ࡱ> ` bjbjss 4tttt\t؝uuuuuuuuWYYYYYY$h~}yuuyy}uuyZuuWyWuu pEnt?(W0؝tgttuH,wxxuuu}}}uuu؝yyyyn|r|r PHYS DX #2 EXAM #2 CARDIOVASCULAR SYSTEM EXAM R side of heart gets the return from the body. R atrium ejects to the lungs. The L atrium receives the oxygenated blood and pushes blood to the L ventricle. *** Remember where to auscultate for specific thingsThis is the toughest thing to do on the cardiac exam *** The heart sounds is very similar to geometry. All you need to know is your anatomy. Understand where you here the sound and in which cycle. CVD CHD leading cause of death in US It contracts more than 4 billion times over a life time 38.5% of all deaths AHA: 64,4000,000 Americans CV ds. Cardiac ouptput can vary from 3-30 L of blood flow 50 million w/HTN 13.2 million w/CHD (coronary disease atherosclerosis) 4.8 million who have suffered a stroke Greater than 13,2000,000 MI/year greater than diede immediately CVD is far greater a cause for death than the next several things on the list combined. CVD CHD: blockage and atherosclerosis HTN Rheumatic heart disease: Incidence has decreased over the use due to antibioticsThere are 5,000 deaths per year and most have sensitivity to group A beta hemolytic strept. Bacertiral endocarditis: M/C cause is hypersensitivity to group A beta hemolytic strept and then followed by IV drug use Congential heart disease: Can be up to 5 per 1,000 birhts. Usually due to premature babies and most are rectified on their own. Some problems are valve prolapse and most often premature infants. There can also be congenital problems in normal term babies. MVP (prolapse) can occur even in healthy individuals. It affects females a little more often and often cant be determined till pregnancy. Grade 1 is often asymptomatic. Grade 2 prolapse can be heard as a midsystolic click with low grade murmur heard even by an inexperienced person. Grade 3 is symptomactic with chest pain palpitatiaons, arrythemias and SOB> Grade 4 is debilitating. PVS Atheroslcerosis: PVS Microvascular disease: Increased risk for microvascular diseaseThe risk is due to diabetes mostly. Cardiac Diseae Risk Fasctors Gender (greater in men than women until postmenopausal) Hyperlipidemia Hypertension (treated or untreated) Smoling High inflammatory index (c-reactive protein) Diabetes mellitus Obesity (or excessive fatty diets) Sedentary Life style Personality type (type A) Family history of CHD, DM, HTN, hyperlipidemia Hyperlipidemia, hypertension and smoking when combined give a greater risk. The medication for hypertension is not curative. The only thing that decreases the risk is lifestyle modifications (diet and exercise modifications are absolutely essential). Other things that can help are the omega fatty acids, stress reduction techniques, stop smoking, etc. There is also an increase risk for fibromyalgia for high stress people. Hypertension In an adult 140/90 Greater than 50 million people 2/3 of Americans greater than 65 years old M/C in African Americans (1 in 2) 50% Greater than 30% with HTN ??? iConditions Associated with HTN Heart diseae, Stroke, Atheroscleoris, Aneurrysm, Kidney Failure, Retinopathy, Dementia Hypertension most often involves L ventricle leading to repsitortry problems, leading to R sided heart failure, leading to dependent edema. Complatins or Symptoms Chest Pain (hallmark), Palpitations, Dyspnea (SOB), Syncope, Hemoptysis (cough), Cyanosis (pallor), Dependent Edema, Nocturia, Fatigue Chest Pain OPPQRST and Associated Symptoms, Treatements Chest wall syndrome (a NMS problem is the #1 cause for chest pain Differential: CV, REspriatorry (Pleural), GI (2nd most common cause of chest pain GERD, esophageal spasm, Gallbladder, pancreas), Chest wall syndrome, Psychogenic LEVINES Sign: consistent with cardiac pain, pushing the first on the precordial areaassociated with SOB and cyanosis. Table 14-2 Cardia: CAD< Aortic valve diseae, pulmonary HTN, mitral valve prolapse, peridarditis, iodpathic hypertorphi subaortic stenosis (pressure overload in L ventricle then volume overload) Vascular: Dissection of aorta Pulmonary: Pumlmary embolish, pneumonia, plueritis, pneumothoras NMS: Table 7.1??? Temporary ischemia is usually due to coronary atherosclerosis. Myocardial infarct: Prolonged ischemia leading to irreversible damage. LocationQulaity of painSevertiy: Can be silent or noticeableThere really are no factors that aggravate or relieve this Embolus, pericarditis have classic holding of the chest or pushing of the chest. Sitting up and leaning forward.FOWLERS POSITION = THINK PERICARDITIS OR PULMONARY EMBOLI Dissecting Aneurysm: A channel created in the wallradiating pain in the neck, chest and abdomenThis people may go into shock and may lose consciousseness Table 14-1 Charactieristsi of Chest Pain Angina: Retrosternal, diffuse, radiation to left arm, jaw and backAching, dull pressing, suqeeing or viselike painIntensity mild to serverDuration of mintuesPrecetidtale by effort emotion, eating, coldRelieved by rest, notrglycerin Not angina: Palpitations Uncomfortable sensation of heart beats associated with various arrhytias Onset, duration, # of episodes, quality Associated foactors: Exercise, chest pain, ehadahces, sweating, dizziness, heat/cold intolerance, alcohol or caffeine usage, medications Some other factors are mitral valve