ࡱ> q` zsbjbjqPqP 4::3kF8<'($h=  I_4t h0'n44&ZL;DX'lqkq TEST 2 CARDIAC CONDITIONS Chest Pain OPPQRST & Assoc Sx, Treatments Differential Cardiovascular Aneurysm, emboli, LEVINE'S SIGN, Respiratory Pleural effusion Gastrointestinal Ulcers, GERD, cholecystitis, Chest wall syndrome subluxation, ribs Psychogenic Table 6-1 The most common causes of cardiovascular problems **4 problems** Q & NB Heart Ischemia Angina Pectoris (temporary ischemia) - due to the fact that cardiac work cannot keep up with the demand of O2 needed Retrosternal, across chest and to shoulders, arms, neck, lower jaw, ***When the pain is myocardial in origin the patient tends to close the fist and push it against the chest wallthis is called LEVINE'S SIGN Tight, heavy occasionally burning pain that is mild to moderate in quality Usually lasts 1-3 min, but up to 20 min Exertion, meals, emotional stress, may occur at rest - All these factors aggravate Nitroglycerine = relieve Heart muscle Myocardial infarct Irreversible tissue damage due to prolonged ischemiacould lead to necrosis A more severe pain than angina Pain Lasts longer than 20 min to several hours (this is from a surviving victim (27% or so die immediately) Things that aggravate or relieve are the same Pericardial Sac inflamed Pericarditis Often severe pain Inflammation of the pericardium Breathing, laying down, rest ONLY TWO CONDITIONS MANIFEST FOWLERS CONDITION Fowlers condition = is sitting up leaning forward Pericarditis & Pulmonary Emboli are the two conditions Aorta Aortic Aneuryism Splitting within the layers of the aortic wall RIPPING OR TEARING pain Lose consciousness, weakness, abrupt onset SEVERE pain Palpitations Uncomfortable sensation of heart beats associated w/ various arrhythmias Onset, duration, # of episodes, quality Associated factors: exercise, chest pain, headaches, sweating, dizziness, heat/cold intolerance, alcohol or caffeine usage, medications Conditions Thyroid problems Thyroid hormones have two effects Protein Synthesis - T3, T4 influence the formation of protein O2 consumption also is effect by the basal metabolic activity Hypoglycemia Decreased glucose releases catecholamines Severe Anemia Increased cardiac activity w/ decreased O2 in blood Stress or anxiety Bronchodilators, digitalis, antidepressants, stimulants Heart blocks Effect the conductivity Pre-excitation syndromes Will parkinsons white syndrome These conditions could be pathological, but not always Cough & Hemoptysis Onset (sudden, recurrent) Descriptor (blood tinged, clots) History of smoking, infections, meds, surgery, ( females - oral contraceptives) Associated symptoms Hemoptysis vs hematemesis (vomiting w/ blood) Cardiovascular disorders Left ventricular failure or Mitral Stenosis May progress to the pink frothy sputum of pulmonary edema or to frank hemoptosis Pulmonary Emboli Can lead to deep vein thrombosis Dyspnea Onset (when, mode, progression) Palliative - what makes it better Provocative - (exertional or positional Pattern Associated symptoms Associated conditions Respiratory problems Left sided heart failure - dyspnea on exertion Dyspnea on exertion GRADING 1-5 Excessive activity Moderate activity Mild activity Minimal activity Rest Positional Dyspnea Paroxysmal nocturnal dyspnea (PND): Sudden onset occuring while sleeping relieved by assuming upright position Orthopnea: lying flat requires > pillows Trepopnea: more comfortable on side Platypnea: problems sitting up, pt. Breaths easier in recumbant position Dyspnea of Rapid Onset Pneumonia, pneumothorax, pulm constriction, peanut (foreign object) Cyanosis (bluish discoloration) Central Dec. O2 in lungs Severe C/R ds Lips, oral mucosa, nail beds > with warming Peripheral Venous Stasis Diabetics are more prone to this due to occlusion Exposure to cold Nail beds, nose, lips < with warming Syncope (fainting) (LOC)- loss of consciousness Onset Has it happened before? Pattern? Did they actually lose consciousness? Activity at the time Position before and after Preceding symptoms or warning signs Medications Syncope Cardiac Pulmonary Pyschogenic Metabolic Neurologic medications From Chart in Book Vasodepressor Syncope Sudden peripheral vasodilation, especially in the skeletal muscles, without a compensatory rise in cardiac output. Blood Pressure falls Postural Hypotension Patient may black out or become unsteady Inadaquate vasoconstrictor reflexes Cough Syncope Associated with increase intrathoracic pressure which decreases