Cvs examination june 2020
1 like249 views
The document discusses examination of the cardiovascular system by assessing arterial pulses. It defines arterial pulses and describes how to evaluate the rate, rhythm, volume, and character of pulses at different arterial sites. Specific pulse abnormalities are also outlined, such as pulsus paradoxus and bisferiens pulse, which provide clues to underlying cardiovascular conditions like constrictive pericarditis or aortic stenosis. The summary evaluates arterial pulses to examine cardiovascular function.
Cvs examination june 2020
- 1. • Dr J P Soni THE PHYSICAL EXAMINATION IN CARDIOVASCULAR SYSTEM THE PHYSICAL EXAMINATION IN CARDIOVASCULAR SYSTEM
- 3. Arterial Pulses: ◆ It is the pressure wave which travels along the walls of arteries when blood is ejected from left ventricle into aorta during systole. • when this pressure wave travels along walls of arteries → expansion of art. Walls → palpated as arterial pulse. • The velocity of pressure pulse wave is 15 time > than velocity of blood in aorta • It is 100 times > than velocity of blood flow in peripheral arteries.
- 4. VELOCITY OF PRESSURE PULSE WAVE IN DIFF. ARTERIES • Aorta 4m/sec • Large arteries 8m/sec • Peripheral arteries 16m/sec
- 5. ◆ The transmission of pressure pulse wave is independent and much faster than the velocity of blood flow. • ◆ Normally Art. Pulse ends in arterioles→ there are no capillary pulsations . ◆ No pulsations in vein except jugular vein. ◆ The amplitude of arterial pulse depends on pulse pressure.
- 6. DEFENITION • Arterial pulse - Rhythmic distension of arterial wall felt along peripheral artery with each effective left ventricular contraction during cardiac cycle is.
- 7. Pulsation • It is caused by pressure changes in aorta. • Systolic ejection of blood from left ventricle to aorta, cause expansion of aorta and then recoil, setting up pressure wave or pulse. • Pulse wave travels faster than blood with velocity of 5-8m/sec( Blood flow at velocity of 0.5msec.
- 8. Pulse pressure: It is the difference between diastolic and systolic B.P: It depends on: • Stoke volume • Elasticity of arteries • Character of ejection of blood from left venrtical.
- 9. Normal Pulse – The normal central aortic pulse wave is characterized by a fairly rapid rise (Anacrotic limb) to a somewhat rounded peak, the anacrotic shoulder, present on the ascending limb, occurs at the time of peak rate of aortic flow just before maximum pressure is reached. – The less steep descending limb(catacrotic limb) is interrupted by a sharp downward deflection, coincide with reflux of blood back into aota, called incisura - dicrotic notch & dicrotic wave coincide with aortic valve closure. – The pulse pressure is about 30-40 mmHg.
- 10. Anacrotic limb Catacrotic limb Dicrotic wave – due to return of same blood by closing semilunar valve P – LV contraction “t” – Elastic recoil of aorta “n” – Regurgitation of blood back form aorta to LV
- 11. Normal Pulse – As the pulse wave is transmitted peripherally, the initial upstrokes becomes steeper, the anacrotic shoulder becomes less apparent, and the incisura is replaced by the smoother dicrotic notch.
- 12. Method of study • Arterial pulse is studied by Palpation of superficial arteries of the body. • E.g. Radial, brachial, femoral, carotid, dorsalis pedis etc. • While palpating radial pulse middle three fingers are used. • Middle finger is used for compression, volume & rate assessment of pulse. • Ring finger is used to study the condition of vessel wall. • Also palmar and plantar pulses in newborns
- 13. Peripheral Pulses Radial pulse • At wrist , lateral to flexor carpi radialis tendon , place your three middle fingers over the radial pulse Simultaneous evaluation of both radial pulses and a femoral pulse
- 14. The Carotids • The patient lies down with the head of the bed elevated 30 degrees • Carotid pulsations is visible just medial to sternomastoid. • Use your left thumb for right carotid pulse & vice versa. • Place the left thumb on the right carotid A. in the lower third of the neck at the level of the cricoid cartilage, Place tip of thumb b/w larynx & ant.border of sternocleidomastoid - just inside the medial border of the sternomastoid and press posteriorly • Never press both carotids at same time
- 15. Brachial pulse • Use your thumb ( rt thumb for rt.arm & vice versa ) with your fingers cupped round the back of the elbow. • Brachial pulse – felt in front of the elbow just medial to tendon of biceps.
- 16. Femoral Pulse • Is felt at groin just below inguinal ligament midway b/w ant.sup.iliac.spine & symphysis pubis.
- 17. Popliteal Pulse • Knee to be flexed 40 deg. Heel resting on bed • Place fingers over lower part of popliteal fossa & fingers are moved sideways to feel pulsation of Popliteal.A against post.aspect of tibial condyles.
- 18. Posterior Tibial Pulse • Felt just behind medial malleolus, midway b/w medial malleolus & tendo achillis.
- 19. Dorsalis Pedis Pulse • Felt just lateral to tendon of ext.hallucis longus. Congenital absence of dorsalis pedis in 10% of population
- 20. Arterial Pulses Evaluation: Assess arterial pulse for rate rhythm volume character Vessel wall Radio-femoral relationship, pulse deficit.
