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Subject: Physical Diagnosis Topic: Physical Examination for CVS 2 Lecturer: Dr. Jaime Pacifico Date of Lecture: 09.09.

11 Transcriptionist: Mating Cats =^.^= Pages: 4

PRINCIPLES Do your auscultation in a quiet room, for practical reasons that you can hear the heart sounds better. Use the bell for the low-pitched sound. (e.g. S3, S4) Bell with an L is for low-pitched sound; Diaphragm with an H is for high-pitched sound Examine the patient in 3 positions. Left lateral decubitus - S3, if you cant find the apex beat, if you turn the patient in this position then you can maximize the contact between the left ventricle and the chest wall - When palpating the patient, what you feel is the vibration of the heart to the chest wall - Exaggerates the apex beat and the heart sounds Supine Sitting - Exaggerates the murmurs found in the base >referring to the pulmonic area, aortic area and the S2 Use the inching technique Move the stethoscope inch by inch and not too fast from different auscultatory areas so that you wont miss any sound in between (from the apex or mitral to the tricuspid area) Listen to one event at a time. At first, try to listen the heart sound in the apex then listen to the first heart sound because it is maximal at the apex Concentrate on one heart sound at a time Listen to whatever there is between the 1st and 2nd heart sound Listen to interval between 1st and 2nd sounds, listen to any extra heart sounds (e.g. murmur).


- Pulmonic Area: left side, 2nd ICS, swallow - Aortic Area: right side, 2nd ICS; radiation of the sound towards the ascending aorta - Mitral Area: Apex, below the nipple; 5th ICS bisected by the midclavicular line - Tricuspid: left side, 4th ICS; shallow FIRST HEART SOUNDS (S1) Caused by closure of mitral and tricuspid valve. There will be motion of blood, chordae tendinae and papillary muscles. This coincides with beginning of systole (contraction of ventricles, closure of MV and TV, 1st heart sound) First heart sound heard, S1 This is best heard over the apex (intensity at the base is decreased). Intensity is affected by strength and contractility of the ventricle and position of valves prior to closure. E.g Tachycardia S1 is louder in: Tachycardia because the valves are widely open and tends to close again Short PR interval Fever because the px tends to be tachycardic Thyrotoxicosis increased metabolism; a.k.a. hyperthyroidism Mitral Stenosis increased metabolism, faster HR; increased pressure in left atrium

SY 2011-2012

S1 is soft in: Bradycardia slow cycle of systole and diastole, valves are practically closed prior to closure, so long diastolic filling time. Prolonged PR interval (exceeding 0.2 second) **semi closure of the mitral valve occurs following atrial systole and before ventricular systole begins Mitral regurgitation most common cause is rheumatic heart disease Acute MI dead myocardium; reduced left ventricle pumps SECOND HEART SOUNDS This is due to the closure of the aortic and pulmonic valve during inspiration. Beginning of diastole, indicates end of systole This is best heard at the base. (+) splitting you can hear separately the aortic and pulmonic components of the 2nd heart sound. During inspiration, there is low intrathoracic pressure->more blood returning to the right side of the heart->prolonging systole->causing delayed closure of pulmonic valve->splitting

Types of splitting: Normal/Physiologic splitting single sound during expiration, 2 sounds upon inspiration. Wide splitting splitting is prominent but variable with respiration. (ex. RBBB) Wide splitting, Fixed there is 2 heart sounds heard regardless if its inspiratory or expiratory. (most common cause is atrial septal defect) Reversed splitting - this is the paradoxical branch block (LBBB), there is a single sound inspiration and split on expiration. Hubbard THIRD AND FOURTH HEART SOUNDS S3 This is associated with early diastole in rapid ventricular filling. This is heard among young individuals age 20 to 25, and it is still normal according to doc. In hearing this, your reference would be the 2nd heart sound (it comes shortly after the 2nd sound) lab-ti-lab Pathologic in 40 years old and above suggests heart failure After the S2 S4 Believed to be because of the flow of blood which coincides with atrial systole (late diastole) Shortly before the S1 Common in ventricular hypertrophy or fibrosis an exaggerated S4 because during this condition, the atrium will contract more to overcome the pressure due to hypertrophy Ventricular Hypertrophy : chronic hypertension; Fibrosis : MI EXTRA HEART SOUNDS Diastole Probably more important than systolic Opening snap -pathognomonic of mitral stenosis which is commonly caused by rheumatic heart disease among Filipinos This is a high-pitched sound heard at the left lower parasternal border. Orienting at S2; shortly after S2 Closure of AV and PV 2

Systole Ejection sound/ Click Mid-systolic click - it is an extra sound between S1 and S2. - Mitral Valve Prolapse CARDIAC MURMURS Extra heart sounds during systole and diastole due to the turbulent flow of blood, in addition this may be due to high output states and structural defects. Occur commonly in diseased valves (e.g. RHD) Other causes: high output states anemia (most common); thyrotoxicosis structural defects ASD altered blood flow in the major vessels patent ductus arteriosus Characteristics of a murmur: Intensity e.g. Grade 1/6 or 2/6 etc. Timing e.g. Systole, Diastole, or continuous Pitch / Frequency e.g. Low-pitched, High-pitched Location where in the chest you best heard the murmur (e.g. Apex, Base, etc.) Radiation common is mitral regurgitation; from apex to the axilla Quality of sound e.g. Stabbing, heavy, etc machinery type of murmur ductus arteriosus Example on how to report: a probing holosystolic 4/6 murmur at the apex radiating to the axilla Most likely diagnosis= mitral regurgitation Example of presentation: *Note: It is important to palpate the carotids/branchial artery to serve as reference point if youre listening for 1st /2nd heart sound o o +systolic thrill (would be at least grade 4 up to grade 6 murmur) 5/6 systolic murmur at 2nd ics parasternal area without radiation

