Prepared by:Dr. Mohammad Shaikhani.

Sulaimani University,College of Medicine.Sulaimani center for GE & Hepatology.

Sulaimanya-Iraqi Kurdistan.

Prepared by:Dr. Mohammad Shaikhani.

Sulaimani University,College of Medicine.Sulaimani center for GE & Hepatology.

Sulaimanya-Iraqi Kurdistan.

General exam: related to CVS 1. FACIESApprehensive facies: from pain, anxiety&respiratory distress (MI, angina, PE, P edema, arrhythmias as VT, fast AF)A. Skin Color / Texture: Malar flush: long-standing MS.Butter-fly rash across the nose/cheeks in SLE(HT,RF). Brick red color of polycethemia ( cause HTN,thrombosis, MI) Bronze skin in hemochromatosis (Cardiomyopathy) Brown + buccal pigmentation in Addison’s disease (hypotension) Flushing & telangiectasia in carcinoid sydrome (tricuspid & pulm valve disease) Moon face in cushing’s disease (HTN) Coarseness & dryness in myxedema (bradycardia, HF, PE)Central cyanosis (right-left intracardiac shunt or lung disease).

General exam: related to CVSB. Eyes/ Lids: Jaundice: CHF causing congested liver. Pallor: anemia of BE, Precipitating HF. Xanthelasma (hypercholesterolemia, DM) Lid edema/Puffy face (myxedema, nephrotic, SVC obst) Exophthalmos, lid retraction in thyrotoxicosis (A.F, high CO) Corneal arcus in youngs indicates severe hypercholesterolemia. Blue sclera in marfan/ Ehlers-Danlos syndrome (AR,MVP, ASD)Lenses (subluxation in Marfan; superior, homocystenuria inferior) Pupils (Argyll Robertson sign) react to accommodation not to light seen in neurosyphilis (AR, calcification in the ascending aorta)

General exam: related to CVSC. Bony developmental Abnormality: Large head (Paget’s disease): High-out failure Acromegaly (HTN, CHF) Marfan syndrome (with long narrow face, lens sublaxation, long arm, arachnodactyly)(AR, aortic dissection, MVP) Williams syndrome (small elf-like forehead, turned up nose, egg shaped teeth, low set ears) associated with supravalvular AS. Noonan’s sydrome (widely set eyes, web neck) with PS

General exam: related to CVSD. Hands Tremor in thyrotoxicosis (AF, CHF) Clubbing (cardiac cause: cong HD, bacterial endocarditis) Capillary pulsation (AR, thyrotoxicosis, pregnancy) Splinter hemorrhage (SBE, acute glomeruloniphritis) Osler’s nodes (0.5-1 cm painful reddish-brown subcutaneous papules occur on the tip of the fingers or toes, palm of the hand, planter aspect of the feet (bacterial endocarditis) Arachnodactyly (long slender hand/ fingers) marfan sydnrome. Peripheral cyanosis: Cardiogenic shock, PVD. E: Feet: Pitting leg edema bilaterally. Cold legs & feet, Any gangrene: PVD. Unilateral swelling: DVT.

General exam: related to CVS

General exam: related to CVSBREATHING PATTERNS: 1. Using accessory muscles of respiration? (P edema,asthma, COPD, fulminant pneumonia) 2. Breathlesness + wheezing (asthma, COPD, LV failure) 3. Stridor (indicating upper airway obstruction) life-threatening 4. Chyne-stokes respiration (CHF, strokes, oversedation, uremia)

General exam: related to CVSCYANOSIS 1. Appears when deoxygenated Hb> 5 gms. 1. Is not apparent when Hb < 5g/dl (central). 2. In CHD cyanosis is observed if R-L shunt is > 25% of CO& not improved by 100% of O2.3. Good exam of tongue, lip, ear lobes, fingers, toes recommended.

General exam: related to CVSFOUR TYPE OF CYANOSISCentral cyanosis: blue tongue, lips, extremities with warm peripheries (CHD, lung disease as emphysema, pneumonia,ARDS, chronic bronchitis, sometimes CHF)Peripheral cyanosis: ( from sluggish circulation in capillaries (extremities are blue & cold): low CO, hypovolemic shock,PVD)Differential cyanosis (lower limb cyanosed, upper limb pink) in PDA with revered shunt due to PHTN.Reversed differential cyanosis. The cyanosis of the fingers exceeds that of the toes; in transposition of the great vessels (blood from RV ejected into the AO reaches the upper limbs/head, blood from LV ejected into PA reaches the lower limb via PDA)

Pulse:1. PULSE:Rate/Rhythm/Volume/Character/RF delay. Rate at rest > 100/min (tachycardia):anxiety, pain, CHF, PE, hyperthyroidism, anemia, fever, medications Rate < 60/min (bradycardia) due to (medications, MI, hypothyroidism, hypothermia, SSS,…)Rhythm (regular or irregular indicating AF, frequent PAC’s, PVC’s, …etc.)