- 21. Rate: Heart rate / minute; count for one full minute. Indicate true rate of ventricular contraction. Normal Bradycardic (conditioning, heart block, digoxin toxicity) Tachycardic (CHF, excitement, fever, anemia, arrhythmia)
- 22. Rate • Count the pulse for 1 min / at least 30 sec • Normal : AGE RATE/MIN 0-1 DAY 94-155(122) 1-3 DAY 90-166(122) 3-7 DAY 106-182(128) 7-30 DAY 106-182(149) 1-3 MNTHS 120-179(149) 3-6MTHS 105-185(141) 6-12MTHS 108- 169(131) 1-3Y 89-152 (!!9) 3-5Y 73-137(109) 5-8YRS 65-133(100) 8-12YRS 62-130(91) 12-16 60-120(80)
- 23. Sinus Tachycardia • Physiological : infants children anxiety , emotion • Pathological : Tachyarrhythmia- SVT, VT High output states ▪ Drugs – atropine nifedipine caffiene, nicotine
- 24. High Output States • Anaemia • Pyrexia • Beri beri • Thyrotoxicosis • Pheochromocytoma • AV fistula
- 25. Sinus Bradycardia • Physiological : Atheletes, sleep • Pathological : severe hypoxia hypothermia sick sinus syn myxoedema obs.jaundice raised ICT ▪ Drugs : beta blockers, verapamil, diltiazem
- 26. Relative Bradycardia • Typhoid • Pt on beta blocker • CNS infection with raised ICT
- 27. Rhythm: Regular Irregular (can be sinus arrhythmia with respiratory variation or PAC/PVC’s) Regularly irregular – extra systole Irregularly irregular (arrhythmia) Atrial fibrillation
- 28. • CATACROTIC PULSE: Normal arterial pulse: 1. Percussion waves, P - Produced by ejected blood in arterial system 2. Tidal wave, T - Generated along arterial wall 3. Dicrotic notch and dicrotic wave – in downstroke of pulse, d/t elastic recoil of vessel *wavy pattern is not felt in health since it is obliterated by normal vascular tone
- 29. CHARACTER OF ARTERIAL PULSE - Pulsus Bigeminus - Pulsus altenunans - Anacrotic Pulse - Pulsus Parvs et Tardus - Bounding pulse - Pulsus Bisferinens - Dicrotic Pulse - Pulsus Paradoxus - Thready Pulse - Waterhammer Pulse
- 30. Pulsus Bigeminus Coupling of the pulses waves in pairs Followed by a pause Alternate premature beats AV block Sinoatrial block with Vent. Escape Pulsus bigeminus is a cardiovascular phenomenon characterized by groups of two heartbeats close together followed by a longer pause. The second pulse is weaker than the first beat. The smaller beat is palpated as either a missing or an extra beat, and on EKG resembles a PVC. These PVCs appearing every other beat are also called extrasystoles.
- 31. Pulsus Alternans • Alternating strong & weak pulse. • Palpation of radial, femoral, brachial pulses • Palpation by light pressure, breath held in mid expiration • Better – recording BP, when sys.pressure alternates by >20mm Pulsus Alternans Strong and weak beat occurring alternately LVF Toxic myocarditis Paroxysmal Tachycardias Following Premature beat
- 32. PULSES IN AORTIC STENOSIS Increased resistance to left ventricular ejection due to fixed obstruction reduces the stroke volume, prolongs left ventricular total ejection time, and retards the rate of initial stroke output into the aorta and distal arterial system. **Characteristics: --Anacrotic character (anacrotic pulse): gives the impression of interruption of the upstroke of the carotid pulse. Aortic stenosis is likely to be hemodynamically significant when the anacrotic notch is felt immediately after the onset of the upstroke. When an anacrotic notch occurs very early on the ascending limb of the arterial pulse, it can be appreciated in the radial pulse and suggests moderate to severe aortic stenosis.
- 33. • **--Delayed upstroke of the ascending limb (pulsus tardus): delayed peak and slower upstroke of the carotid pulse. The delay can be appreciated by simultaneous palpation of the carotid pulse and auscultation of the interval between S1 and S2 (duration of systole). Normally the peak of the carotid pulse occurs closer to S1; in the presence of severe aortic stenosis, it is usually closer to S2. In the presence of fixed outflow obstruction, the central aortic pulse demonstrates a progressively slower rise of the ascending limb, a lower anacrotic shoulder, and a peak closer to the incisura as the severity of obstruction increases. • --Small amplitude (pulsus parvus): The amplitude of the pulse decreases with a diminished stroke volume. • --Shudder (thrill) on the ascending limb: is frequently palpable on the ascending limb of the pulse. • ** The usual changes in the carotid pulse due to aortic stenosis are modified in this situation, particularly the amplitude.
- 34. Anacrotic Pulse Two upbeats, in systole Pulse is typically small slow rising with delayed peak. Aortic stenosis Pulse/ Characteristic Examples Anacrotic Pulse Slow rising Twice beating Both waves felt in systole Aortic Stenosis
- 35. Pulsus Parvus Parvus = small, weak pulse rise slowly and Has late systolic phase. Aortic stenosis Mitral stenosis Hypovolemia Pulsus Parvus et Tardus Slow rising Anacrotic wave not felt Aortic Stenosis
- 36. Pulsus Tardus • Delayed systolic peak resulting from obstruction of lt.ven.ejection • Fixed LV obs – Valvular AS
- 37. Pulsus Parvus et Tardus • Small vol pulse with delayed systolic peak • Severe AS
- 38. Collapsing or hammer Pulse (Corrigan) It is characterized by rapid upstroke and down stroke Of pulse wave, no dichrotic notch w PDA, Aorto-pulmonary window AR Arterio-venous fistula Rupture of sinus of valsulva. Severe Mitral regurgitation Waterhammer Pulse(Corrigan’s Pulse) High volume pulse Sharp rise Ill-sustained Sharp fall Pulse pressure is at least 60mmHg Aortic Regurgitation
- 39. Bisferiens Pulse • 2 systolic peaks ,the percussion & tidal waves separated by distinct midsystolic dip. • Detected more rapidly by palpating carotid artery. • AS+AR Pulsus Bisferiens Rapid rising Twice beating Both waves felt in systole Idiopathic Hypertrophic Subaortic Stenosis(jerky pulse) Severe AR with mild AS HOCM
- 40. Pulsus Paradoxus • Exaggerated reduction in strength of arterial pulse during normal inspiration due to exaggerated insp fall in sys.pressure (> 10 mm) • >20mm Hg – detected by palpating brachial.a. • Milder fall – measuring BP Pulsus Paradoxus SBP fall more than 10mmHg during inspiration (exaggeration of normal) Does not happen if thoracic cage is immobile SVC Obstruction Lung conditions(Asthma, emphysema, airway obstruction) Pericardial effusion Constrictive pericarditis Severe CCF Reversed Bernheim sign
- 41. Pulsus Paradoxus • Venous return normally increases with inspiration • Despite this, BP normally decreases by up to 8 mm Hg on inspiration • This paradoxical response is due to: – Increased pulmonary capacitance – Increased negative intra-thoracic pressure with inspiration and – The phase lag between right and left sided events
- 42. How to measure Pulsus Paradoxus • Pulsus paradoxus is an exaggerated inspiratory fall in BP – Ask the subject to breath normally – Auscultate Korotkoff’s sounds as the BP cuff is slowly lowered. Time respiration simultaneously – Mark when BP sounds are heard only in expiration – Mark when BP sounds are heard both in expiration & inspiration. Korotkoff’s sounds seem to double at this point. – The difference is the measured pulsus paradoxus
- 43. Pulsus Paradoxus An exaggerated drop in SBP (>10mmHg) with inspiration
- 44. Pulsus Paradoxus • Cardiac tamponade, • Constrictive pericarditis, • severe airway obs , • SVC obstruction
- 45. Reverse Pulsus Paradoxus Peripheral arterial systolic and diasdolic pulses pressure increase on inspiration, while heart sounds remain audible Patient on Continuos airway pressure on mechanical ventilator Idiopathic hypertrophic subaotic stenosis Isorhyrthmic ventricular rhyrhtm Reversed Pulsus Paradoxus
- 46. Dicrotic Pulse • 2 peaks . • 2nd peak is in diastole after S2. • Normally a small wave that follows aortic valve closure ( dicrotic notch ) is exaggerated • Due to very low stroke vol & per. Resistance. • LVF Dicrotic Pulse Twice beating First wave in systole, second wave in diastole (seen when PR and DP is low) Felt due to hypotonia of vessel wall Fever (e.g. typhoid fever) Endotoxic shock CCF Cardiac Tamponade Following open heart surgery
- 47. Volume: Indicate amplitude of the pulse, depends upon stroke volume, elasticity of vessel wall & peripheral resistance. This measures amount of blood flowing with every heart beat. Normal Bounding/water hammer (pulse pressure >30 mmHg in infant, >50 mmHg in child) Thready − low output states: shock, severe CHF, large VSD or PDA − L sided obstruction: AS, aortic atresia, HLHS Absent
- 48. Radio – femoral Delay • Usually 2 radial pulses come simultaneously & femoral comes 5msec before ipsilateral radial pulse. • Delay in femoral pulse – obstruction of aorta – coarctation
- 49. Vessel Wall Thickness • Assess the state of medium sized arteries which are palpable. • Method: palpate radial artery with middle 3 fingers. Occlude proximally & with index finger empty artery by pressing out blood distally. Applying pressure on either side – roll the artery over underlying bone using middle finger.