the venous return to the heart Cardiac disorders Arrythmias Decreased oxygenated blood to brain Aortic stenosis and Hypertrophic cardiomyapathy MI Massive pulomonary embolism ***Know the above that cause syncope Dependent Edema Accumulation of excessive fluid in the interstitial tissues System differential: Cardiac, Kidney, Liver, Peripheral Vascular System ds. Pitting edema, swelling with chronic insufficiency Onset, U/L (vascular system) or B/L (cardiac, kidney, liver), timing palliative or provocative, associated symptoms, ulcers/discoloration/pain, SOB, Meds Cardiac Exam Components Peripheral signs Inspections Palpation Percussion - not performed often on exam, and cannot be performed on females with reliability Auscultation CVS - Peripheral signs Any signs of dyspnea: posture, use of accessory muscles of respiration, DOE, cyanosis, clubbing. Signs of elevated lipid levels: corneal arcus, xanthomas - upper and lower lid Splinter hemorrhage of the nails Little brown or reddish slivers (splinters) assoc, with bacterial endocarditis Lichtstein's sign NOT TESTED ON THIS - have seen on NB Associated in between the lobe and tragus Shows a likely hood of cardiac disease KWB (keith wagner barkner) Depending on the amount of hypertensive retinopathy, you would have some narrowing in stage 1 Stage tow, AV nicking Stage 3 - increased exudate, AV nicking, silvery wiring Stage 4 - papilledema JVP - dilated vessels Present even when not mad Peripheral Edema CVS peeripheral signs Pulse: Rate, rhythm (consistent?), amplitude, contour, symmetry, condition of vessel, wall Blood pressure Jugular Venous Pressure (JVP) Vesus Carotid pulse Capillary Refill Assess both upper & lower extremities Evaluation: 1st time 1 minuter Regular 30 Sec X 2, 20 X3, 15 X 4 Irregular always 60 sec Pulse characteristics 60-90 min, reg rhythm (interval), strong amplitude (2), smooth upstroke & descent, symmetrical After puberty child's pulse decreases to adult Pulse Characteristics (Rate) Rate > 100: Tachycardia Inc. Blood requirement by tissues: Exercise, fever, thyrotoxicosis, severe anemia Decrease stroke volume: CHF, severe anemia, pericardial effusion Meds that increase sympathetic N.S. -stimulants Rate < 60 BPM Bradycardia Decrease blood requirement by tissues: Hypothermia, myxedema Increased stroke volume: Well conditioned athlete Heart blocks or Altered conduction Parasympathetic stimulation: CNS depressants, increase in intracranial Regular vs Irregular Pattern (Rhythm) Regular - consistent interval btn pulsations Irregular - regular or irregular pattern Irregular regular: predictable pattern such as a heart block every 3rd or 4th beat etc Irregular irregular: no pattern such as Atrial ventricular fibrillation No Pattern Amplitude Described on a 0-4 scale 4 = bounding pulse 3 = full, increased 2 = expected, normal 1 = diminshed, barely palpable 0 = absent, not palpable Pulse pressure: 30-40 mm Hg Systolic - diastolic pressure INSERT INFO HERE Pulse Deficit Difference b/w the distal pulse & the apical pulse rate indicates: Vascular occlusion TOS Aneurysm (produces a widened pulse interval) Atrial fibrillation Pulsus alternans (left V-failure or CHF) Apical pulse = left 5th ICS at mid-clavicular line (also area where we assess mitral valve) Blood Pressure Beginning p. 75 p. 79 --> Blood Pressure Classification Chart Postural hypotension== drop of 20 mmHg or more in systolic pressure when going from lying down to standing Systolic Pressure: the force exerted against the arterial wall w/ ventricular contraction (cardiac output & volume) Diastolic pressure: force exerted against the arterial wall when the heart is relaxed (peripheral vascular resistance). Pulse pressure = systolic - diastolic pressure Jugular Venous Pressure (JVP) Method used to asses right side heart status Know what can lead to abnormal JVP: Atrial fibrillation Tricuspid valve stenosis or regurgitation R ventricular failure (causing regurgitation into jugular vein) Pulmonic valve stenosis or regurgitation Pulmonary hypertension p. 267 Use of the Rt. Jugular is optimal The Level at which the pulse is visible gives an indication of R atrial pressure Avg = 2-3 cm above sternal angle Distinguish IJ from Carotid pulse Hepatojugular (abdominojugular) Reflux Test for venous congestion and R sided heart status Pt. is supine breathing through open mouth. Apply firm pressure over the liver for 20-30 sec. Normal response is increased JVP distension< 1cm & returns to