prolapse or migraines, uncotrollled thyroid conditions, dehydration, electrolyte imbalances. Palpatiations are foten described as jumping, skipping of the heart with the beat heard in the ears and heart. Myocardium Extensive Electrical Pathway.Anything altering pathway increasing or decreasing excitation can lead to palpitationsExcitation of sympathetics or problems with parasympathetics can lead to heart palpitations. Tehre are case studies out there that people with palpations may benefit from chiro care. Table 14-2 Common Causes of Palptations Medications can lead to Palpatations Extrrasystoles (Atrial premature beats) Anemia Not all causes of palpitations are pathological in nature. Dyspnea (SOB) Onset (when, mode, progression) Palliative Provocative (exertion, positional) Pattern Associate symptoms Associated conditions With myocardium in erarly stages exertion is a problem and in later stages position is a problem Table 14-4 Common Causes of Dyspnea Carida: Left ventricular failure Dyspnea on Exertion (DOE) Grading 1-5 1: Excessive activity 2: Moderate activity 3: Mild activity 4: Minimal activity 5: Rest *** this may be on the final *** Positional Dyspnea Paroxysmal Nocturnal dyspnea (PND): Sudden onset Table 13-4 Positional Dyspnea Orthopnea: CHF, Mitral Valve Diseae, Severe Asthma (rare), emphysema (rare), chronic bronchitis (rearely), neurologic diseases (rare) Trepopnea: CHF Platypnea: Status post-pneumonectormy, neurologic diseases, cirrhosis (intrapulmonary shunts), hypovolemia Table 13-8 Common Cnditions Associated with Dyspnea *** Know this again for the exam *** Syncope (Fainting) (LOC) Onset Has it happened before? Pattern? Didy they acualltally lose consciousness? Activity at the time Position before and after Preceding symptoms or warning: Possibility for seizuresSeizures are the most common cause of syncope. If the patient is on depressants, this is more common. Electrolyte imbalances can lead to syncope. Medications Table 14-5 Common Causes of Syncope Cardiac: Decreased cerebral perfusion secondary to cardiat rhytm distrubaance, L ventricular output obstruction Metabolic: Hypllycemia Syncope: May be more common in trauma patientsTrauma or severe pain may be the reason for syncope. Descriptors of Coughing Dry, Hacking Chronic (productive) Wheezing Barking STridor Morning Nocturnal Associated with intake Inadequate Table 13-1 Descrptiors of Coughing Appearance of Sputum (Table 13-2) Hemoptysis Table 13-3 Cahracterisiting Distinghting Hemoptysis from Hematemesis Dependent Edema Accumulation of excessive fluid in the interstitial tissues. System Differential: Cardiac, Kidney, Liver (cirrhosis, tumors, etc). Onset: U/L or B/L, Timing, Palliative or Provocative, associated symptoms, ulcers/discoloration/pain, SOB, Meds Arthritis can lead to edema. A person can say it is painful with activity depending on activity. Pitting fluid can trigger micturation reflex in the sacral plexus. Nocturia Any cause of polyuria: Diabetes insipidus, solute diuresis We void 700-2000 mL offluid per day, depending on the fluid you drink a daySugar tends to retain water in fluids. That is why we give athletes Gatorade PHYS DX. 6/13/08 Nocturia Any cause of Polyuria Diabetes Insipidus Solute Diuresis DM, diurectic use Excessive fluid intake Fluid retentaion states Decreased concentrating ability of the kidneys Cardiac Exam Components Peripheral Signs Inspection Palpation Percussion Auscultation CVS Peripheral Signs Any signs of dyspnea: psture, use of accessory muscles or respiration, DOE, cysanosiss, clubbing Sings of elevated lipid levels: corneal, aruscs xanthomas Splinter hemorrhage of the naisl Lictensteins sign KWB Peripheral Edema (dependent) Flame shaped hemorrhages, vscxualr narrowing, change of light refeflex (coopper wirte), crossing deficts in the vessels with nicking Cyanosis Picure of Cnetral cynsanosis Late Clubbing Occurs with various conditionschange in nail bed Clubbing Of Nails Itnrathoracic tumors Congenital Heart Malformation: Misecd venous to arterial shutns Acquried Carigpuklary Disease Chronic Pulmnary diseaew Chronic Hepatic Fibrosis Neck Vein Distention Look for dilation (picture of dilation of the jugular vein) Xanthelasma An important signThisis associated with high lipid levels (dermatology). Tuberous Xanthomata People have cholesterol levels that are very highDevelopment in the tendons indicates cholesteraol 1500-2000 mg/dL Tendon Xanthomata Deep xanthomatas that develop mostly on extensore tendons Splinter Hemorrhages Occurs with traumaIn multiple nails, think bacterial endocarditis (Particularly if there is an URTI). Lichsteins Sing Occurs with severe CVDThere is a lot of false + and false -. It is not a strong/consistent sign Palatal Petechiae Associated with infective endocarditisThis person has other problems as well. We wont see this person in the office much. Arcus Senilis White or grey ring around limbus of iris. This is another condition that is an absolute. If it occurs under 40, if would warrant a lipid profile. This change is more consistent with people over 50. In young people, it would mean a lot of atherosclerotic plaque. Hpertension Flaem shaped, hermorrhages, cotton whool spots CVS Peripheral Sings Pulse: Rate, rhythm, amplitiusde, contour, symmetry, condition of vessel wall Blood Pressure Jugular