- 50. Condition of vessel wall • Sufficient pressure should be exerted on the artery to abolish pulsation in vessel. • Artery should be rolled beneath the finger against underlying bone. • Arterial wall cannot be felt, soft in young. • It become tortuous, easily palpable & whip cord • Like in old age due to arteriosclerosis.
- 51. Pulse Apex Deficit • Diff b/w heart rate & pulse rate , when counted simultaneously for one minute. • Diff b/w AF & Ectopics Features Atrial fibrillation Ectopics Pulse deficit > 10 / min < 10 / min On exertion Persists/increase Decrease rhythm Irregularly irregular Regularly irregular
- 52. Blood Pressure ▪ Definition: the force exerted by the blood against the blood vessel wall. The highest pressure in the cycle is the systolic blood pressure and the lowest is the diastolic. ▪ BP = Heart Rate x Total Peripheral Resistance* * blood volume, viscosity, vessel elasticity sympathetic activity, kidney function
- 53. How to take the measurement • Palpate the location of the brachial artery • Position the arm cuff over the brachial artery Width of cuff40% of circumference Length of cuff 80 -100 % of circumference
- 54. How to take the measurement • Palpate the location of the brachial artery • Position the arm cuff over the brachial artery • Obtain an estimated systolic pressure by palpation prior to auscultation • Inflate cuff to 30 mmHg above the estimated systolic BP • Deflate the cuff slowly, 2-3 mmHg/second • Note the first of 2 regular beats as systolic pressure. • Use Kortokoff V (last sound heard as the diastolic pressure) • Continue deflation for 10 mmHg past last sound to assure sound is not a skipped beat • Record as an even number and to the nearest 2 mmHg (round upward)
- 55. Cuff Sizes Cuff Name Bladder Width Bladder Length Mid Arm Circumference Child 8 21 16 to <22cm Small arm 10 24 22 to <27cm Average arm 13 30 27 to<33cm Large arm 16 38 33 to <41cm Extra Large 17 43 41 to <52cm Based on AHA Guidelines
- 56. Equipment • Aneroid • Ocillometric • Hybrid • Mercury (used only for accuracy check in MI)
- 59. Jugular Venous Pressure • Which vein to inspect for - JVP ? Internal/External jugular vein
- 60. Why Internal Jugular Vein? • IJV has a direct course to RA. • IJV is anatomically closer to RA. • IJV has no valves( Valves in EJV prevent transmission of RA pressure) • Vasoconstriction Secondary to hypotension ( in CCF) can make EJV small and barely visible.
- 61. Why Right Internal Jugular Vein? • Right jugular veins extend in an almost straight line to superior vena cava, thus favouring transmission of the haemodynamic changes from the right atrium.
- 62. Why Right Internal Jugular Vein? • The left innominate vein is not in a straight line and may be kinked or compressed between Aortic Arch and sternum, by a dilated aorta, or by an aneurysm.
- 63. What is Normal JVP • The normal JVP reflects phasic pressure changes in the right atrium - • It consists of three positive waves a,c,v. And two negative troughs x,y.
- 64. How to distinguish JVP- Carotid pulsatation • Simultaneous palpation of the left carotid artery aids the examiner in relating the venous pulsations to the timing of the cardiac cycle. Venous pulsation Arterial pulsation Best seen Best palpable Lateral medial Have Upper limit No upper limit Sinuous
- 65. JVP Inspection
- 66. The centre of the right atrium is 5 cm below the angle of louis in any position. At 45 degree angle of louis and supraclavicular fossa comes in one plane. Thus JVP pulsatation above the 5cm will be visible at 45 degree only.
- 67. --------------------------------------------------------- --------------------------------------------------------- Angle of louis • Usually JVP is less than 8 cm water that is < 3 cm above level of sternal angle.
- 69. Normal JVP Waveform • a wave - atrial systole • x descent – onset of atrial relaxation • c wave - small positive notch in the 'x' descent due to bulging of the AV ring into the atria in ventricular contraction or due carotid pulsatation • x' (prime) descent !!! – occurs during systole due to RV contraction pulling down the TV valve ring “descent of the base” – a measure of RV contractility • v wave - after the x' descent - slow positive wave due to right atrial filling from venous return • y descent - rapid emptying of the RA into RV due to TV opening
- 70. A- Atrial contraction C- Tricuspid closure • V- f
- 72. • Venous distension due to RA contraction Retrograde blood flow into SVC and IJV • Synchronous with S1, Follow P of ECG • Precede Carotid pulse a WAVE
- 73. • The x descent: is due to X Atrial relaxation X` Descent of the floor of the right atrium during right ventricular systole. Begins during systole and ends before S2 • The c wave: Occurs simultaneously with the carotid pulse Artifact by Carotid pulsation Bulging of TV into RA during ICP
- 74. v WAVE • Rising right atrial pressure when blood flows into the right atrium during ventricular systole when the tricuspid valve is shut. • Synchronous with Carotid pulse • Begins in early systole, Peaks after S2 and ends in early diastole
- 75. y DESCENT • The decline in right atrial pressure when the tricuspid valve reopens • Following the bottom of the y descent and before beginning of the a wave is a period of relatively slow filling of the ventricle, the diastases period, a wave termed the h wave.