normal level within 2 cardiac cycles. Abnormal > 1cm & remains elevated Heart lies underneath and to the left of the sternum R atrium and R ventricle on the anterior aspect of heart (R ventricle largest area of ant. Heart) Remember the valves of the heart Hepatojugular reflex test JVP Inspection of Precordium Abnormal pulses, lesions, shape of chest wall, apical impulse (indicative of LVF contractility Left 5th intercostal midclavicular line) Precordial Inspection Shape of chest wall Apical impulse Pulsations Masses, lesions, vascular distentions Apical Impulse/Distentions Apical Impulse 5th ICS, Left MCL Masses lesions, Vasc Dist Aortic arch dilation w/ aortic regurg Tumors Superior vena cava obstruction Abnormal Pulsations Sternoclavicular: aortich arch aneurysm Sternal Notch: carotid artery transmission Sternal Border: Aorta Aneurysm of ascending portion - UPPER Ventricular Enlargement - LOWER Epigastric Abdominal Aortic Enlargement ventricular enlargement Palpation of the Precordium Confirm inspection findings Locate and define tender areas Locate and evaluate apical impulses Evaluate/ define abnormal pulsations Detect any palpable thrills Compare to the PMI (Point of Maximal Impulse) LEFT LATERAL DECUBITAL POSITION - rolling partly onto the left side form supine (PG 273) Table 7.1 (pg 286) **Know the increased values*** Normal Apical Impulse - assess the pulse like the carotid Located = 5th or 4th ICS, medial to the MCLine (could be above or below) Diameter = a little more than 2cm in adults Amplitude = small gentle Duration = Hyperkinetic - tests, anxiety, severe anemia, hyperthyroidism, fevercould cause this Increased amplitude Pressure overload - increased after load, hypertrophy, hypertension, aortic valve stenosis Increased diameter, amplitude, duration Volume overload - caused by the fatigue of pressure overload (ventricle dilated) Increased location = displaced to the left and possibly downward Increased diameter, amplitude, duration Could lead to mitral regurgitation Palpation around the heart Triscuspid (LL Sternal Border) - RIGHT VENTRICAL - TABLE 7.1 Pt. Instructions: Esxhale & hold breath Location: (L) 4-5th ICS parasternally Tricuspid valve assessment area Normal: Children & thin adults Abn: ventricular enlargement Conditions of increase cardiac output S3 or S4 heart sound conditions COULD BE FROM R VENTRICULAR HEART ENLARGEMENT Left Upper Sternal Border Pt. Instructions: Exhale & hold breath Location: L 2nd ICS parasternally Pulmonic valve assessment area Normal: Children & thin adults Abnormal: Pulmonary hypertension, Pulmonary valve stenosis, Condition of increase cardiac output R Upper Sternal Border Pt instructions: exhale & hold breath Location: R 2nd ICS parasternally Aortic valve assessment area No pulsations felt there normally Conditions: Systemic Hypertension Aortic valve stenosis Dilation/aneurism of aortic arch Percussion of the precordium Purpose: determine myocardial size Left ventricle - 5th ICS on Left Compare cardiac dullness vs resonance Method start parasternally -- lateraly Or Method start laterally -- medially Auscultation of heart sounds Pattern - inch from point to point concentrating on each of the auscultatory locations Assess with both the diaphragm & bell PG 271 in TEXT Patient positioning is talked about Four standard pt. Evaluation positions: Supine with head elevated at 30 degrees 2nd interspace, palpate precordium, listening for RV, Apical Impulse, LV S1, S2, and systolic murmurs in all areas This one accentuates the aortic area, mitral valve, apical activites Left lateral decubitus Apex accentuated Upright Accentuate sounds from aortic and pulmonic Upright, leaning forward Accentuate sounds from aortic and pulmonic Base Heart Sounds Assessment*** Normally, only closing of the heart valves can be heard********** S1 = 1st heart sound = closure of the mitral (left) and tricuspid (right) valve (AV or atrioventricular valves) S2 = 2nd heart sound = closure of the semilunar valves (aortic & pulmonic) S1 & S2 characteristics & changes Increase vs decrease intensity S1 & S2, how does one sound compare to the other in volume & length Extra Discrete HS Splits - physiologic vs Pathologic (S2 splits common) These are very common Ejection click & opening snaps Opening of stenotic valves S3 & S4 (could be either norm or pathological) S3 = Usually CHF, or unknown issue S4 = associated with MI (atriodiastalic gallop) Herd with bell in supine position or