Venous Pressure (JVP) Carotid Pulse CVS Peripheral Signs Assess both upper and lower extremities Evaluation: 1st time 1 minute Regular 30 second x 2, 20 x 3, 15 x 4 Irregular always 60 seconds Pulse Characterisitcs 60-90/min regular rhtym (interval), strong amplitude (20< smooth upstroke and descent, symmetrical Pulse Charatcterisitcs Rate greater than 100 is tachydardia Increased blood requi4eent by tissues: exercise, fever, thrytoxicosis, server anemia Decrease Stroke Volume CHF, servere anemia, pericardial effusion Meds that increase sympathetic NS Stimulates Pulse Characteristics (Rate) Rate less than 60 minutes (bradycardia) Decreased blood requirement by tissues: hypothermia, myxedema Increased Stroke Voulme: Well condition athletes Heart Blocks or altered conduction Parasympathetic stimulation CNS depressants, Increase in intracranial pressure Meningitis may increase intracranial pressure. Aneurysms may increase intracranial pressure. Pulse Differeneces Chart in Textbook Anacrotic: Small slow rising delayed pulse with a noutch or shoulder on the ascending limbCause == Aortic Stenosis Waterhammer: Rapid and sudden systolic expansion Cause: Aortic Regurgitation Bisferterus: Double peaked pluse with a midsystolic dip: Aoritic regurtiationcombined arotic stenosis and aortic regurgitation, iodepathtic hpuertrohic subarotic stenos Atlernans: Classic for CHF (also L ventricular failure)Atlernating amplitusde of pulse pressureCause = CHF Paradixical: Detected by blood pressure assessement. An exaggerated drop in systolic blood pressure during inspiration. Cause = Tamponade, constrictive pericardidtis, COPD Rhtym Regular vs. Irregrulat REgualr: Conssiten interval betweee pulsations Irregular: reguar or irreguarl pattern Contour Best evaluated Carotid pulse Assess the cartotid pulseIt should be assessed before the bifurcation. Most indicative of cardiac activity??? PUse cahrtarctireis Amplitude 4 = bounding 3 = full increaeed 2 = expected normal 1 = diminished barely palpable 0 = absent, not palpable Pulse Pressure: 30-40 mm Hg Systolic diastoilic pressure Symmetry Symmetrical side to side Asymemetry: Obstruction or occlusion (normal variance side to side should be under 5 beats vs. under 10 for older adults) Pulse defitict: compare to to apex Assesss lower extremity: should be essentially the sam Weaker and delayed in legs: occlusive aortic disease The bifurcation of the iliacs is a common site for problems Vessels Condition of vessel wall: Assess ppulse with 2 fingers. Lightly press proximal finger to occlude folwo, forll attery over bone with distal finger Normal arterial wall is not felt Atherosclertoic plausge feels like a cord Be Careful The only way you would perform this is because of a testing situation. You could break the plaque lose. Pulse Deficit Difference bwtween the distal pulse and the apical impuse rate (apical impulse L 4-5th intercostal space at MC Line) Vascular occlusion TOS Anerurm Atrial Fib Pulses Alternans Blood Prssure Guides New patient: B/L baseline n the arms in more than 1 position (less than 10 mm Hg difference) Korotkoff Sounds BP considerations Read to the nearest 2 mm mercury BP readings may different Table 15-3 Know the levels Optimal - -Less than 120 and Less than 80 Prehypertension 120-139 or 80-89 Hypertension Stage 1: 140-159 0r 90-99 Stage 2 160-179 or Hypertension Silent Kilelr Chest pain, dyspnea, fatigue, nausea, pain vision problems, excessive sweating Assessmetnet Treatmetn options for HTN Lifestyle mOdifications Orhtostatic hypertension Fall in sysptolci pressure of 20 mm or more when patient stands Ausculates and palpate carotid Table 14-6 Differentiation of Jugular and Carotd Wave Forms Internal Jugular Pulse: Palpation = Not palpableWave forms = multiform: two or threee componentsQuality = Soft, undulatingPressure = Wave forms obliteratedInspiration = Decreased height of vwave formsStiting Up = decreased height of wave forsValsava = increased height of wave forms Carotid pulse: Platption = palpabeWave forms = Singlequality = vigorousPressure, inspiration, stitting up, valsalva = all no effect Inspiration decreases the fill level, because the lungs can draw more blood from R side of heart into to it,temporarily. Jugualr Venous Prssure (JVP) RElfets status of R side of heart Level at which the pulse is visible gives and incatino f R atrial pressure For the exgernal jugular vein sat 45 degree angle 30, 60, ditting upright (no distaention upright normally) JVP Pattern Depends on patient position and shape of chest Abnormal JVP Finginds Absent a wave: ATrial Firbillation Increased JVP: Indicates R sides Heart problems as the cause More prominent a wave Increased JVP: tricuspid valusve stenosis, valve regurititsaiton, R vent. Vailrure, pulmonary stenosis, pulmonary hypertension (5 choices) Hepatogjugular Reflex Test for venous congestion and R sides heart states Pt. is supin gbreathing through open mouth. Apply firm pressur fove the liver for 20-30 seconds. N response is increased JVP distension less than 1 cm and returns to normal level within 2-3 cardiac cycles. Abnormal greater than 1 cm and remains elevated IN normal patient, the jugular vein fill level will increase just a little (you can use dot marks to measure). At the 1 cm or below, the patient is OK as the blood leaves and goes back to