- 76. • The x descent occurs just prior to the second heart sound ( during systole), while the y descent occurs after the second heart sound (during diastole). • Normally X descent is more prominent than Y descent. Y descent is only sometimes seen during diastole. Descents are better seen than positive waves. • The a wave occurs just before the first sound or carotid pulse and has a sharp rise and fall. • The v wave occurs just after the arterial pulse and has a slower undulating pattern. • The c wave is never seen normally. Identifying Wave Forms
- 77. Abnormalities of jugular venous pulse A. Low jugular venous pressure 1. Hypovolaemia.
- 78. B. Elevated jugular venous pressure 1. Intravascular volume overload conditions Right ventricular infarction Left heart failure Myocardial infarction. Valvular Heart Disease Cardiomyopathy 2. Constrictive pericarditis. 3. Pericardial effusion with tamponade
- 79. Elevated “a” wave Increased Resistance to RV Filling. Tricuspid stenosis R Heart Failure PS PAH
- 80. Cannon “a” wave • Atrial- ventricular Dissociation (atria contract against a closed tricuspid valve) Complete heart block VPC Ventricular tachycardia Ventricular pacing Junctional rhythm Junctional tachycardia.
- 81. Absent “a” wave • 1. Atrial fibrillation
- 82. Elevated “v” wave 1. Tricuspid regurgitation. 2. Right ventricular failure. 3. Restrictive cardiomyopathy. 4. Cor Pulmonale
- 83. Tricuspid regurgitation • Absent X Decsent • CV/ Regurgitant Wave • Has a rounded contour and a sustained peak • Followed by a rapid deep Y descent • Amplitude of V increases with inspiration. • Cause subtle motion of ear lobe with each heart beat
- 84. “a” wave equal to “v” wave ASD Prominent X descent followed by a large V wave M Configuration Indicates a large L-R shunt With PAH A wave becomes more prominent If L JVP > R JVP indicates associated PAPVC
- 85. 1. Cardiac tamponade. 2. Constrictive Pericarditis 3. RVMI 4. Restrictive Cardiomyopathy 5. Atrial septal defect Prominent “x” descent Blunted “x” descent 1. Tricuspid regurgitation. 2. Right atrial ischaemia
- 86. Prominent “y” descent 1. Constrictive pericarditis. 2. Tricuspid regurgitation. 3. Atrial septal defect. 1. Cardiac tamponade. 2. Right ventricular infarction 3. Restrictive Cardiomyopathy Absent “y” descent Slow “y” descent 1. Tricuspid stenosis. 2. Right atrial myxoma.
- 87. Constrictive pericarditis. • M shaped contour • Prominent X and Y descent (FRIEDREICH`SIGN) • Y descent is prominent as ventricular filling is unimpeded during early diastole. • This is interrupted by a rapid raise in pressure as the filling is impeded by constricting Pericardium • The Ventriclar pressure curve exhibit Square Root sign
- 89. The Abdomino-jugular Test: Technique and Hemodynamic Correlates Abdominal pressure of 35mm Hg applied with rolled up manometer Patient instructed to breath normally JVP estimated 12 seconds after compression
- 90. Abdomino-jugular reflux • Is positive when JVP increase after 10 sec of abdominal pressure followed by a rapid drop in pressure of 4 cm on release of compression. • Most common cause of a positive test is RHF • Positive test in: Borderline elevation of JVP Silent TR Latent RHF • False positive: Fluid overload • False Negative: SVC/IVC obstruction Budd Chiari syndrome • Positive Test imply SVC and IVC are patent
- 91. Specific JVP patterns Condition Pattern Normal waveform X' deeper than Y Post CABG X' shallower, now = Y Atrial fibrillation CV wave Tricuspid regurgitation CV wave Complete heart block Irregular cannon A waves Tamponade JVP brisk X' > Y Constriction JVP brisk X' & Y descents X' less exaggerated than Y RV infarction JVP –low amplitude
- 92. 2000’S Pulse Oximetry saturation Pulse oximetry – right upper limb and lower limb, three time at interval of 60 minutes
- 94. Central cyanosis •noted in the trunk, tongue, mucous membranes •due to reduced oxygen saturation Peripheral cyanosis •noted in the hands and feet, around mouth due to reduced local blood flow The cyanosis usually correspond to oxygen saturation of 70-80%. Therefore mild desaturation may clinically be missed.
- 95. Differential cyanosis 1. pink upper, blue lower CoA, IAA, Pulm Htn Blue lower Pink Upper Pink Upper
- 96. blue upper and pink lower limb d-TGA with pulm Htn *indicates serious underlying cardiac Deep Blue upper Less blue
- 97. Pulse Oximetry •Easy to use, harmless when done correctly •Accuracy of 2% in the range of 70 to 100% •Consider for CHD’s when Sat <94% at 24 hours of age •Should be obtained prior to discharge from nursery = Policy for newborn’s - Measure sat in foot If <95%, gets evaluation
- 98. The patient: Male Should have their shirt(s) off, or wear an examination gown Females nine years old and older should wear a gown with the opening in the front CVS examination Should be in calm and quiet room.
- 99. 99 Inspection & Palpation 1 Pre-cardial projection and excavation 2 Apical impulse 3 Abnormal pulsations of precardium
- 100. Precordium -Inspection Palpation• Apex beat – Location – Character • Heaving • Thrusting • Double • Tapping • Paradoxical • Left parasternal heave • Thrills (palpable murmurs) – Systolic – Diastolic • Palpable P2 (pulmonary hypertension) • Pacemaker box
- 101. PALPATION Lay a prewarmed hand very gently on the chest, remembering the heart may not be in its normal position. With the tips of the right first and second fingers, depress the thorax just left of the xiphoid process The fingertips are now lying on the right ventricle. A faint impulse is allowable, but if the heart is enlarged, a definite forceful movement will be present
- 102. INSPECTION & PALPATION: Asymmetry can indicate RVE Kyphoscoliosis--can have cardiopulmonary effect Poland’s anomaly (unilateral absence of pectoralis major/minor) Harrison’s grooves seen in the lower chest Pulsations/rocking seen with large shunts, MR, or AI
- 103. PALPATION: Use the most sensitive portion of the hand Lay the heel of R hand at left sternal border with fingertips pointing to left axilla
- 105. Apical Impulse: It is lower most, outer most, definite cardiac pulsation, felt in 3rd ICS medial to left mid-clavicular line in new born. 4th ICS medial to left mid-clavicular line in infant 5th ICS medial to left mid-clavicular line in Adult. This apical area corresponds with mitral area & is due impact of left ventricle. . It help in assessment of ventricular size / thickness.
