ rib to the level of the 6^th^ or 7^th^ rib, from the sternal edge to the anterior axillary line - "tail" of the breast extends into axilla and is thicker than other breast areas because the upper outer quadrant has the most mammary tissue - Often site of neoplasia - Normal breast overlies the pectoral muscles & contains glandular tissue, ducts, supporting muscular tissue, fat, blood vessels, nerves, and lymphatic vessels - 15 to 25 lobes make up breast glandular tissue and they each drain into separate excretory ducts that terminates in the nipple - Each duct dilates as it enters the base of the nipple to form a *milk sinus(=* reservoir for milk during lactation) - Each lobe subdivides in 50-75 lobules that drain into a the excretory duct - Smooth muscle contracts the areola and compresses the nipple to make them erect and firm, aiding the emptying of milk sinuses - The nipple and areola are deeply pigmented but only the nipple is hairless - Dermal papillae have sebaceous glands that are grouped near milk sinus openings - Areolar Sebaceous glands are *Montgomery tubercles* which look like small nodules - *Cooper ligaments* project & suspend breast tissue with outer layers of superficial fascia - Internal mammary artery supplies the breast and there is an extensive venous and lymphatic drainage network - Most lymphatic drainage empties into nodes of the [axilla] - Other nodes lie under the lateral margin of pectoralis major muscle, along the medial side of the axilla, in the subclavicular region A diagram of a breast Description automatically generated - Cannot evaluate internal mammary LNs and the ones frequently associated with metastatic spread, the **rotter's nodes** [Physiologic changes in the breast are caused by:] - Puberty and aging/menopause - Menstrual cycle - Pregnancy [Development of the breast] - At birth: branching system of ducts empty into a developed, slightly elevated nipple - Shortly after birth: slight milky material secretion - 5-7 days: secretion stops - *Breast bud stage* before puberty: elevation of breast & nipple, areola size increase; development of contour of breast = earliest sign & its associated with development of fatty tissue before glandular - Stage 3 - Puberty onset: areola enlarges and darkens; areola looks pasted on - Stage 4 - Menstruation onset: well-developed breasts, forward projection of nipple and areola at the apex of the breast - Stage 5 - 1-2 yrs later: breast is mature, only nipple projects forward, areola receded to natural contour of breast [Tanner stages of breast development]  Many females never go from stage 4 to stage 5 [Characteristics of the adult breast] - Nodularity, density, fullness - Most important factor = excess adipose tissue - \# of glandular tissue is equal in all women so size of breast doesn't affect nursing - Menopause: decreased breast size, less dense, and less elastic tissue - 3-5 days before menstruation **engorgement** AKA increased size, density, nodularity, and sensitivity of the breasts; **don't diagnose breast mass at this time;** reevaluate during midperiod of next cycle - Pregnancy fuller & firmer, areolae darken, nipples erect as they enlargen - 3^rd^ trimester *colostrum* -- thin, yellow secretion; stops being secreted in the mother begins nursing within 24hrs of birth - Breastfeeding? softer, less nodular breasts, markedly engorged; lactation continues for a short time after female stopped nursing [Neuroendocrine control of the breast] - Suckling hypothalamus (stimulates 2 areas) - anterior pituitary produces *prolactin* causes glandular tissue to produce milk - posterior pituitary produces oxytocin stimulated contraction of muscle surrounding glands to force milk out [Accessory nipples] - often form along the *milk line* which is an embryological epithelial ridge from the axilla to the symphysis pubis (inguinal region); multiple rudiments for future breast development - may be glandular (may have milk letdown), nipple, or only areola - most common site = axilla followed by just below normal breast - 50% are bilateral - Little clinical significance  **[Review of Specific Symptoms]** - Mass or swelling - Pain - Nipple discharge & nipple changes - Change in skin over breast - Inflammation (mastitis) 1. Mass or swelling a. Could be physiologic nodularity or fibrocystic changes that occur throughout menstruation cycle; unless dealing with someone that has family history, most breast masses are benign b. Biopsy and do imaging if associated with nipple discharge, nipple inversion, or skin changes 2. Pain c. Cyclic pain is due to hormone level changes throughout menstruation d. Fibrocystic changes are usually painless, while rapidly enlarging cysts may be painful e. Uncommon to have in breast cancer but it can still occur f. Never delay evaluation of a painful breast mass g. Nonabnormal breast pain can be treated by: avoiding tight bras, applying warm or cold compresses, using NSAIDs h. Can be from mastitis (caused by suckling that causes a tear in the areola infection can occur from skin flora) or a carcinoma 3. Nipple discharge i. Uncommon; always raises suspicion of benign or