the heart. Abnormal = If it rises above 1 cm mark or it will not return to 1 cm mark. This indicates further testing. *** Know the Hepatojugular Reflex for National Boards and this exam *** *** Know the fill rates for JVP for the class exams *** PHYS DX #2 6/16/08 Cardiac Exam Components Peripheral Signs Inspection Palpation Percussion Auscultation Precordial Inspection Shape of Chest Wall Apical IMpuslse Pulsaitons Masses, Lesions, Vacuslar Distention (?) Shape of Chest Wall Normal Apical Impulse/Distention Apical Impulse 5th ICS, Left MCL Masses, Lesions, Vascular Distention Aortic Arch Dilation with aoric regurgiations Tumors Supeiror vena cava obstruction Point Masxilam Impulse (PMI)Pulations can be palpated here. Base of the heart tips posterior and the apex is closer to chest wall (more anterior located). You can tell apical limpulse due to the location a little better. CHF: R side of heart increae and you may feel palaptions near the sternal border (PMI impulse then state locationex. Left lower sternal border). Abnormal Pulsations Sternoculavicular: Aortic Arch Aneurysm Sternal Notch: Carotid Artery transmission R STernal Border Aorta aneurysm R Ventricular Enlargement Epigastric Andominca Aortic Enlargement R Ventiricalar Enlargement *** Picture of Doctor assessing PMI with pateins seated (can also be assess supine)Thrills can be felt in either position (preferably supine) *** Areas to Auscultate Aortic area, pulmonary area, tricuspid area, Erbs Pont, Mitral Area Erbs Point (know where it is) Apical Impulse is only located over the mitral valve iApical IMpuluse Pt. intstriction: Exhale and hold breath Location: 5th ICS left MCL (mitral valve) Diameter: 2-3 cm (1-1.5 ICS) Amplitutute: Small, gentle tap Duration: Less than 2/3 of systole Abnormal: Inc, cardiac output, systemic HTN, Aortic/Mitral Valve Regurgiation, Aortic Valve, Stenosis The grade is 0-4. for amplitutede. 0 is no amplituted. 4 is bounding amplitutede with heaving and bounding. Duration is assessed by stethoscope. Listen for the lub-dubCorrelate time it take for impulse to remain on your finger. If it covers the whole period (S1-lub and ends at S2-dub it is too long). It should be quick. HTN typically increases the LV size. Apical impulse may move more lateral and inferior away from the 5 ICS and lateral to the MC line. Aortic/Mitral Stenosis: Aortic Stenosis may be a dangerous condition causing strain on the heart. Table 7-1 VAritations and Abnormaliteis of the Ventricular Impulses Left Lower Sternal Border Pt. instructions: Exhale and Hold breath Location: (L) 4-5th ICS parasterinally Tricuspid Left Upper STernal Border Pt. instructions: Exhale and Hold Location: L 2nd ICS parasternally Pulmonic Valve assessement area Normal: Chiodren and thin adults Abnormal: Pulmonary HtN IRight Upper STernal Border Pt. instructions: Exhale and hold breath Location: R 2nd ICS parasternally Aortic Valve assessment ara NO pulsations felt there normally Conditions: systemic HTN Aortic valve stenosis Percussion of Precordium Purpose: Determine myocardial size Compare cardiac dullness vs. resonsance Method start parasternally ----- laterally OR Method start laterally ------- medially Mitral Valve Closure and Tricuspide valve cosure: S1 sound, best heard at the apex S2 sound is best heard at base (level of 2nd ICS). Auscultation Ausculations allows for assessment of cardiac valve activity and blood flow patterns Dr, assesses form patietns right side Ausculatation will be performed with the patients in more than 1 position Assess akk regions wthe diaphragm and bell of stethoscope. S1 and S2 heard with diaphragm. High pitched sounds are S1 and S2 (lub-dub). Regurgitation(valve don close and leak, called a regurgitation murmurthese can be stenotic valve or leaky valves) also heard with diaphragm. The bell is needed for low pitched sounds. S3 and S4 are pathological and indicate filling problems, best heard with the bell. Stnotic murmurs are also best heard with the bell. S1 and S2: S2 is caused by closure of aortic valve and pulmonic valve. S1 is caused by close of mitral and tricuspid valve. The aortic does close slightly before the pulmonic valvue Ausculataiton of Heart Sounds PHYS DX #2 6/23/08 Heart Sounds Assesssment S1 and s2 Characteristics and changes Increase vs. Decreae Intensity Extra Discret HS Splits Physiologic vs. Pathologic Ejection Coick and Opening Snaps S3 and S4 Continuous Sounds or Murmurs Physiologic vs. Pathologic S2 split is the most common split to be heard. Clicks are due to stenosis of the valves which delays closure and opening of the valve. They close with greater intensity increasing the intensity of the sound. Stenosis (mild moderate) increases intensity of closure of valves and causes an extra heart sound when the valve opens. S1 split is perceived btter with expiration and heard at the tricpusod. S2 is heard on inspiratin at th pulmonic and merges. S3 and S4 Variations in S1 Sound S1 is softer than S2 at the base. S1 is often but nto walwys louder than S2 at the apex Accentuated: high cardiac output states, especially with tachycardia, early/mid stage Mv stenosis Diminished: Calcfified Mv, MV regurgitation, LVF or CHD, first degree heart block Split at the tricuspid, accentuated by expiration S1 is composed of mitral and tricuspid closure Intensity