History & physical examination of cvs


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History & physical examination of cvs

  1. 1. HISTORY & PHYSICALEXAMINATION OF CVS Presented by: Mandeep Duarah (CRI)
  2. 2. HISTORY TAKING IN CVSShould record the details of: PRESENTING SYMPTOMS – chest pain, fatigue & dyspnoea, palpitations, and presyncope or syncope. PREVIOUS ILLNESS HABITS – smoking, alcohol abuse FAMILY HISTORY DRUG HISTORY
  3. 3. PRESENTING SYMPTOMSCHEST PAIN1. Myocardial ischaemia Ischaemia of the heart results from an imbalance between myocardial oxygen supply & demand, producing pain called angina. The patient describes retrosternal pain which may radiate into the arms, the throat or the jaw. It has a constricting character, is provoked by exertion & relieved rapidly by rest.
  4. 4. 2. Pericarditis Also causes central chest pain, which is sharp in character & aggravated by deep inspiration, cough or postural changes. Usually idiopathic or caused by coxsackie B infection.
  5. 5. 3. Aortic dissection Severe tearing pain in either the front or the back of the chest. Onset is abrupt, unlike the crescendo quality of ischaemic cardiac pain.
  6. 6. DYSPNOEA A major symptom of many cardiac disorders, particularly left heart failure.1. Exertional Dyspnoea Most troublesome symptom in heart failure. Exercise causes a sharp increase in left atrial pressure & this contributes to the pathogenesis of dyspnoea by causing pulmonary congestion.
  7. 7. 2. Orthopnoea In patients with heart failure lying flat causes a steep rise in left atrial pressure, resulting in pulmonary congestion & severe dyspnoea.3. Paroxysmal Nocturnal Dyspnoea Caused by congestion (excessive or abnormal accumulation of blood) in the lungs, along with accumulation of excess fluid in the lungs (pulmonary edema), which occurs as a result of left sided heart failure.
  8. 8. FATIGUE Important symptom of heart failure. Caused partly by deconditioning & muscular atrophy but also by inadequate oxygen delivery to exercising muscle, reflecting impaired cardiac output.
  9. 9. PALPITATION Description of the rate & rhythm of the palpitation is essential. Rapid irregular palpitation is typical of atrial fibrillation Rapid regular palpitation of abrupt onset occurs in atrial, junctional & ventricular tachyarrhythmias.
  10. 10. DIZZINESS & SYNCOPE Cardiovascular disorders produces dizziness & syncope by transient hypotension, resulting in abrupt cerebral hypoperfusion. Recovery is usually rapid.
  12. 12. INSPECTION OF THE PATIENT Chest wall deformities such as pectus excavatum (hollowed chest) should be noticed. Most common congenital deformity of anterior chest wall Sunken appearance of sternum, may compress the heart & displace the apex Hypothesized that there is impairment of CVS function.
  13. 13.  Large ventricular or aortic aneurysms may cause visible pulsations. Superior vena caval obstruction is associated with prominent venous collaterals on the chest wall. Prominent venous collaterals around the shoulder occur in axillary or subclavian vein obstruction.
  14. 14. ANAEMIA May exacerbate angina & heart failure. Pallor of the mucous membranes is a useful physical sign but for confirmed diagnosis lab measurements of haemoglobin concentration is required.CYANOSIS Bluish discoloration of the skin & mucous membranes caused by increased concentration of reduced haemoglobin in the superficial blood vessels.
  15. 15. a. Central cyanosis Caused by reduced arterial oxygen sauration caused by cardiac or pulmonary disease. Affects not only the skin & lips but also the mucous membrane of the mouth. Causes include pulmonary oedema (which prevents adequate oxygenation of the blood) & congenital heart disease (tetralogy of fallot, eisenmenger’s syndrome).
  16. 16. b. Peripheral cyanosis Cutaneous vasoconstriction slows the blood flow & increases oxygen extraction in the skin & lips. Can be seen in fingers, underneath fingernails, other extremities. Occurs in heart failure and mitral stenosis.
  17. 17. CLUBBING Congenital cyanotic heart disease & infective endocarditis.OTHER CUTANEOUS AND OCULARSIGNS OF INFECTIVEENDOCARDITIS Splinter haemorrhages in nail bed Oslers nodes (tender erythematous nodules in the pulp of the fingers) Janeway lesions (painless erythematous lesions on the palm)
  18. 18. COLDNESS OF THE EXTREMITIES Important sign of reduced cardiac output in severe heart failure. Caused by reflex vasoconstriction of the cutaneous bed.PYREXIA Infective endocarditis is associated with pyrexia Can also occur for the first 3 days after myocardial infarction.
  19. 19. OEDEMA Subcutaneous oedema that pits on digital pressure is a cardinal feature of congestive heart failure. Pressure should be applied over a bony prominence (tibia,lateral malleoli,sacrum) In advanced heart failure oedema may involve the legs, genitalia & trunk.
  20. 20. ARTERIAL PULSEShould be palpated for evaluation of:1. RATE & RHYTHM Rate, expressed in beats per minute (bpm), is measured by counting over a timed period of 15 seconds. An irregular rhythm usually indicates atrial fibrillation.