Pulse:Character1. Collapsing pulse (water hammer pulse) jerky pulse with full expansion followed by sudden collapse (AR, PDA, A-V fistulas, pregnancy, paget’s disease, thyrotoxicosis, anemia)2. Alternating pulse or pulses alternans (regular rate, amplitude varies from beat to beat) seen in LVF3. Pulses bisferiens (two strong systolic peaks separated by a midsystolic dip) seen in HOCM, AS/AI4. Anacrotic pulse slow rising pulse in A.S. (Parvus et tardus)5. Diacrotic pulse, two systolic/ diastolic peaks (sepsis, hypovolemic, cardiogenic shock)6. Paradoxic pulse (amplitude decreases with inspiration & increases during expiration) seen in cardiac tamponade, COPD, massive P.E.

Peripheral pulses: Symmetry: Exam both radial, carotid, femoral, tibial, dorsalis pedis.

JVP:

JVP:

JVP:

JVP:

Don’t worry too much about the wave form, just try to see it first!

JVP:Normal JVP waves:H Period of slow filling of atria before atrial contractiona Atrial systoleX Atrial relaxationC Bulging of TV into RA during V systoleX´ RA pressure falls because of pulling of RA floor during V systole. Some authors refer to this as X waveV filling of RA while TV is closedY Decline in RA pressure when TV opensX´ descent: systolicY descent: diastolic

JVP: Abnormal waves1. Giant “A” wave seen in RA contraction against an obstructed TV (TS, atresia, myxoma) high resistance to RA emptying (RVH, PHTN, PS, PE, …)2. Cannon “A” wave: (RA contracts against closed TV) seen in CHB.3. Prominent “V” wave (V wave caused by RA filling against TV closure coincide with S2 & T wave on the ECG) seen in significant TR, VSD, ASD causing distolic RA overloading4. Kussmaul’s sign: paradoxical rise with inspiration (constrictive pericarditis, severe RHF)

Precordial exam: inspectionAny deformities. Pulsations. Scars. Asymetry.

Precordial exam: Palpation APEX BEAT localization. Character of apex beat. Any thrils in all precordial areas; mitral, pulm, aortic & tricuspid areas.Thril is a palpable murmur, has localizing benefit. Left parasternal heave.

Precordial exam: Palpation1. APEX BEAT:Patient should be examined in the supine, sitting, left lateral decubitus position. Normal apical impulse occurs during early systole with an outward motion imparted to the chest wall.Apex beat: is outermost lowermost palpable cardiac pulsation.Normal apex beat is palpable as brief outward impulse (intersection of left MCL & 5th intercostal space by the fingers.Apex beat > 2cm indicate LV enlargement.Double apical impulse caused by LVH &forceful LA contraction.2. LEFT PARASTERNAL LIFT,Best appreciated by the distal palm or with the finger tip, Palpable anterior systolic movement sustained up to S2,indicate RVH.Giant presystolic lift seen in HCM.

Auscultation:AREAS TO AUSCULTATES1. Apex (mitral area) murmur from the MV are best heard.2. Right Lower sternal edge (tricuspid area)3. Lower left parasternal (4th ICS) murmur of AR is best heard4. Upper left parasternal (pulmonary area, 2nd left ICS)5. Upper right parasternal (aortic area, 2nd right ICS, murmurs arising from aortic valve area best heard)6. Below the left clavicule: continuous murmur of PDA is best heard7. Posterior chest for bruits caused by bronchial collaterals in case of coarctation of the aorta8. Other areas: (abdominal aorta, renal arteries, carotide, femoral arteries)

Auscultation:

Auscultation: S1Produced by M&T valve closure Best heard at the apex. Occurs just before the palpable upstroke of the carotide pulse. Factors influencing intensity of S1:1. PR interval : - short PR-loud S1,long PR-soft S12. Mitral Valve Disease: MS typically causes loud S1,but later in the course of the disease, when the valve becomes calcified/immobile, S1 intensity decreases. Soft S1 occur also in AR due to premature closure of MV. Intensity of S1 increase in (MS, TS, myxoma, short PR) Intensity of S1 decrease in (fibrosis or cacification of MV, prolong PR, HF, MR, AR) Variable intensity of S1 in A.F., CHF, VT.