- 106. LV apical impulse (PMI): Found with fingertips with the patient upright One should always note interspace location, relation to the midclavicular /anterior axillary line, amplitude compared to RV impulse
- 107. LV apical impulse : Strong impulse is due to increased cardiac output or LVH Downward/leftward displacement--LVE (with or without LVH)
- 108. Apical Impulse : Hyper-dynamic : Forceful but illsustained Hyper-dynamic impulse in normal location: think increased cardiac output or LVH Hyper-dynamic and downward/left wardly displaced: think LVE Indistinct impulse associated with RVH Precordial heave is seen with RVE
- 109. Apical Impulse : Normal S1 is not palpable Tapping : Normal apex beat, S1 palpable Heaving : Forceful and sustained Hyperdynamic : Forceful but not sustained
- 110. Left para-sternal heave RV impulse: Felt at the LSB--usually slight RVH (without RVE)--parasternal tap (sharply localized, quickly rising) RVE (with or without RVH)--parasternal lift (diffuse, gradually rising)
- 111. Thrills: Palpation of a loud murmur Found in the precordial, suprasternal, or carotid artery area If low intensity murmur, probably just a pulsation and NOT a thrill
- 112. 112 Percussion • Aim:to determine the size and shape of the heart . • Absolute dullness: contain no gas Relative dullness : real size
- 113. 113 Maneuver Of Percussion • Patient should be in erect position –the pleximeter is vertical with the intercostal space • Patient should be in the recumbent position –the pleximeter is parallel with the inter-costal space
- 114. AUSCULTATION:
- 115. The stethoscope: Should be own!!! Should have a separate bell and diaphragm Bell allows in all sounds Diaphragm lets in middle and high frequency sounds, attenuates low pitched sounds
- 116. The stethoscope : Bell should be used relatively lightly (avoid diaphragm effect) Diaphragm should be small enough to fit on the chest of the patient Should have tubing which is short (16-18 inches) Should have earpieces that are comfortable and snug
- 117. Auscultation • Use the diaphragm for high pitched sounds and murmurs • Use the bell for low pitched sounds and murmurs
- 118. Where to listen: Apex/5LICS (mitral area) Left lower sternal border/4LICS (tricuspid and secondary aortic area) Right middle sternal border/2RICS (aortic area) Left middle sternal border/2LICS (pulmonary area)
- 119. Auscultation 1. Position the patient supine with the head of the table slightly elevated. 2. Always examine from the patient's right side. A quiet room is essential. 3. Listen with the diaphragm at the right 2nd intercostal near the sternum (aortic area). 4. Listen with the diaphragm at the left 2nd intercostal near the sternum (pulmonic area). 5. Listen with the diaphragm at the left 3rd, 4th, and 5th interspaces near the sternum (tricuspid area).
- 120. 6. Listen with the diaphragm at the apex (mitral area). 7 Listen with the bell at the apex. 8. Listen with the bell at the left 4th and 5th inter-costal near the sternum. 9. Have the patient roll on their left side. ➢ Listen with the bell at the apex. ➢ This position brings out S3 and mitral murmurs. 10 Have the patient sit up, lean forward, and hold their breath in exhalation. ➢ Listen with the diaphragm at the left 3rd and 4th inter- costal near the sternum. ➢ This position brings out aortic murmurs. 11. Record S1, S2. 12. Auscultate the carotid arteries.
- 121. Other site for auscultation Lungs Cranium (temples/orbits/fontanelle) Liver Neck (carotid area) Abdomen Lumbar/abdominal region over renal area Mouth/trachea with respiration Femoral artery
- 122. How to listen: Have a system, e.g. method of inching Listen systematically: S1, S2, S3, S4 Murmur systolic sounds, systolic murmurs, diastolic sounds, diastolic murmurs
- 123. Normal heart sounds
- 124. S1: May be due to acceleration/deceleration phenomena in the LV near the A-V valves Best heard at the apex and LLSB Often sounds single unless slow heart rate Differentiate S1 from S2 by palpating carotid pulse: − S1 comes before and S2 comes after carotid upstroke
- 125. Decreased S1: Slowed ventricular ejection rate/volume Mitral insufficiency Increased chest wall thickness Pericardial effusion Hypothyroidism
- 126. Decreased S1 : Cardiomyopathy LBBB Shock Aortic insufficiency First degree AV block
- 127. Other Abnormal S1 : Increased S1: − Increased cardiac output − Increased A-V valve flow velocity (acquired mitral stenosis, but not congenital MS) Wide splitting of S1: − RBBB (at tricuspid area) − PVC’s − VT
- 128. S2: From closure vibrations of aortic and pulmonary valves Divided into A2 and P2 (aortic and pulmonary closure sounds) Best heard at LMSB/2LICS Higher pitched than S1--better heard with diaphragm
- 129. S2 splitting (normal): Normally split due to different impedance of systemic and pulmonary vascular beds Audible split with > 20 msec difference Split in 2/3 of newborns by 16 hrs. of age, 80% by 48 hours Harder to discern in heart rates > 100 bpm
- 130. S2 splitting (normal): Respiratory variation causes splitting on inspiration: pulmonary vascular resistance When supine, slight splitting can occur in expiration When upright, S2 usually becomes single with expiration
- 131. S2 splitting (abnormal): Persistent expiratory splitting − ASD − RBBB − Mild valvar PS − Idiopathic dilation of the PA − WPW
- 132. S2 splitting (abnormal): Widely fixed splitting − ASD − RBBB Wide & varible splitting − Mild PS − RVOTO − Large VSD or PDA − Idiopathic PA dilation − Severe MR − RBBB − PVC’s
- 133. S2 splitting (abnormal): Reversed splitting − LBBB − WPW − Paced beats − PVC’s − AS − PDA − LV failure
- 134. Single S2: Single S2 occurs with greater impedance to pulmonary flow, P2 closer to A2 Single and loud (A2): TGA, extreme ToF, truncus arteriosus Single and loud (P2): pulmonary HTN!! Single and soft: typical ToF Loud (not single) A2: CoA or AI
- 135. Normal Sounds Heart sound S1 S2 Event Due closure of AV Due to closure of semilunar valve Pitch Lower Higher Duration Longer Shorter Point of maximal intensity At cardiac Apex Base of the heart Location in cardiac cycle At the end of the long pause At the beginning of the long pause S3 ventricular gallop S4 atrial gallop Event Due rapid ventricular filling Due Atrial contraction Timing During early diastole During late diastole Feature May be normal, physiological Always abnormal Suggest Can be sign of systolic ventricular failure Can be sign of diastolic ventricular failure Ventricle is compliant Ventricle noncompliant HEART SOUND