lateral position If S3&4 are together - this is a problem Continuous Sounds or Murmurs Physiologic vs pathologic Murmur can be physiological or pathological Many things will effect the sounds of the heart, this is why you should just know thee characteristic features. Chart in library about the different characteristics - LISTENED TO HEART SOUNDS Closure of the mitral valve - this contributes the most to the S1 heart sound However S1 could be diminished if mitral valve disease is present Closure of the aortic contributes the most to the S2 sound The second heart sound is identified at the aortic area first, this way people know which is S2 Systole - begins with the opening and closure of the mitral valve (Mc & Tc sounds) Diastole - is the s2 to s1 beat using the Ac & Pc Pg 280 in text**** Identifying the 1st and second heart sound Splitting may occur from the effect of respiration on the heart JVP Fluttering or palpatory frill Duration of the normal apical impulse The right side of the heart is effected by respiration much more than the left Why? The blood is returing from the right side of the heart into the lungs Inspiration is going to delay the closure of the pulmonic valve & a little bit to the tricuspid More blood flows since there is more room Expiration can step up the tricuspid valve closure Normal respiration can lead to the splitting of sound (especially S2 can be delayed because of respiration Looking for width, timing, intensity, when does it disappear, Variations in the 1st heart sound and second heart sound should be read by wed (table 7.2) Chart 7.2 S1 is often, but not always louder than S2 at the apex This is where the mitral valve is located, tissue can effect the volume What would increase the intensity? S1 - tachycardia, exercise, high cardiac output states, louder in growth spurts Why? - because the ventricles have to contract harder and more frequently Stenosis - causes greater pressure for the valve to open and close Click when they open, and increased intensity when closing What could diminish the intensity? CHF, Coronary heart disease, decreased contractility, Mitral regurgitation, late stage stenosis of the mitral or tricuspid valve causing it to be immobile. What could make it vary? Complete heart block - what would you anticipate would be the intensity of S1 with complete heart block = varying or alternating What could make a split? **************** S1 split - can be normally and will be perceived along the left lower sternal border (heard at the TRICUSPID area) APPEARANCE = Anything that could be associated with increased myocardial activity with respiration, early stage mitral valve stenoisis Usually on young people (growth spurts) or well conditioned athletes EXPIRATION = will accentuate the split Can be heard during inspiration and expiration CARDIAC disease, coronary artery disease, immobility (CALCIFIC STENOSIS, complete mitral valve stenosis) CANNOT appreciate at the mitral valve What increase intensity, decreases intensity, splits*** S2 split - this is common *************** These splits are common and have A2 and P2 (physiologic) These are separate components of S2, Closure of the aortic valve, right second intercostal space, A2 sound, this is caused by systemic hypertension, INCREASE IN A2 = EARLY AORTIC VALVE STEOSIS will increase the intensity of A2 DECREASED OR ABSENT A2 - calcific and immobile aortic valve, aortic valve regurgitation P2 pulmonic valve INCREASED - pulmonary hypertension DECREASE - late stage pulmonic valve stenosis or regurgitation Heart sound sequence Sequence of valve closure MVc TVc M1 T1 -S1 Avc PVc A2 P2 S2 We should only hear the closing of the valve S2 SPLITS***** These are very common, if we hear S1 best at the tricuspid Inspiration is when S2 becomes split more often 2nd or 3rd left ICS 98% of the time it disappears on expiration IF it does not disappear have the patient sit up On any person if there is splitting during inspiration and expiration have them sit up to double check ****Heard at the pulmonic area (erbs point) and is heard during inspiration and merges on expiration ANYTHING different from the above is considered pathological If heard during ins and exp it is ABNORMAL (wide split during inspiration and it approximates during expiration), Fixed Split (wide spilt) during inspiration and expiration Paradoxical split - S2 split on expiration but not inspiration (supposed to be on inspiration) - this is abnormal (bundle