  21. 21. 2. CHARACTER Defined by the volume & waveform and should be evaluated at the right carotid artery (pulse closest to the heart & least subject to damping & distortion) Pulse volume is small in heart failure & large in aortic regurgitation. Pulsus alternans – relatively high amplitude or normal amplitude pulse followed by a pulse of lower amplitude, occurs in severe left ventricular disease.
  22. 22.  Pulsus paradoxus – occurs when the pulse prssure falls by >10mm hg with each inspiration, found in constructive pericarditis & cardiac tamponade. Bisferiens pulse (biphasic pulse) – with 2 systolic peaks is usually attributed to a combination of aortic stenosis & aortic regurgitation.
  23. 23. 3. SYMMETRY Symmetry of the radial, branchial, carotid, femoral, popliteal & pedal pulses should be confirmed. Coarctation of the aorta causes symmetrical reduction & delay of the femoral pulses compared with the radial pulses.
  24. 24. MEASUREMENT OF BLOODPRESSURE Measured using sphygmomanometer Patient is placed at supine position A cuff of atleast 40% the arm circumference in width is attached to a mercury manometer & inflated around the extended arm Auscultation over the brachial artery reveals 5 phases of korotkoff sounds as the cuff is deflated:
  25. 25.  Phase 1: the first appearance of the sounds marking systolic pressure Phase 2 & 3: increasingly loud sounds Phase 4: abrupt muffling of the sounds Phase 5: disappearance of the sounds.Conditions where korotkoff sounds remain audibledespite complete deflation of the cuff (aorticregurgitation, arteriovenous fistula) phase 4 mustbe used for the diastolic measurement.
  26. 26. JUGULAR VENOUS PULSE Best examined while the patient reclines at 45 degrees with patients head partially rotated to one side. Sternal angle is reference point for JVP Differentiate from carotid - multiple wave forms - can be abolished by gental digital pressurewhere as carotid pulsation is always palpable & cannotbe abolished by gentle digital pressure.
  27. 27. JUGULAR VENOUS PRESSURE• Position the patient so that the upper level of JV pulse is visible• Place ruler at sternal angle which is 5cm above the RA• Hold another ruler horizontally at the top of JV pulse• Note how many cms this is above the sternal angle , add 5cms to this number & total is JV pressure• Normal pressure is less than or equal to 9cm.
  28. 28. CAUSES OF ELEVATED JUGULARVENOUS PRESSURE Congestive heart failure Cor pulmonale Pulmonary embolism Right ventricular infarction Tricuspid valve disease Tamponade Constrictive pericarditis Superior vena cava obstruction
  29. 29. PALPATION OF CHEST WALL Used for detection of parasternal heaves & apex beat Parasternal heave is discerned with the heel or flat of the right hand against the left parasternal region, right ventricular hypertrophy causes a left parasternal heave. Apex beat is defined as the lowest & most lateral point at which the cardiac impulse can be palpated. The apex beat is normally located in the fifth left intercostal space in the mid-clavicular line. Apex beat is displaced in left ventricular dilation.
  30. 30. AUSCULTATION OF THE HEART Use the diaphragm for high pitched sounds & murmers Use the bell for low pitched sounds & murmers Sequence of auscultation- Upper right sternal border (URSB) withdiaphragm(aortic area)- Upper left sternal border (ULSB) with diaphragm(pulmonary area)- Lower left sternal border (LLSB) with diaphragm(tricuspid)- Apex ( mitral area)
  31. 31.  After the age of 40 S3 is nearly always pathological, usually indicating left ventricular failure, mitral regurgitation S4 is also pathological and heard in aortic stenosis, hypertrophic cardiomyopathy.
  32. 32. systolic clicks & opening snaps Valve opening is normally silent In aortic stenosis valve opening produces a click, the click is only audible if the valve cusps are pliant & non-calcified, and is prominent in bicuspid valve. In mitral stenosis, elevated left atrial pressure causes forceful opening of the thickened valve leaflets, this generates a snap.
  33. 33. Heart murmurs Caused by turbulent flow within the heart & greater vessels. Turbulence is caused by increased flow through a normal valve usually aortic and pulmonary. Murmurs may also indicate valve disease or abnormal communications between the left & right sides of the heart (septal defects).
  34. 34. According to the phase of systole or diastole duringwhich it is heard murmurs are classified as:1. Systolic murmurs Midsystolic murmur – caused by turbulence in the left or right ventricular outflow Pansystolic murmur – mitral regurgitation, tricuspid regurgitation, ventricular septal defect Late systolic murmur – mitral valve prolapse, tricuspid valve prolapse.
  35. 35. 2. Diastolic murmurs Early diastolic murmurs – caused by regurgitation through aortic and pulmonary valves Mid diastolic murmurs – caused by turbulent flow through the atrioventricular valves (mitral stenosis) Presystolic murmur – mitral & tricuspid stenosis.3. Continuous murmurs Heard during systole & diastole Patent ductus arteriosus
  36. 36. THANK YOU