- 136. S1 abnormalities Decreased S1 Loud S1 Split Reverse split MR, TR MS,TS RBBB Ectopic beats Absent if Av calcified High output state Pul. Hypertension S2 abnormalities Decreased S2 Loud S2 Single S2 Loud A2 Loud P2 Absent A2 Absent P2 AS, PS CALCIFIED SEMILUNAR VALVE Hypertension, Aortic aneurysm Dilated aorta ASD, PDA, VSD AS PS,TOF, TGA S2 Splitting Wide & fixed Wide & variable Narrow Narrow splitting ASD, MR VSD, RBBB SEVERE AS & PS AS, HOCM
- 138. Extra heart sounds
- 139. S3 (gallop): Usually physiologic Low pitched sound, occurs with rapid filling of ventricles in early diastole Due to sudden intrinsic limitation of longitudinal expansion of ventricular wall Makes Ken-tuck-y rhythm on auscultation
- 140. S3 : Best heard with patient supine or in left lateral decubitus Increased by exercise, abdominal pressure, or lifting legs LV S3 heard at apex and RV S3 heard at LLSB
- 141. S3 (abnormal): Seen with Kawasaki’s disease--disappears after treatment If prolonged/high pitched/louder: − can be a diastolic flow rumble indicating increased flow volume from atrium to ventricle
- 142. S4 (gallop): Nearly always pathologic Can be normal in elderly or athletes Low pitched sound in late diastole Due to elevated LVEDP (poor compliance) causing vibrations in stiff ventricular myocardium as it fills Makes “Ten-nes-see” rhythm
- 143. S4 : Better heard at the apex or LLSB in the supine or left lateral decubitus position Occurs separate from S3 or as summation gallop (single intense diastolic sound) with S3
- 144. S4 Associations: CHF!!! HCM severe systemic HTN pulmonary HTN Ebstein’s anomaly myocarditis
- 145. S4 Associations: Tricuspid atresia CHB TAPVR CoA AS w/ severe LV disease Kawasaki’s disease
- 146. What is a Murmur? Murmur is the Sounds made by turbulence in the heart or blood stream Can be benign (innocent, flow, functional) or pathologic Murmurs are the leading cause for referral for further evaluation Don’t let murmurs distract you from the rest of the exam!! • .
- 147. Basics of murmur 1. When does it occur - systole or diastole 2. Where is it loudest - A, P, T, M
- 148. Describing a heart murmur When does it occur - systole or diastole 1. Timing – murmurs are longer than heart sounds – HS can distinguished by simultaneous palpation of the carotid arterial pulse systolic, diastolic, continuousI. Systolic Murmurs: 1. Aortic stenosis - ejection type 2. Mitral regurgitation - holosystolic 3. Mitral valve prolapse - late systole II. Diastolic Murmurs: 1. Aortic regurgitation - early diastole 2. Mitral stenosis - mid to late diastole
- 149. Shape of Murmurs Systolic Murmurs • Aortic stenosis • Mitral insufficiency • Mitral valve prolapse • Tricuspid insufficiency Diastolic Murmurs • Aortic insufficiency • Mitral stenosis S1 S2 S1 2. Shape : crescendo (grows louder), decrescendo, crescendo-decrescendo, plateau
- 150. Describing a heart murmur –Where is it loudest ? Location of maximum intensity is determined by the site where the murmur originates e.g. Aortic Pulmonary Tricuspid Mitral listening areas
- 151. Describing a heart murmur : 4. Radiation – reflects the intensity of the murmur and the direction of blood flow 5. Intensity – graded on a 6 point scale • Grade 1 = very faint • Grade 2 = quiet but heard immediately • Grade 3 = moderately loud • Grade 4 = loud • Grade 5 = heard with stethoscope partly off the chest • Grade 6 = no stethoscope needed *Note: Thrills are assoc. with murmurs of grades 4 - 6
- 152. Describing a heart murmur : 6. Pitch – high, medium, low 7. Quality – blowing, harsh, rumbling, and musical 8. Others: i. Variation with respiration • Right sided murmurs change more than left sided ii. Variation with position of the patient iii. Variation with special maneuvers • Valsalva/Standing => Murmurs decrease in length and intensity EXCEPT: Hypertrophic cardiomyopathy and Mitral valve prolapse
- 153. Systolic Murmurs Derived from increased turbulence associated with: 1. Increased flow across normal SL valve or into a dilated great vessel 2. Flow across an abnormal SL valve or narrowed ventricular outflow tract - e.g. aortic stenosis 3. Flow across an incompetent AV valve - e.g. mitral regurg. 4. Flow across the interventricular septum
- 154. Early Systolic murmurs 1. Acute severe mitral regurgitation – decrescendo murmur – best heard at apical impulse – Caused by: i. Papillary muscle rupture ii. Infective endocarditis iii. Rupture of the chordae tendineae iv. Blunt chest wall trauma 2. Congenital, small muscular septal defect 3. Tricuspid regurg. with normal PA pressures
- 155. Midsystolic (ejection) murmurs • Are the most common kind of heart murmur • Are usually crescendo-decrescendo • They may be: 1. Innocent • common in children and young adults 2. Physiologic • can be detected in hyperdynamic states • e.g. anemia, pregnancy, fever, and hyperthyroidism 3. Pathologic • are secondary to structural CV abnormalities • e.g. Aortic stenosis, Hypertrophic cardiomyopathy, Pulmonic stenosis
- 156. Pansystolic (Holosystolic) Murmurs • Are pathologic • Murmur begins immediately with S1 and continues up to S2 1. Mitral valve regurgitation – Loudest at the left ventricular apex – Radiation reflects the direction of the regurgitant jet i. To the base of the heart = anterosuperior jet (flail posterior leaflet) ii. To the axilla and back = posterior jet (flail anterior leaflet – Also usually associated with a systolic thrill, a soft S3, and a short diastolic rumbling (best heard in left lateral decubitus 2. Tricuspid valve regurgitation 3. Ventricular septal defect
- 157. Diastolic Murmurs • Almost always indicate heart disease • Two basic types: • 2. Rumbling diastolic murmurs in mid- or late diastole suggest stenosis of an AV valve e.g. mitral stenosis • Two components: 1. Middiastolic - during rapid ventricular filling 2. Presystolic - during atrial contraction; therefore, it disappears if atrial fibrillation develops • Is low-pitched and best heard over the apex (w/ the bell) • Little or no radiation • Murmur begins after an Opening Snap; S1 is accentuated