of sound is accentuated in times of high cardiac output (exercise, stress, anxiety, fever, thyroid toxicosis, and even during 3rd trimester of pregaancy with increased cardiac demands, stenosis ) Stenosis hardens the valve so it taknes more pressure to open and close valves (mitral and tricuspid valves). Ex. 65% cardiac capacity so valvfes dont open and dont close well and ehart must pump faster to accommodate Regurgitation is blood flow back to previous area Split S1 is accentuated by expiration and heard at the tricuspid valve. If you suspect an extra sound at the mitral vavle, it is not a normal S1 split. *** Know what affects the intensity *** Varitions in S2: A2/P2 A2 ncreased: systemic HTN, early stage Av stenosis A2 decreased: calcific Av stenosis, Av incompetent greater than regurgitation P2 increased: pulmonary HTN, early stage Pv stenosis, atrial septal defect, dilater plomonary arter P2 decreased: I increased AP diameter S2 Splits Normal S2 split whichis extremely common is heard at the pulmonic area (2 sounds) with inspiration and merges (heard as 1 sound) on expiration. This is the normal or physiological split. It is heard best with the diaphragm (higher pitched). Anything other than that is pathological. The split delays pulmonic valve closure. There wll be greater colsoing pressure. Lub Dub, Dub (Inspiration 2 sounds).Lub-Dub (expiration 1 sound) 3 Types of Pathological S2 Splits Wide Split During inspiration arotic and pulmonic component may have a small delay (A2 and P2 delay) and with expiration the 2 components are still heard separtately (Dub is closer together).Wider during inspiration and approximates during expiration, but doesnt occur at the same time Vent. Septal Defect, Pulonary Dilateion, *** She wont ask the causes of this, but is going to describe the split and tell you if it is normal or abnormal *** Paradoxical Split You see pulminc before arotic component and they merge during inspiration and split during expiration Fixed split: Duration of separation is the same during inspiratin and expiration *** Knw that the above conditions are pathological or not *** Wide Splitting: Pulmonic Senosis, RBBB, mitral regurgitation,, VSD, PDA Paradoxical Aortic Stneosis, LBBB Fixed: Atrial Septal Defect Table 14-8 Cardiac Sounds Early Ssytolic: Ejection click, aortic prosthetic valve opening sound Mid-late Systolic Midsystolic click, rub Early Diastolic opening snap, S1, Mitral Prosetetic valve opening sound, tumor plop Mid-diastolic: S3, summation gallop Late Diastolic (sometimes called presystolic): S4 , pacemaker sound S1 ystolic: Mitral Closed & Tricuspid Closed ----- Aortic Open & Pulminic Closed S2 Diastolic: Aortic Closed & Pulmonic Closed ---- Mitral Open & Tricuspid Open Aortic or Pulmonic Stenosis may present with ejection click in early systole. A pulmonic ejection clicks (pulmonic click) will be heard best at the L 2nd ICS parasternally and perceived best with expiration (increases intensity of click). Aortic valve stenosis (l side of ehart) tends not to be affected by respiration as much. Aortic click is heard best at R 2nd ICS and is not affected by respiration. Stenosis of the Mitral or Tricuspid is called an opening snap. This is moderate stenosis. Respiration doent affect intensity of opening snap for mitral or tricuspid. It is also heard better with the diaphragm. S1 Split and Pulmonic Click: S1 split is decreased by expiration (location) S1 is ehard at tricuspind and heard by expairtion. Pulmonic click is heart at the puloimic. You should not be perceived a pathologic click of pulmonic valve at other areas so location is the key. Know where you are auscultating and what sounds should be there. S2 split and Mitral Valve Opening Snape: Location plays a role. Opening snape is not affected by respiration. S2 split is heard at the pulmonic area is 1 component on 1). Location 2). Respiration 3). Diaphragm or Bell Ways to help differentiate Mitral Valve stenosis is ehard in early disstole over the mtrial valve L 5th ICS midclavicular line. S3 or S4 Sounds: Isolated SoundsThe presence of either gives a triple sound or when both present a quadrouple sound (galloping horse). S3 and/or S4 may be normal or patholigcal. They occur during filling of the ventricles. The first part is most of diastole when the mitral and tricuspid are open and blood passively fills the ventricles and distends the ventricles. This is like a water balloon. Put a balloon on the end of the facet and turn water on. At first the balloon recoils, like compliant myocardium (as in children). In children, this can create a new heart sound. In adults, hearts decrease compliance S3 and S4 Heart Sounds Diastolic filling has 2 steps: Opening of AV valves: 80% of filling, distention of ventricular walls = S3 Atrial Contraction: 20% of filling, vibration of valves, walls or papillae = S4 S3: Normal up to age 30-40. Abn: CHF, CAD, post MI, valve regurgitation S4: Normal up to age 30-40. Abn: HTN, valve senosis, acute MI, well conditioned athletes (may actually have an S4 beyond age 40) Either S3 or S4 is normal in young people, but both sounds together in a child is abnormal. In adults, either sound is abnormal. Heart attacks can present with S4 heart sound. S4 can disappear following an MI and even turn into an S3 sound. An S3 sound is a clue that