Auscultation: S2Closure of AV & PV,normally AV closes before PV. Inspiration splitting of S2 is due to delay in P2 due to:1. Increase capacitance of pulmonary vascular bed2. Increase-RV volume.Normally intensity of A2 exceeds that of P2.A) Loudness of A2 or P2 is proportional to the respective pressures in Ao or PA at onset of diastole, i.e., higher pressure – louder A2 or P2 A2 is louder with HTN, dilated aorta. P2 is louder with pulmonary HTN, dilated PAB) Decrease intensity of A2 or P2 is due to decrease pressure beyond the valve, stiff semilunar valves (A.S, P.S.), chest wall or lung deformity (emphysema)

Auscultation: S2Wide but not fixed splitting of S2:1. Delayed electrical activation of RV (RBBB, PVC from LV)2. Prolonged RV mechanical systole (massive PE, Pulm HTN,P.S.)3. Early aortic closure (MR).Reversed Splitting:1. Delay electrical activation of LV (LBBB, PVC from RV)2. Prolonged LV mechanical systole (HTN, A.S., severe LV dysfun)3. Early pulmonic closure (TR), early electrical activation of RV (WPW)

Auscultation: S2Fixed Splitting: A.S.D., severe RV failure

Auscultation: S3Normal findings in younger patientsDue to passive diastolic filling of ventricle (0.14 to 0.22s after S2)Best heard at the apex patient on the LLP Causes of S3 includeAbnormal ventricular relaxationVentricular failureDilated and hypertrophic cardiomyopathySevere TR, MRLV dyskenesia or aneurysmHyperdynamic states (AV fistula, thyrotoxicosis)

Auscultation: S4Due to vigorous atrial contraction to propel blood into a stiff ventricle (absent in AF)Best heard at the apex, patient on LL decubitus S4 is heard in:LVHAcute MIHOCM, DCMSevere AS, PS S4 occurs just before the S1 (# diagnosis with split S1: firm ressure by the diaphragm eliminates S4 but not split S1)

Auscultation: Ejection clicksThree mechanisms:1. Intrinsic abnormality of AV or PV (congenital bicuspid AV, congenital P.S.)2. Pulsatile distension of dilated great artery (HTN, PHTN, dilated PA,aortic aneurysm)3. Increase flow states (ASD, pulmonic EC) (truncus arteriosus aortic EC)Mid to Late Systolic Clicks:Commonly heard in MVPSharp high pitched soundManeuvers that decrease LV volume move the click earlier.Maneuvers that increase LV volume move the click later.

Auscultation: Opening snap Caused by the opening of the stenoic but pliable MV or TV (disappears in severe calcified MS or TS). Higher LA pressure leads to short S2-OSOccurs 0.08 s after S2Best heard between apex and left sternal borderDD: Split S2. However, having the patient stands help to differentiate the two. The S2 – OS internal widens, while split S2 does the change or narrow.

Auscultation: MurmursGrading:Grade I - So faint and heard only with special effortGrade II - Soft but readily detectedGrade III - Prominent but not loudGrade IV - Loud usually with palpable thrillGrade V - Very loud with thrillGrade VI - Heard without stethoscope on the chest wallHigh pitch sounds (use diaphragm of stethoscope) S1, S2, murmurs of valvular regurgitation OS, clicks, obstruction of semilunar valves (AV, PV) Pericardial knock Low pitch sound (use of bell of stethoscope) S3, S4 obstruction of AV valve (MV, TV)

Auscultation: MurmursClassification of Murmurs: (Systolic, Diastolic, Continuous)I. Systolic Murmurs (SM)Stenosis of semilunar valve causes delay in peaking of SM related to prolongation of ejection. The duration not the intensity is proportional to severity of obstruction. Commonly encountered clinic problem is the differentiation of AS Vs benign aortic sclerosis. With aortic sclerosis there should be no clinical, ECG, or radiological evidence of heart disease. The carotid upstroke is normal.

Auscultation: MurmursThe SM peaks early with normal S2.MR murmur is usually pansystolic, It can be late systolic in timing (suspect MVP, papillary muscle dysfunction). It can also be early systolic in acute severe MR with markedly increased LA pressure reducing late systolic LV-LA gradient.The SM of TR is best heard at LLSB or over xyphisternum & associated with large V-wave. The murmur of VSD parallels the pressure difference between the two ventricles. The murmur is typically pansystolic and associated with thrill. With significant pulmonary HTN, the murmur duration shortens. SM heard in the back may be caused by coarctation, aortic dissection, peripheral PA stenosis or pulmonary AV fistula.