- 160. Diastolic Murmurs 2. Early decrescendo diastolic murmurs – signify regurgitant flow through an imcompetent semilunar valve • e.g. Aortic regurgitation • Best heard in the 2nd ICS at the left sternal edge • High pitched, decrescendo • Blowing quality => may be mistaken for breath sounds • Radiation: i. Left sternal border = assoc. with primary valvular pathology; ii. Right sternal edge = assoc. w/ primary aortic root pathology • Other associated murmurs: i. Midsystolic murmur ii. Austin Flint murmur
- 161. Continuous Murmurs • Begin in systole, peak near s2, and continue into all or part of diastole. 1. Cervical venous hum – Audible in kids; can be abolished by compression over the IJV 2. Mammary souffle – Represents augmented arterial flow through engorged breasts – Becomes audible during late 3rd trimester and lactation 3. Patent Ductus Arteriosus – Has a harsh, machinery-like quality 4. Pericardial friction rub – Has scratchy, scraping quality
- 162. MANEUVERS
- 163. Routine positions-- Supine and standing or sitting examinations should be performed on all patients
- 165. Increases afterload/systemic vascular resistance, initially increased venous return, increased stroke volume, decreased HR Reduces the murmur of AS w/ HCM Increases the murmur of MR Squatting:
- 166. Sudden standing: Decreased afterload, decreased venous return and stroke volume, increased heart rate, increased SVR): Accentuates the murmur and S4 of subAS, MVP, and HOCM
- 167. Left lateral decubitus positioning or leaning forward in an upright position: Apex of the heart falls toward the chest wall Brings out mitral valve and aortic valve murmurs
- 168. Summary A. Presystolic murmur – Mitral/Tricuspid stenosis B. Mitral/Tricuspid regurg. C. Aortic ejection murmur D. Pulmonic stenosis (spilling through S20 E. Aortic/Pulm. diastolic murmur F. Mitral stenosis w/ Opening snap G. Mid-diastolic inflow murmur H. Continuous murmur of PDA
- 169. Whoop (sometimes called a honk): Loud, variable intensity, musical sound heard at the apex in late systole Classically associated w/ MVP and MR Seen w/ VSD’s closing w/ an aneurysm, subAS, rarely TR Some whoops evolve to become systolic murmurs
- 170. Friction rub: Creaking sound heard with pericardial inflammation Classically has 3 components; can have fewer than 3 components Changes with position, louder with inspiration
- 171. INNOCENT MURMURS
- 172. INNOCENT MURMURS: Also known as flow, benign, normal, non- pathologic, functional, inorganic, or physiologic Occur in up to 77% of neonates, 66% of children, and can be increased to up to 90% with exercise or using phonocardiography
- 173. General “Rules” of Innocent Murmurs: Grade I-III intensity No thrills associated at any area of precordium Only minimal transmission Not harsh Brief duration (usually early to mid-systole)
- 174. More General “Rules” of Innocent Murmurs: Never solely diastolic Never loudest at the RUSB/R base No clicks Normal S2
- 175. Occur at areas of mismatch of normal blood flow volumes with decreasing vessel caliber size e.g. LVOT, RVOT, branch PA’s, etc. Better heard in children due to their thinner chest walls with greater proximity of stethoscope to vessel
- 176. Having more than one innocent murmur in a patient is normal, too!
- 177. Some maneuvers for innocent murmurs : Jugular vein compression/turning the head can abolish venous hum Lying the patient perfectly flat is the most reliable method of quieting the hum. Compression of the subclavian artery or shoulder extension can abolish supraclavicular bruit
- 178. Other maneuvers: Transient arterial occlusion Breath-holding in end-expiration in the upright position or leaning forward Deep breath inspiration in upright position Lower extremity elevation (passive) while lying down Exercise (running in place)
- 179. Other maneuvers : Isometric handgrips Valsalva (straining) maneuver--forced expiration against a closed glottis after full inspiration for at least 10 seconds Chemical maneuvers--rarely, if ever, performed today due to better imaging techniques
- 180. Vibratory Systolic Murmur (Still’s Murmur): Most common innocent murmur of childhood Needs maneuvers normal ECG to differentiate from sub AS, HOCM, VSD
- 181. Still’s Murmur (Characteristics): Location—max at LLSB Radiation—may radiate to LMSB, apex, and R-L base (“hockey-stick” distribution), although may not completely radiate Timing—mid-systole Intensity—grade I-II Pitch—mid to low
- 182. Still’s Murmur : Character—vibratory, groaning, musical, buzzing, squeaking, “guitar-string twanging,” “cooing dove” Variation—loudest supine, after exercise, with fever, anemia, or excitement Disappears or localizes to LLSB when upright
- 183. Still’s Murmur : Age range—uncommon in infancy, commonly age 2 to 6 years, rare in teens Etiology—unknown, may be associated with LV ejection Similar murmur seen with LV false tendons (but does not tend to diminish as much when upright)
- 184. Innocent Pulmonary Systolic Murmur: Need to differentiate from ASD, PS, subAS, VSD, and true/organic PPS
- 185. Innocent Pulmonary Systolic Murmur : Location—LUSB Radiation—possible to hear at LMSB Timing—early to mid-systole with peak in mid-systole
- 186. Innocent Pulmonary Systolic Murmur : Intensity—grade I-III Pitch—mid to high-pitched Character—soft, blowing, somewhat grating, diamond-shaped
- 187. Innocent Pulmonary Systolic Murmur : Variation—louder when supine, fever, exercise, anemia Age range—most commonly age 8-14 years, but early childhood to young adults Etiology—normal ejection vibrations into MPA
- 188. Physiologic Peripheral Pulmonic Stenosis (PPS): Need to differentiate from valvar PS, ASD, true/organic PPS, and ToF
- 189. Physiologic PPS : Location—LUSB Radiation—LMSB, bilateral axillae, mid- back, approximately same intensity over entire precordium Timing—early to mid-systole
- 190. Physiologic PPS : Intensity—grade I-II Pitch—high-pitched Character—blowing, not harsh, diamond- shaped Variation—none
- 191. Physiologic PPS : Age range—newborns, especially premies. May last 3 – 6 months but not longer (requires further eval if persistent) Etiology—small relative size of branch PA bifurcation to MPA at birth with acute angle → turbulence and relative obstruction