malignant breast disease j. If a pt has recently given birth, ask if there were any problems during delivery k. Most common types are serous (thin & water, may look yellow) and bloody l. Serous discharge is often from an intraductal papilloma is one of the large subareolar ducts; oral contraceptives can also induce bilateral form m. Bloody discharge is associated with an intraductal papilloma, which is common in pregnant and menstruating women i. May also be associated w malignant intraductal papillary carcinoma n. *Galactorrhea* is common for a few months after pt stopped nursing; in rare cases, milky secretion occurs for a yr; caused by any prolactin release ii. May also be due to **pituitary tumor** that interferes with normal hypothalamic-pituitary feedback loop or certain **psychiatric tranquilizing medications** iii. Can also be induced by mechanical stimulation or suckling 1. There is glandular tissue in a male breast!! 4. Any nipple that was inverted/everted and becomes everted/inverted is cancer unless proven otherwise 5. Change in skin over breast o. Important sign of breast cancer p. Dimpling (=underlying sign of carcinoma), puckering, and scaliness warrants further investigation q. Unusually prominent pores, indicative of edema is an important sign of malignancy and is called *Peau d' orange* (means orange peel in French) iv. Thick and pitted skin; edema v. In early cancer stages, lymphatic vessels are dilated and contain occasional emboli of carcinoma cells limited peau d' orange over the lower half of the areola vi. Ligaments contract vii. As disease progresses, more vessels blocked generalized edema  **[General suggestions]** - Pay attention to family history - Acquire about mammograms, breast biopsies and surgeries, radiation treatment (whether its premenopausal or post), birth control pills, estrogen therapy, etc - Chemotherapy and chemoprophylaxis can alter hormone levels, alter a woman\'s sexual arousal/response, and cause early menopause - Breast cancer pts live with fear of bad prognosis AND disfigurement - Alternative to mastectomy for early, small cancers = lumpectomy **[Physical examination]** No special equipment needed! Done in 2 parts: sitting & lying down - Inspection - Axillary examination - Palpation - Inspects LNs when pt is sitting - Palpate entire breast using firm, gentle pressure exerted by pulp of fingers when pt is lying down - Divide breast into 4 quadrants and imagine two lines running through the nipple at right angles to each other - By visualizing the breast as a clock face, one line is the 12 o clock -- 6 o clock line, while the other is the 3 o clock -- 9 o clock line 1. Inspection a. Ask pt to remove gown to waist and have their arms at their side b. "I am inspecting the breasts for any changes in the skin, contour, or symmetry" c. Size, shape, symmetry, contour, color, edema, inversion/eversion of nipples, discharge; nipples should be symmetric; is there abnormal bulging? d. Erythema can be from infection or inflammatory carcinomaA close-up of a breast cancer Description automatically generated e. *Retraction phenomena* -- dimpling from neoplasm & its fibrotic response f. skin retraction is commonly associated with malignancy that causes abnormal traction on Cooper ligaments g. Cancer can cause larger mammary glands to shorten & invert/flatten nipple h. ANY change in nipple position is important because women can have congenitally inverted nipple on one or both sides  Nipple inversion due to breast cancer i. Red, scaling, crusting plaque around one nipple, areola, or surrounding skin *Paget disease,* associated w underlying invasive or intraductal carcinoma i. Looks like eczema but is unilateral ii. Skin may also weep and erode iii. Less common form of Paget's is in the anus or genitalia and is associated with malignant disease of the adnexa, bowel, or GU tract  j. Inspect the breasts in various postures to see if there are less evident signs of retraction A person with her hands on her hips Description automatically generated  2. Axillary examination i. Have pt be seated facing examiner w relaxed pectoral muscles ii. Right axilla exam: support pts right forearm with right hand and use fingertips of left hand, starting low in axilla, going up with slow rolling motions, and drawing patients arm medially when you're at the mid axilla so you can get higher up in the actual axilla iii. Palpate supraclavicular, subclavian, and axillary regions iv. Use small, circular motions over ribs to detect adenopathy v. Freely mobile nodes of 3-5mm are common and indicates lymphadenitis secondary to minor trauma of hand or arm 3. Palpation a. Ask pt to lie down b. Often better to examine left breast from left side for large breasted women (but normally stand on the right side) c. Small-breasted women may have their arms at their sides while larger-breasted women should be instructed to place their arms behind their head d. Place a pillow beneath the shoulder on the side being examined e. Use the "spokes of a wheel", concentric circle, or vertical strip method f. ["spokes of a wheel" method]: start at the nipple and move out