Continuous Murmurs

6,809 views 56 slides Apr 02, 2017
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About This Presentation

Cardio Class


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CONTINUOUS MURMURS DR AMZATHKHAN PG GENERAL MEDICINE

A murmur that begins in systole and continues without interruption through S2 into all or a part of diastole without change in the character of the murmur is defined as a continuous murmur. Continuous murmurs are usually generated by uninterrupted flow from a high pressure vascular bed into a low pressure vascular bed without phasic interruption between systole and diastole.

CAUSES 1. Due to high to low pressure shunts (i) From systemic artery to pulmonary artery Aortic run off into pulmonary artery : PDA, AP window, truncus arteriosus with pulmonary artery stenosis, surgically created aortopulmonary anastomosis (Blalock , Waterston or Pott’s shunts ).

Bronchial collaterals (bronchial to precapillary pulmonary arterial anastomosis and resultant aortic pulmonary fistula): Pulmonary atresia, TOF . Anomalous left coronary artery from pulmonary artery (ALCAPA).

(ii) From systemic artery to right heart: Aortic run off into right heart: RSOV into RA or RV . Coronary cameral fistula: Coronary artery fistula into RA or RV (LA).

Patent ductus arteriosus (PDA) Gibsons murmur (George Gibson in 1900) rough machinery murmur due to the combination of high and low frequency vibrations and associated thrill is common .

It peaks at S 2 , after which it gradually wanes until it terminates before S 1 (crescendo -decrescendo murmur).

LOCATION The murmur is best heard in the left infra clavicular and pulmonary areas during expiration. The systolic component is widely audible, while the diastolic component is restricted to pulmonary and infra clavicular areas.

INTENSITY Isometric hand grip increases the intensity and duration of the murmur and may bring out the diastolic component when it is not heard . The murmur disappears or decreases with Valsalva maneuver. Amylnitrate inhalation decreases the diastolic component.

2) Continuous murmur associated with bronchial collaterals: It is heard in the same location as that of PDA, but radiates widely especially over the posterior thorax.

3) Continuous murmur in anomalous origin of left coronary artery from pulmonary artery (ALCAPA): The murmur is continuous when the left-to-right shunt is large and is usually best heard at left sternal border.

4) Continuous murmur in RSOV (rupture of sinus of valsalva ) The murmur is usually continuous when RSOV occurs into RA or RV . But it is early diastolic when sinus of Valsalva aneurysm ruptures into LV. It also becomes early diastolic when PH supervenes with high RVSP which shortens or abolishes systolic flow and systolic component of the murmur.

Superficial murmur, with prominent diastolic thrill. “ Purring of a cat” SITE – Lower left sternal border (or) xiphoid process.

5) Continuous murmur in coronary cameral fistula soft, superficial and high pitched . In 90%, coronary artery (CA) fistula drains into right heart and resultant murmur is continuous . But in case of CA fistula draining into RV, the murmur softens during systole (when the systolic flow decreases due to compression of the fistula during RV contraction).

CHARACTER The murmur is louder in systole as the pressure gradient is more in systole in case of CA fistula draining into RA or LA. The murmur is not continuous if it empties into LV. It may be purely diastolic or systolic and diastolic. Continuous murmur is also absent and may be silent if multiple coronary artery fistulas empty into pulmonary artery.

LOCATION The murmur is best heard either left or right of the lower sternal area when CA drains into RA. It is maximally heard at left mid to lower sternal border or in sub xiphoid region in CA draining into RV. In CA draining into LA, it is best heard in upper to mid left sternal border and may radiate leftward as far as the anterior axillary line

Other shunts Left to right shunts (mitral valve obstruction) Lutembachers syndrome Mitral atresia with ASD Post PTMC AV fistula Venovenous shunts Portosystemic shunts Curveiller Baumgartens syndrome)

2. Due to rapid blood flow Cervical venous hum Mammary souffle Hyperthyroidism Hemiangioma Hyperemia of neoplasm: Hepatoma , renal cell carcinoma, Paget’s disease.

Venous Hum First recognized by Potain in 1867. The normal flow of blood across the normal veins in the neck is noiseless. But increased velocity of blood flow gives rise to a continuous bruit over the neck veins which is known as cervical venous hum . CHARACTER - It may be rough and noisy and typically louder in diastole.

MECHANISM The laminar flow in internal jugular vein may be disturbed by the deformation of the vein at the level of the transverse process of the atlas during head rotation designed to elicit the hum.

POSITION The venous hum is best heard in sitting posture with head rotated to the opposite side and chin upwards, placing the bell of the stethoscope at the base of the neck in between the two heads of the sternocleidomastoid muscle and may be more prominent on the right side. Sometimes it may radiate below the clavicles and may be confused with the continuous murmur of PDA if not evaluated carefully

The murmur is abolished by the digital compression of the internal jugular vein with head in neutral position – It is poorly heard in supine position, while – Anemia and thyrotoxicosis initiate or reinforce the venous hum.

Mammary souffle This innocent continuous arterial murmur occurs in 10–15% of pregnant women during 2nd and 3rd trimesters and in early postpartum period in lactating mothers. MECHANISM - It is due to increased blood flow to the breast tissue.

PITCH AND CHARACTER This medium to high pitched murmur is best heard over the breast on either side between 2nd and 6th anterior intercostal spaces with no significant change with respiration and may be confused with the continuous murmur of PDA or AV fistula. The mammary soufflé usually begins after S1 with a distinct gap and systolic component is the loudest.

INTENSITY Light pressure with the stethoscope augments the murmur, whereas the firm pressure with the stethoscope or digital compression abolishes the murmur. Valsalva maneuver has no significant effect on the murmur. It disappears after the termination of lactation.