branch block) You will be tested on what is normal & what is abnormal Discrete HS Assessment Location S1 - tricuspid area S2 - pulmonic area Intensity Cardiac cycle Which side of the heart is effected by respiration (right side) Affect of respiration Split - timing & width Extra Sounds Cardiac Auscultation Right sided cardiac events are most often affected by respiration ***S1 - McTc & AoPo Blood is ejected into the pulmonic system causing the Aortic & pulmoinc valve to open Early stage stenosis will cause you to hear an ejection click from the Aortic or pulmonic valve opening Location & effects of respiration will tell you what you are listening too PG 289 in text book (extra heart sounds in systole) Table 7-4 Early systolic ejection sounds have to do inconjunction with Opening of A or P valves Ejection click is heard better with diaphragm of the stethoscope HEARD at the aortic valve (AORTIC CLICK) Pulmonary valve heard at 2nd and 3rd interspace *******MITRAL VALVE PROLAPSE - - - any exam when they talk about the click-murmur syndrome (especially heard over the apex) is mitral valve prolapse******** Turbulent blood flow through closed valves More common in females At some point in time we will develop this (if we live long enough) S1 & S2 is heard over all precordium parts S1 - (SYSTOLIC) - S2 - (DIASTOLIC) - S1 McTc AcPc AoPo MoPo EC (early Stenosis) Osnap (early St) S1 split or EC S2 split and an opening snap (how do we tell the difference) Location (early diastole) pulmonic area (erbs point) - S2 split - heard with inspiration Early diastole - at mitral area - early mitral valve stenosis - (accentuates the opening of valve, S2 heart sound increased S3 - Dull and low in pitch, better heard at the apex with the BELL Pathological - decreased myocardial activity, volume overloading, could be left or right sided Heard after opening snap S4 - heard right before S1 Displacement of the ventricle with VOLUME OVERLOAD If it is emanating from the base - lean forward If it is emanating from the apex - sit up Table p. 280 What is it? R 2nd ICS Parasternally Upstroke of cycle Heard in early systole = S1 split What is it? L 5th ICS parasternally Heard just before the upstroke (prior to S1) =S4 (heard best w/ bell and respiration would affect it) Murmur Features Location Cycle-- Timing & Duration Intensity-- how loud is it? Table 9-11 (handout) 6 levels (p. 282) Grade 1 --> 6 Majority of time Grade 1 & 2 are benign (unless a diastolic murmur--all diastolic murmurs are pathologic) Respiration-- Quality & Pitch how does respiration affect it? Bell vs. Diaphragm Radiation Body Position **Began video of heart sounds** Aortic Area, Pulmonic Area, Erbs point, Tricuspid area, Mitral area PMI = Apical impulse Inspection and palaption Found at 4th or 5th ICS medial from the MCL S3 - key sign of heart failure (after S1) S4 - diminshed ventricular compliance (mechanism unclear) Murmur grading system 1-6 1 heard barely 3 moderately loud 5 heard with touching the edge of stethoscope Patient Positioning with murmurs & breathing - know how they effect murmurs Under age 5 about 90% of children have murmurs, till age 10 about 50% have murmurs, still as young adults some people have innocent murmurs Incompetent valve can cause the regurgitation Systole - it is the mitral or tricuspid regurgitation murmur Diastole - it is the pulmonary or aortic regurgitation murmur TABLE 7.6 Innocent or physiological murmurs**** Innocent murmurs - result from turbulent blood flow, there is no evidence of cardiovascular disease. Theses are common in children and sometimes in older adults Grade 1-2 are usually not considered pathological Grade 3 murmur is pathological until confirmed Grade 4-6 are pathological Crescendo decrescendo or DIAMOND shape Charactieristics No thrill, grade 2 or less Systolic (ALL INNOCENT MURMURS WILL BE WITHIN SYSTOLE) No alteration of pulse Short midsystolic ejection murmur Changes with respiration or position Disappears with inspiration Decreased with standing Most common at mitral or pulmonic areas Aortic valvular sclerosis in an elderly pectus excavatum - pulmonary ejection murmur Pts with hyperdynamic circulation Physiological Murmur Turbulance due to temoprary increased blood flow, it is heard over the breast usually Pathological ****** (organic murmur) Any diastolic murmur Loud murmur (3-6 grade) Associated with palpable thrill Increased duration Radiation of sound Ventricular Semtal Defect Systole Mitral