Auscultation: MurmursII. Diastolic Murmurs: Early diastolic murmurs:Aortic regurgitation: configuration of the murmur reflects volume & rate of regurgitation flow,therefore, with chronic AR, the aortic diastolic pressure consistently exceeds the LV diastolic pressure and the murmur is heard throughout diastole.However, with acute AR, the LV diastolic pressure is very high (because the LV is not dilated and unprepared), so the murmur tend to short.Pulmonary regurgitation murmurs secondary to pulmonary HTN (Graham-steel murmur) is high velocity blowing murmur that can last throughout diastole. While PR without elevation of PA pressure results in mid diastole murmur because the diastolic pressure exerted on PV is minimal in early diastole.

Auscultation: MurmursMid diastole murmursMajority originates across mitral or tricuspid valves.Murmur is easily appreciated with increase flow through the valves.Duration of the murmur correlates with severity.Mid diastolic murmurs occur with: (1) obstruction of AV valves (MS, TS, Austin flint) & (2) Increase flow across AV valves (functional obstruction), e.g., ASD, VSD.

Auscultation: MurmursLate diastolic murmur (presystolic)Represented by increased flow through obstructed mitral or tricuspid valves during atrial contractionCan be heard (opposite to common belief) in MS or TS in patients with atrial contraction (AF).

Auscultation: MurmursIII. Continuous Murmurs – due to(1) Aortopulmonary connection (PDA)(2) AV connection (AV fistula, anomalous origin of left coronary from PA)(3) Disturbance of flow in arteries or veins (mammary soufflé, cervical venous hum)

Auscultation: common valve lesionsMS: Malor flush, small volume pulse, S1, opening snap, middiastolic murmur (MDM), presystolic accentuationSigns of Severity:1) duration of murmurs (longer is severe).2) S1 ¾ OS interval (shorter is severe).MR: Soft S1, wide splitting of S2, S3 present, systolic murmur (pansystolic, early, mid or late systolic).Signs of Severity: Longer duration or confined to early systole

Auscultation: common valve lesionsAS: Slow-rising pulse, S1, (N or soft), S2 (single, paradoxicalsplitting), S4 present, ejection click if valve is mobile, ejection systolic murmur with late peaking.Signs of Severity:1. Single S2 or paradoxical splitting2. Longer murmur3. Late peaking of murmur.

Auscultation: common valve lesionsAR: Peripheral signs with chronic not acute AR. S1 (soft), S2 (absent, single),S3 present.Early diastolic murmur – short in acute AREjection systolic murmur due to increase flow across AVAustin flint – MDM due to narrowed mitral valve due to rising ventricular diastolic pressureSigns of Severity:1) Duration of murmur – longer is severe in chronic2) Systolic ejection flow murmur3) Austin flint4) Reduced diastolic BP

Auscultation: common valve lesionsT.S.: Prominent A-wave, OS, MDM at LSB with presystolic accentuationBoth the OS and the murmur are accentuated with inspiration,leg raising, squatting and manoeuvres that increase transtricuspid valve flowSigns of Severity:1) duration of murmurs (longer is severe)3) S1 ¾ OS interval (shorter is severe)

Auscultation: common valve lesionsTR: Prominent V-wave, pulsatible liver, soft S1, S3 present,pansystolic murmur at LSB increase in inspirationSigns of Severity: Peripheral signs with TR, longer duration of the murmur

Auscultation: common valve lesionsPS: Ejection click, S1 (N)S2 (wide splitting), S4 presentEjection systolic murmur increase with inspiration

Auscultation: common valve lesionsPR: S1 (soft), S2 wide splittingS3 present, S4 presentDiastolic murmur increase in inspiration. If secondary to PHTN it begins in very early diastole. If secondary to organic valve lesion, it begins slightly later and ends in mid diastole.

Auscultation: common valve lesionsPulmonary HTN: Prominent A-waveEarly systolic click (sudden opening of P.V. into high pressure artery)Prominent P2 (due to increase force of pulmonary valve closure) Left parasternal left (RVH)Mid systolic ejection murmur (turbulent transvalvular pulmonary flow)Signs of Severity: 1. Murmur of PR 2. Murmur and peripheral signs of TR 3. If advanced pulmonary HTN – look for signs of RVF

Maneuvers to differentiate murmurs:

Valsalva: During active strain phase most murmurs decrease in intensity except murmur of: 1) HOCM – typically get louder 2) MVP – longer and louderRespiration: Right sided sounds and murmurs get louder with inspiration (except for pulmonary ejection click)Handgrip: By increasing BP (afterload), augments murmur of MR, AR but does not affect murmur of AS and tends to decrease murmur of HOCMPrompt Squatting:Causes a rapid increase in venous return and increase in peripheral resistance. Because LV volume and peripheral resistance increase, the murmur of HOCM gets softer. The murmurs of MR/AR get louder because of increase resistanceExtrasystolic beats: Both HOCM/AS murmur get louder because of increased post-extrasystolic contractility, while MR unaffected.