Inspiration: increase blood flow turbulence exaggerating the murmur


Intensity/Grading of Murmurs (LEVINES GRADING SYSTEM) Grade 1 so faint, heard only with special effort; in optimal environment Grade 2 faint but can be heard readily by an experienced observer; quiet, can be recognized readily after placing the stet on the chest wall. Grade 3 moderately loud Grade 4 loud murmurs, although the stet must be in complete contact with the chest wall to hear them; may/ may not be associated with trill Grade 5 very loud, with stethoscope lightly pressed on the skin; always associated with thrill Grade 6 exceptionally loud with the stethoscope slightly above the chest wall; always assoc with thrill *Note: Grade 1-3 lack thrills, Grade 4-6 have thrills Thrill a palpable murmur; a sensation of running water on the fingertips; comes in terms of intensity

TIMING OF MURMUR Systolic occurs at anytime from S1 to S2 Diastolic occurs at anytime from S2 to S1 Continuous starts from S1 and continues to S2 Mid-systolic starts after S1 before S2, seen in aortic stenosis ends

Holosystolic starts at S1 and ends at S2, from the start the intensity doesnt change; appreciate the murmur throughout the systole

Systolic Murmur If the murmur starts or coincides with the pulse of the carotid artery Two causes: It is an abnormal flow over an outflow tract or semilunar valve. Eg. aortic stenosis It can also be a regurgitant flow from a ventricle into a low pressure chamber. Eg. mitral regurgitation Early Systolic Murmur Begins in S1 and ends in mid systole This can be heard in tricuspid regurgitation in the absence of pulmonary hypertension Mid Systolic Murmur Also called systolic ejection which starts after S1 Diamond shape-characteristic of intensity of murmur/ ascend-crescendo description- it increases then decreases typical of aortic stenosis may be seen in aortic stenosis

during diastole aortic and pulmonic should close to fill the RV and LV) May be also due to an abnormal forward flow across and atrioventricular valve. (e.g. mitral stenosis the hole is small which causes a turbulent flow from LA to LV which causes the loud noise)

Early Diastolic Murmur Starts with 2nd heart sound, begins with or shortly after S2 E.g. Aortic Regurgitation Mid Diastolic Murmur Usually occurs across the MV and the TV during early ventricular filling. Severity of stenosis is proportional to the duration rather than the loudness of the murmur Pre Systolic Murmur Late Diastole Usually this is due to atrioventricular valve stenosis

Late Systolic Murmur Starts after ejection, does not obliterate S1 and S2 This is heard in mitral regurgitation due to mitral valve prolapse which is late systolic timing Holosystolic or Pansystolic Murmurs Starts from S1 and ends within or extends beyond S2 occurring between chambers that have widely different pressures. (e.g. tricuspid regurgitation, ventricular septal defects) Turbulence is throughout the systole Diastolic Murmur Two causes: o May be due to an abnormal backward flow across a leaking semilunar valve. (e.g. aortic and pulmonic regurgitation normally

Continuous Murmur Begins in systole, peaks near S2 This is due to the communication between high and low pressure chambers. (e.g. murmur that sounds like a machine due to a patent ductus arteriosus) Can be heard at the left supraclavicular area PERICARDIAL FRICTION RUB Not a heart sound perse Parietal/visceral pericardium This is due to an inflamed layer of the pericardium sliding over one another This is described as scratching, grating, crunching or creaking sounds which is better heard during deep inspiration and the patient leaning forward (to maximize contact between pericardium) Described always as to and fro, systolic plus one or two diastolic component This is sometimes just transient so examine your patient everyday to note for any changes Seen in patient with pericarditis-chestpain fever; an ECG will differ pericarditis from myocardial infarction

EFFECTS OF PHYSIOLOGICAL AND PHARMACOLOGICAL INTERVENTIONS OF THE INTENSITY TYPE OF MURMURS Respiration right sided murmurs increase with inspiration To differentiate between mitral and tricuspid regurgitation ask the patient to inspire, if the intensity increases, it is tricuspid = Carvallos Sign Valsalva most murmurs decrease in intensity (due to decreased blood volume) and duration except in hypertrophic cardiomyopathy (HCOM; presents with systolic murmur) and mitral valve prolapse (MVP) Positional Changes with standing (decrease cardiac output) most murmurs decrease in intensity except HCOM and MVP Exercise with hand grip exercise, MR, VSD, and AR increase; Left-sided S3 and S4 also increase (increase total peripheral resistance> more blood will go back to left side of the heart > increase intensity). Pharmacologic Amyl nitrite decreases murmur of MR, VSD, AND AR. (Amyl nitrite is a vasodilator> decreases TPR, therefore blood in aorta will move forward rather than go back to the left side of the >decrease intensity) Transient arterial occlusion Compression of both arms increases the murmur of MR, VSD, AR.

~ The Notebook "Know in your heart that all things are possible. We couldn't conceive of a miracle if none had ever happened." ~ Libbie Fudim "Between you and every goal that you wish to achieve, there is a series of obstacles, and the bigger the goal, the bigger the obstacles. Your decision to be, have and do something out of the ordinary entails facing difficulties and challenges that are out of the ordinary as well. Sometimes your greatest asset is simply your ability to stay with it longer than anyone else." ~ Brian Tracy

Notice that in Hypertrophic CM, valsava exaggerates the murmur; it is prolonged. In other murmurs like in aortic stenosis there is a decrease in intensity; in mitral regurgitation there is a decrease in intensity as well as a decrease in duration. --------------END OF TRANSCRIPTION---------Always listen to your heart, because even though it's towards your left; it's always right. <3