- 192. Supraclavicular or Brachiocephalic Systolic Murmur (Carotid Bruit): Need to differentiate from supravalvar or valvar AS, CoA, bicuspid AoV Bruit is French for “noise”
- 193. Carotid Bruit : Location—suprasternal notch, supraclavicular areas Radiation—carotids, below clavicles Timing—early to mid-systole
- 194. Carotid Bruit : Intensity—grade I-III, ?IV (may have a faint localized thrill) Pitch—mid-pitched Character—may be slightly harsh
- 195. Carotid Bruit : Variation—decreased intensity with hyperextension of shoulders; louder with anxiety, anemia, or trained athletes w/ resting bradycardia Age range—children and young adults Etiology—unknown, ? turbulence at takeoff of carotid or brachiocephalic vessels
- 196. Venous Hum: Most common continuous innocent murmur, and probably the second most common innocent murmur Need to differentiate from AS/AI, AVM, anomalous left coronary artery arising from the PA, or PDA if L-sided
- 197. Venous Hum: Location—anterior neck to mid- infraclavicular area, R side > L side Radiation—may go to LMSB Timing—continuous with diastolic accentuation Intensity—grade I-III Pitch—mid to low
- 198. Venous Hum: Character—soft, whispering, roaring, or blowing, distant-sounding Variation—disappears when supine, with head turn AWAY from the side listened to, with gentle manual compression of jugular venous return w/ fingers, or w/ Valsalva
- 199. Venous Hum : Age range – pre-school through grade school age (very common) – adol. to young adults (rarely heard, can be seen w/ increased blood flow states e.g. anemia, pregnancy, thyrotoxicosis) Etiology—turbulence in jugular and subclavian venous return meeting in SVC
- 200. Mammary Souffle: Occurs in certain circumstances of breast development/activity and disappear otherwise Differentiate from PDA, AVM, or AS/AI Souffle is French for “breath”
- 201. Mammary Souffle: Location—heard over/just above breasts in late pregnancy or in lactating women Radiation—none Timing—may be systolic only, systole with diastolic spill-over, or continuous with late systolic accentuation (most common)
- 202. Mammary Souffle: Intensity—grade I-III Pitch—mid to high Character—blowing or breath-like Variation—obliterated by increased stethoscope pressure or compressing the tissue on both sides of the stethoscope
- 203. Mammary Souffle : Age range—rare (hopefully!) in pediatric population Etiology—increased blood flow to the relatively smaller mammary blood vessels
- 205. don’t forget it!! THE REST OF THE BODY--
- 206. Vital signs: Temperature Respiratory rate Weight and height
- 208. NYHA Class Symptoms I Cardiac disease, but no symptoms and no limitation in ordinary physical activity, e.g. shortness of breath when walking, climbing stairs etc. II Mild symptoms (mild shortness of breath and/or angina) and slight limitation during ordinary activity. III Marked limitation in activity due to symptoms, even during less-than- ordinary activity, e.g. walking short distances (20–100 m). Comfortable only at rest. IV Severe limitations. Experiences symptoms even while at rest. Mostly bedbound patients.
- 209. Lungs: Pulmonary congestion probably nonexistent in infants (more manifest by tachypnea or retractions) Cardiac asthma: fine crackles heard in older children associated w/ CHF (coarse crackles indicate a pneumonia)
- 210. Lungs : Possible signs of increased pulmonary blood flow − Tachypnea − Dyspnea − Retractions − Flaring − Grunting − Panting
- 211. Edema: Caused by systemic venous congestion Seen more in older children and adults (little evidence of this in infants) More often seen in renal- or liver-induced hypoproteinemia (esp. if marked)
- 212. Edema : Locations: − Periorbital − Scrotal − Pre-sacral − Hand/foot area Non pitting pedal/hand edema or lymph edema in a newborn: think Turner’s or Noonan’s syndrome
- 213. Liver: Measure at mid-clavicular line where it crosses the 9th costal cartilage Can be right-sided (situs solitus), left-sided (situs inversus), or midline (situs ambiguous--measured subxiphoid)
- 214. Liver : Measurements: – 2-3 cm below the RCM in the infant – 2 cm below the RCM from 1-3 years of age – 1 cm below the RCM from 4-5 years of age Use warm, gentle hands
- 215. Liver--abnormal: Hepatomegaly caused by systemic venous congestion Right-sided CHF: liver enlarges, becomes firm, loses distinct edge Pulsatile liver: tricuspid regurgitation or other cause of elevated R sided pressures Hard liver may be more serious than large, soft liver
- 216. Spleen: Normally felt in newborns under the LCM Significant enlargement can indicate TORCH infection with an associated cardiac lesion Isolated splenomegaly is usually not seen w/ CHF
- 217. Infective endocarditis: Splenomegaly New/changing murmur Fever Positive blood cultures Neurologic changes Peripheral signs of embolic phenomena
- 218. Ascites: Severe right or right AND left sided CHF-- from Fontan anastomosis, dilated cardiomyopathy
- 219. Nutrition/muscle mass: Wasting (systemic, bitemporal)--from poor nutrition/high metabolic demand (CHF)
- 220. Skin: Sweating and pallor (diaphoresis) -- associated with increased adrenergic tone
- 221. Cyanosis of the mucus membranes: Central--from > 3g reduced Hb in the arterial blood due to cardiac or pulmonary shunting Acrocyanosis--from low cardiac output Differential cyanosis
- 222. Clubbing: Thickening of tissues at the base of the nails Due to capillary engorgement associated with chronic hypoxemia and polycythemia. Seen in cyanotic congenital heart disease and pulmonary disease Can reverse after improvement of hypoxemia, can disappear with anemia
- 223. OTHER SYSTEMS
- 224. Facial features of certain syndromes, chromosomal anomalies, and associations important to recognize: Anomalies of the eyes and lens, nose, ears, mandible/maxilla, tongue, dentition and gingiva, asymmetry of the facial musculature, etc.
- 225. CNS: Developmental delay Seizures Certain personality traits associated with these findings (usually not in isolation)
- 226. Extremities: Abnormal palmar creases Polydactyly Arachnodactyly Thumb/radial anomalies Phocomelia Pseudohypertrophy Nail anomalies