the person had a previous heart attack. PHYS DX. 6/25/08 S3 AND S4 Heart Sounds Diatstolic filling has 2 steps: Opening of AV valves 80% of filling, distetion of ventricular walls = S3 Atrial Contraction: 20% of filing, vibration of valves, walls or papillae = S4 S3: Normal up to age 30-40. Abnormal CHF, CAD, post MI, valve regurgigtation S4: Normal up to age 30-40. Abn: HTN, valve stenosis, acute MI, Well conditioned athletes *** S3 and S4 combined is never bening and it IS ALWAYS PATHOLOGICAL *** S2 Split or opening snaps are heard best with the diaphragm S3 and S4 are heard best with the bell. S2 spilt vs. S3 Locaiton helps differentiate. S2 is heard over the pulmonic (heard during inspiration and merges during expiration) vs. S3 heard on R side over R ventricle in the same location as the tricuspid (L 4-th ICS parasternally). The right ventricle dilation we coluld hear activity on the R lower sternal border (hypothetically) or over the epigastric area. L sided s3 or S4 is heard in the same spot as mitral valve activity (L 5th MC line and5th ICS). R sided S3 or S4 intesnity should increase during L sided S3 or S4 is increased in the lateral decubitus position during expiration. Video The Creation of Heart Sounds Aortic Area Pulmonic ValveTricuspid Area (tricuspid and RV) Mitral Valve (MV and L Ventricle) Herbs Point (Aortic and PUlmonic soudds) PMI: Point of maxial impulse found over apex of heart medial to MC line in 4th or 5th ICS. Location where you here the sound best is defined best by boney structures Aortic: 2nd R ICS space Pulmonic: 2nd L ICS Tricspuid: 5th ICS left of sternum Mitral: 5th ICs medial to MC line over left Vtnerical apuls Herbs: 3rd ICS Supine, Left Lateral, and Hunched over Seated positions are recommended S1= Closure of Mitral Valve (and closure of tricuspid valve) = M1 and T1asococtated with QRSMitral area is where it is hear best and is louder over mitral area than S2. S2 = Closure or Aortic Valve(pulmonic contricutres to S2). A2+P2 = S2.S2 is heard during the T wave and hear best over aortic area. S2 has higher pitch, short. S3 = Associated wih reapied ventricular filling in early diastole. Children and youn aduts it is normal. It could indicate failure via a ventricular diagnostlic gallop. S3 is best heard at the apex in L lafteral position with the bell. It is dull and low pitched. Associated with CHF. S4 = diminiested vent. Complicance. ATrial sound is associated with MI (atrial diastoclic gaollpp). S4 precedes S1. Best heard in supine and L lateral positon. Location, INtesnity, duration, Pitch, Quality, Timing in relation to S1 or S2Help note characteristics Column Method: Height is intensity, width is duration Label S1 and S2 Descritpive words pitch (high medicm lovw) Quality: sharping booing, snapping dull blowing, musical Valve dysfunction: REsutls REgurgiration: relex of blood and foeces affected chamber to accomeodrate a larger volumen Mitravl vavle regurg: Retrograde flow Stenosis: Reduces channgel for flow reduslt in pumping force increased ot overcome resistance Murmurs are based on timing. Late diastolic are called presystolic sometimes. Grade 1 murumr: Bareely head 2: Faint bt as soon as scope is palce on wall 3 = moderated lloud 4 = loud 5 = Edge of sethocscpe touching chest wall 6 = S1 and S2 are often greded as 3 normally. Crescendo murmur (soft loud) Decreasecndo murmur )loud soft) Patient Positioning cvan change sounds as well as Inspiration and expiration Radiation of Sound: Depeds on chamber affected and direction of flow. Listen over multiple sites. All Diastolic murmurs tend to be pathological! Systolci murmurs can be functional or physiological (tendency to be resolved), innocent (in children during growth spurts), . functional murumurs can occur during pregnancy due to hyperdynamic blood flow. By the age of 50 by our diet and lifestyle, 50% of adults have sclerotic or stenotic murmurs of the AV vavle. We dont consider this lifethreating, till later in life. Murmurs: Continuos Sounds Originate in the heart or great vessels: Valve Stenosis: Causes previous chamber to work heardr to get blood through nearrowed valve Abnormal valve shape: Normal Structure icnreasec flow: anemia, growth spurts, anxiety, stress, hyperthyroidism, etc. Incompetent valve: Regurgitation (doesnt close and leads to regurgitation) Dilater chamber: Aneurysmal dilatation (aortic arch or ventricular dilation) Shutning: Ventricular septal defect (also patent ducturs arteriorsus) Murmurs are continous heart sounds and area a hemodynamc phenomenon. They occur with increased flow or abnormal flow because of a problem. Murmurs Characteristics Location Cycle: Timing and duration Intensity: Graded 1-6 (We see that Level 1 or 2 which are mild murmurs in systole are usually beningn. 