Localized arterial obstruction Continous murmur (obstruction >80%) with no adequate collaterals pressure gradient produced throughout the cardiac cycle with systolic accentuation. Systolic gradient +/ No diastolic gradient

Coarctation of aorta Pulmonary artery stenosis Carotid/femoral/renal/celiac mesenteric artery occulusion

COARCTATION OF AORTA Continuous murmur in coarctation of aorta (COA) heard over the thorax and over the back in the midline between the scapulae. rapid blood flow through tortuous intercostal collaterals.

ADDED SOUNDS

Pacemaker sounds Pericardial rub Mediastinal crunch

PACEMAKER SOUNDS These sounds are brief and high frequency sounds occasionally produced by transvenous pacemakers implanted in RV apex, due to stimulation of the intercostal muscles(through intercostal nerves) by the endocardial electrodes.

Pectoral muscles and diaphragmatic stimulation can also occur. They occur synchronously with pacemaker spike and often associated with twitching of the muscles. The audible high frequency pacemaker sounds always suggest myocardial perforation by the endocardial lead, although it is not always present.

PERICARDIAL RUB Pericardial rub is the hallmark of pericardial inflammation. a) Mechanism of production of pericardial rub (PR): It is due to the movement of the parietal and visceral surfaces of the pericardium moving against each other. b) Components of PR: The classic rub is triple phased: systolic, mid-diastolic and late diastolic (or presystolic / atrial systole).

However, it is often biphasic, i.e. to and fro rubs due to ventricular systolic and atrial systolic components. The diagnosis is the simplest when all the three phases are present, which occurs only in 50% of the cases. It is commonly audible in uremic pericarditis especially when associated with hypertension. The systolic phase is most consistent followed by the presystolic phase. In the setting of atrial fibrillation presystolic component disappears.

c) Causes: Acute pericarditis of any etiology: especially tubercular in origin Following open heart surgery: post cardiotomy pericarditis Uremic pericarditis Rheumatic pancarditis Acute phase of transmural MI giving rise to post MI pericarditis , which dramatically responds to steroids Infective endocarditis due to ring abscess.

d) Clinical recognition: These friction rubs are high-pitched, leathery and scratchy in nature. They are best heard over the 2nd and 3rd left intercostal spaces over the ‘bare area’ of the heart. They seem close to the ear and are auscultated best with diaphragm of the stethoscope with the patient leaning forward or in knee-chest position and holding the breath after forced expiration.

Unlike pleural rub, pericardial rub can be present even with large pericardial effusion and cardiac tamponade . Occasionally, the short scratchy pulmonic ejection systolic murmur heard in hyperthyroidism (Means- Lerman sign) is misinterpreted as pericardial rub.

MEDIASTINAL CRUNCH It is a series of high-pitched scratchy sounds heard in mediastinal emphysema, which is designated as Hamman’s sign. These sounds are common following cardiac surgery. They occur most frequently during ventricular systole in a random fashion. They may be prominent during different phases of respiration or different postures. The mediastinal emphysema is clinically confirmed by noting the crepitations in the neck secondary to subcutaneous air.

OPENING SNAP The opening of the normal AV valves is noiseless, but with thickening and deformity of the leaflets, a high frequency clicky sound is generated in early diastole, which is called as ‘ opening snap. This term ‘ opening snap ’ was coined by Thayer WS in 1908.

CHARACTER AND INTENSITY OS is an early diastolic crisp, sharp sound, which correlates with the mobility of the AV valve i.e. anterior mitral leaflet (AML) in MS and septal leaflet in TS . The intensity of OS parallels the intensity of mitral component (M1) of S1. The mobile valves in MS have a loud OS and an accentuated M1, while immobile valves have an attenuated M1 and a decreased or absent OS, though OS may be found in 50–60 % of the calcified MS patients, since mere presence of valvular calcium does not preclude the mobility of valve leaflets .

OS follows A2 by an interval of 0.03 to 0.15 s and A2–OS interval has been used to predict the level of left atrial pressure (LAP) and the severity of MS

MECHANISM Thickened but mobile AV leaflets: immobile valve precludes OS as in severely calcified MS High atrial pressure ( LAP or RAP): OS may occur early or late depending upon the atrial pressure High velocity flow across AV valves causes rapid excursion of leaflets producing OS in the absence of MS or TS.

Margolies and Wolferth theory : It is due to sudden stopping of the opening movement of the valve. This has been confirmed by hemodynamic and angiographic studies.

Absent OS in MS is noted in: Severly calcified (immobile) mitral valve Associated with significant MR severe AR severe AS CAD and LV dysfunction.

MITRAL AREA As OS is a high frequency sound, it is best heard with diaphragm of the stethoscope in the midprecordium between the left sternal border and just inside the apex without any significant change with respiration. It is often well heard at the base of the heart (pulmonary area) and may be confused with S2 split. The MDM follows the OS after a short interval. It becomes more prominent with exercise. A2–OS interval: It sounds like a split S2 with the shortest interval (about 40 ms ), simulates wide fixed split of ASD with moderate A2–OS interval and it may be mistaken for S3 of MR or severe heart failure with widest A2–OS interval (120 ms).

TRICUSPID AREA It is frequently not detected due to prominence of the findings of coexisting MS. It is best heard with diaphragm of the stethoscope with the maximum intensity closer to the left sternal border during inspiration. When audible, it generally follows the mitral OS.

EJECTION CLICK Occurs in early systole after S1. Heard in aortic and pulmonary stenosis .

MID SYSTOLIC CLICK Mitral valve prolapse . High pitched. Heard at apex. Abrupt halting of prolapsing mitral leaflets into the chordae .
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