or tricuspid regurg (holosystolic) Mitral valve prolapse - click murmur syndrome Aortic or pulmonic stenosis (diamond) NOT concerned about the pattern of diastolic murmur since it is pathological Pericardial friction rub - sound that can be heard in systole or diastole (venus hum) Due to inflammation of the cardial sac Heard above the clavicle (low intensity) Heard above the medial clavicles by the jugular vein Patent ductus arteriosus Cyanosis present Grade 4 mitral valve prolapse (could have systolic and diastolic murmur) Walking up the stairs is too much for this person Peripheral Vascular Exam Older aged individuals Loss of elasticity Stenosis Legs cramp with decreased blood flow (when they sit the cramping goes away (10%)) Skin changes take place Peripheral Vascular Exam Same as cardiac exam PVS Complaints Pain or cramping of muscles Swelling or lymph edema Dysesthesia Changes to the skin Reynauds, loss of hair, increased pigmentation, ulceration, callous formation Poor healing of superficial wounds Prominent vessels Chest pain Shortness of breath Palpitations Cold hands/feet Usually due to decreased fat Risk of vascular insufficiency Risk for deep vein thormbosis Varicose veins Women are more often the recipients Due to pregnancies Factory workers People who are on there feet all day Sedentary life style Genetics Age Race AA - more valves less pooling of blood Vascular insufficiency Recent trauma or surgery Hyperlipidemia Hypertension Smoker History of cancer Diabetes I & II Previous thrombosis or family history HX of cancer Diabetic Neuropathy PVS More common (4 times) Occurs in younger individual Equal incidence in female and males More widespread Progresses more rapidly Multisegmental Bilateral Deep Vein Thrombosis Risk Advanced age Injury, fracture, infections Right sided heart failure, CHF Varicose veins Family history of blood clots Prolonged bed rest For older individuals it could be from a long drive or ride Postpartum Difficult pregnancy History of cancer Post operative Obesity Hormone supplement Arterial Exam Inspection Palpation: temp & pulses Postural color changes Capillary refill Blanching of nails Ankle: Arm index BP Auscultation Carotid, posterior tib, popliteal, dorsalis pedis The arms Size symmetry, skin color Radial pulse, brachial pulse Amplitude scale for pulses Arterial Exam: Palpation Chronic Arterial occlusion: Postural color cahnges Trophic changes to the skin Intermittent claudication PG 454 History of symptoms: pain, coldness, numbness, tingling Constan paine: acute occlusion If excrutiating: major artery If distal pulse diminished or absent : ER If co-lateral circulation is good the patient may only have numbness and coldness as only sx Postural color changes Patient lies supine raises leg 60 degrees until pallor develops usually < 1 min Have patient sit up/ stand & note return of color limb Normal almost immediately, normal - 15-20 seconds, elderly 35 seconds 2 minutes severe claudication TABLE 14.1 - claudication talked about Arteries palpable Brachial, radial , ulnar artery Femoral, popliteal, dorsalis pedis, posterior tibial Arms have two types of veins Superficial (subcutaneous tissue) Deep (thinner walls) Leg Deep Superficial Great and small saphenous vein Perforators Join deep and superficial Lymphatics Lymphnodes form a major part of the Inguinal nodes, horizontal and vertical groups Arterial Exam** Inspection Palpation: temp & pulses Postural color changes Capillary refill Ankle : arm index (BP) ( >1 in a young patient) Ankle (on calf)- 120mmhg Calf - 140mm/hg Above kneee - Take the ankle reading and divide it by the arm (ankle arm index) .7-.9 mild claudication .5-.7 moderate claudication < .3 Severe claudication Auscultation Capillary Refill Blanch Nail bed & observe return to normal color - < 2 sec INSPECTION FROM TABLE 14.2 (MATCHING SECTION)**** Arterial CLAUDICATION CLAUDICATION CLAUDICATION Pain - at rest Pulse - decreased or absent Temp - cool Edema - mild or absent Gangrene Callous - neuropathic ulcers Venous Exam Varicose veins Thrombosis - you won't see much if it is deep (could have pooling discoloration) Swelling of foot and ankle Hyperpigmentation Venous stasis causes the build up of stasis dermatitis Ulcer Pitting edema Manual Compression test Used with dilated vessels on LE Trying to determine if there is back flow Retrograde filling or Trendelenburg Test Is there any rapid filling? 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