3-6 in systole are pathological. Diastolic murmurs are always pathological). Radiation Pitch and Quality: Affect or respiration: R sided heart murmus tend to increased with inspiration vs. L sided it varies (respiration may not affect it or it is appreciated with expiration in L lateral position or it is not appreciated as well in inspiration) Affect or patient position Murmur: Innocent or Functinal Murmurs Pts with a hyperdynamic circulation Stills murmur: Noted in over 50% of children. In most cases it disappears at puberty. Early systole, low intensity and at pulmonic or mitral area. Most common at pulmonic or mitral valve Short midsystolic ejection murmur of grade 2 or less: Consistent with innocent or functional murmur No alteration of pulse, no radiation: Pulse with LV failure or CHF becomes pulsus alternans (alternating increased and decreased intensity) Decreases with inspiration or standing: These are normally positions that would tax the heart. R sided problems normally should increase with inspiration. Aortic Vavle sclerosis murmur: By age 50, over 50% adults have this type of murmur with early crescendo-decrescendo murmur. Characterisistc of Innocent/Funcitonal Murmurs Stills murmur N in greater 50% of children and Most common at paulmonic or mitral vavle Short misystolic ehection murmur of grade 2 orless No alteration of pulse, no radiation Decreases withinspiration or standing Aortic valve sclerosis murmur Characterisstics of Pathological Murmurs Any diastolic murmur is pathological *** Any stystoic murmur with : Greater than 3/6 Assoicated with a palpable thrill Incrased duration (holo or pansystolic): HOlo or panysystolic means the murmur is appreciated all the way through S1 and S2. Radiation of sounds: distant from the site. During an exam, if you hear radiation to other areas, that indicates a problem. Shape (chart in textobook) Cresenceo mu Gradations of Murmurs 1: Very faint, heard only after listener has tuned in; man not be heard in all positions 2: Quite, but heard immediately after placing the stethoscope on the chest 3: Moderately loud 4: Loud, with palpable thrill 5: Very loud, with trhill. May be heard when the stethoscope is partly off the chest. 6: Very loud, with thrill. Ay be heard with stethoscope entirely off the chest. Grade 5 or 6 may be heard through the back. Systolic Mumurs Aortic Stenosis: Location: Aortic Area Radiatio: Neck Shaped: diamond Ptch: Medium Quality: Harsh Associated in Sings Decreased A2, Ejection click, S4, Narrow pulse pressure, Slow rising and delayed pulse Mitral Regurgitation: Location: Apex Radiation: Axilla Shape: Holosystolic Pitch: High Quality: Blowing Associated Signs: Decreased S1, S3, Laterally displaced diffuse (PMI) Mitrla Valve Prolapse is called the Click Murmur Syndrome and occurs mostly in systole. In Grade 1 prolapse, is usually incidental. If valve doesnt open as well as it should, it is temed a stenotic murmur. If valve doesnt close as well as it should, it is termed a regurgitation murmur. Systole is typically where a regurgitation murmur occurs. Ex. Murmur Scenario Continous Heart Sound (murmur) heard at L 2nd ICS space parasternally.Murmur heard with upstroke of carotid pulse (S1 upstroke systole with S2 immediately following the carotid pulse)Systolic murmur.Grade 2 and not affected with respirationMurmur decreases in intensity with exerciseType of murmur = Pulmonic AreaNo radiation of soundPattern is crescendo, decrescendo = Innocent, pulmonic valve ejection murmur. An innocent murmur in a child does not require a referral. Regurgitation and stenosis always indicates pathology! Example of a Murmur: L 4-5 ICS, following peak of carotid pulse, Grade 2, increase with inspiration, no radiation of sounds = Tricuspid, heard during diastolic (tricuspid should open during diastolicalso tricuspid due to location auscultated over) A tricuspid stenotic murmur, that is patholigcal (because it during diastole it is automatically pathological). CLASSICALLY SPEAKING, CAN WE HAVE A MV REGURGITATION MURUMUR DURING DIASTOLE? NO Example of a Murmur: Diastolic, continous sound, at the R 2nd ICS PS = Aortic Valve Regurgitation murmur during diastole (it is pathological because it is during diastole) *** This will be on the exam, comp boards and national boards parts 2-4 *** Table 14-9 *** Know it for the exam *** Murmurs Systolic and Diastolic (during both systole and diastole) Pericardial Firction Rub Severe Mitral Valve Prolapse Venous Hum: Innocent, above the clavicle, right sidede, continuous sound, high pitched, roaring or humming sound, appreciated often in children during growth spurts Patent Ductus Arteriosus: Opening that remains between descending aorta and bifurcation of pulmonary aretery Coarctation of the Aorta Tetralogy of Fallot: Dual Murmur Transposition of Great Vessels Atrial Septal Defect PHYS DX #2 6/27/08 Murmurs: Grade 1 Low sound and often missed. Sytolic murumur is often beninn and if diastolic is often pathological. Grade 2 is a little louder than 1 (2 in systole is not a problem and 2 in diastolie is pathological). Grad 3 is louder than 2 and can be pathological. Grade 4 = Turbulent Flow (Grade 4-6 is always pathological and has a associated thrill) Grade 5 = Louder murumur, palpable thrill (Grad 4-6 occur through systole and can be appreaciate with radiation) Grade 6 = can be appreaciated with the stethoscope removed from the chest wall but over the vicinity (above the chest) Peripheral Vascular System Part of a complete physical exam Complaints Risk Factors Pain is a common complaint. Other things to note, asymmetry, weakness, discoloration. Risk factors are trauma and post-srugical Peripheral Vascular System Arterial Atheroscleoriss, Aneurysmal dilatation, Microvascular disease (DM), Gangrene Venous PVS Complaints Pain or cramping of muscles Swelling or lymph edema Dyesthesia: abnormal