to the 12 o clock position; return to the nipple and move along the 1 o clock position; start at the areola go out to the tail g. [Concentric circle method]: start at the nipple and move from the nipple in a continuous circular manner h. Can describe lesions as "3 cm from the nipple along the \_\_ o\'clock line." i. [Vertical strip or grid method]: divide breast into 8 or 9 vertical strips, each one finger's width; hold 3 middle fingers together and use pads of the fingers to make dime-sized circles at light, medium, and deep levels of pressure i. Superior, most sensitive method but more time consuming ii. Patients should do the exam j. May mistake **inframammary fold** for a breast disorder; often seen in older women & it is where mammary tissue is bound tightly to chest wall k. **How to describe mass:** size in cm and its position, shape, delimitation (borders), consistency/hardness, mobility iii. benign = freely mobile; carcinomas = usually fixed l. Evaluate retraction phenomenon (how mass induces molding of the skin)  m. Palpate subareolar area which is directly under the areola iv. Breast tissue is less dense v. Abscess of Montgomery glands may cause a tender mass here n. Examine the nipple for retraction, fissures, and scaling o. To examine for discharge, place each hand at the sides of the nipple and gently compress it; can ask pt if they would like to do it themselves p. Place fingers and press them down on the areola to feel for any masses (should feel hollow in males) **[Breast Self-Examination (BSE)]** - Has limited value in detecting early cancer - Monthly BSE has been replaced by "breast self-awareness" where women older than 20 become aware of the normal appearance and feel of their breasts but without a specific schedule or examination technique - Physician should encourage women to report changes of the breast but reassure them that most findings are not cancer - [BSE techniques] - Stand with your arms at your side and inspect - Raise your arms and clasp them behind your head - Press hands forwards and look for any changes in breast tissue - Put hands down and place them on hips - Bend slightly towards the mirror as you pull shoulders and elbows forward - Rase right arm and palpate your right breast with your left hanf - Gently squeeze nipple for any discharge - Repeat raising your arm and palpating while laying down, with a pillow under the right shoulder - Repeat steps with left breast - Examine each underarm **[The male breast]** - *Gynecomastia* -- enlargement of one or both breasts in men; often occurs at puberty, with aging, or is drug-related - 2500 new cases of invasive breast cancer in men - Average diagnosis at age 59 - Most common manifestation (75% of cases): painless, firm, subareolar mass, or mass in upper outer quadrant of breast - Highest incidence (for breast cancer in both sexes) in north America and British Isles; lowest in Japan and Finland - Just like women, most commonly metastasizes to bone, lungs, liver, pleura, lymph nodes, skin, and other visceral sites **[Examination of the male breast]** - Should be done on all men - For swelling, discharge, and ulceration - Palpate areola and subareolar tissue as well for any masses - Axillary examination is indicated for women  **[Cancer of the breast]** - More than 2000 mutations in *BRCA1* (chr17) and *BRCA2* (chr13) **tumor suppressor genes** have been described; they are associated with proteins like p53 abd RAD51 - Higher prevalence in Ashkenazi Jews (2.5x more in Ashkenazi women) - Increases risk for early-onset, familial breast or ovarian cancer - 50% of all heritable breast cancers - Only found in 5-10% of women with early-onset breast cancer though and are very rare in the general population overall so **widespread genetic testing is not recommended** - *BRCA1* gene mutation? 60-80% lifetime risk for breast cancer & 33% risk for ovarian cancer; increased risk of prostate cancer in men - *BRCA2* gene mutation? increased breast cancer risk for men and women - ALWAYS biopsy breast mass, even in a normal mammogram; any lump increases cancer risk by 20% - Breast palpation has a much lower true-positive rate (sensitivity) than mammography and has many false-negatives - Of all breast cancers, 60% are freely mobile, 40% have well-delineated borders, and 50% feel soft or cystic. - Fixed lesion = 50% chance of being malignant. If this lesion has irregular borders 60% chance **[Screening guidelines for early detection of breast cancer]** - Have a mammogram every 1-2yrs starting at age 40 and every yr after age 50 - They detect 85% of all breast cancers - Abnormality detected? breast imaging - Tumors can be missed if they are - Very small - In an area not easily imaged (ex. Axilla) - If obscured by other shadows - Clinical breast exam should occur every 3yrs for women in 20s and 30s and every yr for women over 40 - Women should know how their breasts normally feel and report any changes - Women at increased risk should speak to their provider about benefits and limitations of starting mammography screening earlier, having additional tests or having more frequent examinations.