sensation Changes to the skin Poor healing of superficial wounds Prominent vessels Chest pain SOB Palpitations: could be due to decreased blood to the heart, hormones, toxicity, etc. Cold hands/feet: Lack of circulation, venous stasis Risk of Vascular insufficiency Risk for DVT Pseudoclaudification = Stenosis vs. Vascular claudficiation = caused by activity and relieved by rest Vascular Insuffidicney risk Recent trauma or surgery, Hyperlipidemia, Hypertension, History of Cancer, Smoker, Diabetes type 1 and 2, Previous thrombus or family history Cancer medications, radiation and surgery can impact the vascular system. Adhesions and other problems can develop form surgery. Medications and radiation can damage the cells within the vessels. Smoking impacts vascular compliance and increases the risk of cardiac and respiratoy problems. It can also decrease compliance of vessel walls. Smoking is classically associated with AAA. Claassic is an older white male, smoker with history of HTN and lack of exercise that has pain with activity relieved by rest.. Diabetic Neuorpathy: PVS DS More common (4 times) Occurs at younger age Equal incidence in males/females More widespread Progresses more rapidly Multisegmetnal Bilateral Diabetes is a system disease affecting the nervous and vascular systems. The distal areas are often affected. The problem is peripheral and works its way up faster than in other conditions. The condition is more widespread and is multisegmetnal. DVT Risk Advanced age, injyry, fracture, inectiosn, CHF, R sided heart failure, varicose veins, family history of blood clots, prolonged bed rest, postpartum, difficult pregnancy, history of cancer, post operative, obesity, hormone supplement A person who stands for a living (assembly line) are at risk for varicose veins and blood clot formation because they frequently dont move around. We see people whose jobs require them to stand a lot that have DVTs. Chiropractors may be at risk because they stand a lot. Family history is another important risk factor. Table 15-2 Preceiptianting Facotrs in Thromboembolism Stasis: Arrhythmia, Heart Failure, Immobilization, Obesity, Varicose Veins, Dehydration Blood Vessel Injury: Trauma, Fracture Increased Coagulability: Neoplasm, Oral contraceptives, Pregnancy, Polycythemia, Previous thromboembolism PVS Exam: Inspection Upper and Lower Extremity with pt. in more than 1 position Size, Symmetry, Swelling Venous Patterun Note color of skin Nail beds, thickness, color, clubbing Hair pattern (loss) Lesions Video on Peripheral Vascular System and Lymphatics Vascular System: ARetiers, veins, lymphatics Arteries: Have apressure wave (pulse) and felt superficially. Brachial Artery, Radial Artery, Ulnar artery, femoral artery, popliteal aretery, dorsal pedis, and post tib are common locations. Veins: Superficial veins and deep veins (wide)Leg Veins (deep femoral and popliteal, superficial - -great saphenous running from foot to trunk, Perforators join deep and superficial veins) Lymphatics: Lymph Nodes small oval clumps of lymph tissue that aid immune reposed. Groin: Inguinal Nodes Arm: Apitrochlear Nodes Physical Exam Arms Inspection of color, nail beds, temp, texture and turgronr, checking for edema and lesions. View the finers for clubbing (Normal angle is 160 degress). Palpate: Radial pulse (rate, rhythm, and grade 0-4). Palpate the brachial pulse (medial to biceps tendon). Plate the epitrochlear node above the medial epicondyle. The epitrochelar node is not palpable. Modified Allens: Perform the test for radial and ulnar patency. Normal filling is 2-5 seconds. Legs Inspect: color, size, hair distribution, venous pattern, ulcersColor should matach. Even hair colorin and amount. Thin shiny skin, haird loss can be caused by arterial insufficiency or aging. DM is common to some cultures. Coolness, pallor, diminished puluses, thin shiny skin and foot ulcers may be found. Measure calf circumference (should be within 1 cm of each other). Palpation: Asses temperature (warm and equal bilaterally), Calf tenderness (flex the knee and squeeze the calfIt should not be painful), palpate the inguinal nodes (ndoes should 1 cm or less, moveable and non-tender). Peripheral arteries femoral pulse (inguinal area), popliteal pulse (slight flexed position), post tibial pulse (medial malleolus area between malleolus and Achilles dorsiflexion can help find the pulse)Dorsalis pedis (near the big toe) Normal pulse should be regular, 2+ and symmetrical Pretibial edema palpation press and hold for 5 secons then releaseNO pits should remain IN pregnancy their may be diffuse pitting edema. Stand to assess leg veins. Veins should not be visible or turtours. Manual Compression Test to test for valve competence of vein Compress the vein superiorly and palpate for a change infriorly. There should be no change. Raise the Legs, wiggle the feet (30-60 seconds) and check for postural color changes (pale). Have the patient sit up dangling the leg over the table, noting the time to color to return (should be about 10 seconds). Note how long it takes for veins to fill (normally about 15 seconds). Ankle Brachial Index Take the systolic measurement of the post tib or dorsal pedis and the brachial atery. Compare the systolic measurements. 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