Systole - the time during which the ventricles contract and eject blood into the pulmonary artery and aorta.

Diastole - the time during which the ventricles relax and fill with blood

As heart rate increases, the relative proportion of time spent in diastole compared to the time spent in systole decreases. This makes it more difficult to identify systole and diastole in patients who have heart rates in excess of 120 BPM.

Systole

ventricles contract and eject blood into the pulmonary artery and aorta

isovolumetric contraction: ventricular pressure increases but the ventricular volume does not change because the ventricular pressure is lower is lower than that needed to force open the semilunar valves and eject blood into the great vessels

mitral valve closes: electrically stimulated first, L ventricular pressure exceeds L atrial pressure;

tricuspid valve closes: electrically stimulated second; R ventricular presure exceeds L ventricular pressure

ventricular ejection: ventricular pressure exceeds the pressure inside the great vessels and the ventricular volume decreases when blood is ejected into the large arteries

pulmonic valve opens: R ventricular pressure exceeds pulmonic arterial pressure

aortic valve opens: L ventricular pressure exceeds aortic pressure

diastole:

the time during which the ventricles relax and fill with blood

isovolumeic relaxation: the aortic valve is closed; exceeds atrial pressure; ventricular pressure is decreasing but still exceeds atrial pressure

aortic valve closes: L. side was stimulated first; L.  ventricular diastolic pressure drops below aortic pressure

pulmonary valve closes: R. side stimulated second; R ventricular diastolic pressure drops below

passive ventricular filling: ventricular diastolic pressure drops below atrial pressure and blood flows passively into the ventricles. During this time, diastole is further subdivided into periods of rapid ventricular filling followed by slow vnetricular filling.

tricuspid valves opens: R. ventricular diastolic pressure drops below r. atrial diastolic pressure

mitral valve opens: l. ventricular diastolic pressure drops below L atrial diastolic pressure

M_cT_cP_oA_o

A_cP_cT_oM_o

JVP is the vertical distance in centimeters between the mid right atrium and the top of the JV column of blood in the neck. Since the position of the mid right atrium is not easily determined, the sternal angle of Louis is used as a point of reference.

S4 occur late in diastolic filling;

s1 occurs with mitral and tricuspid closing during isovolumetric contraction

ejection sound occurs with pulmonic and aortic opening

at the end of isovolumetric contraction and at the beginning of ejection

s2 occurs with aortic and pulmonic closing during isovolumetric relaxation

opening snap occurs with tircuspid and mitral valve opening at the end of isovolumetric relaxation and passive ventricular filling

s3 occurs with early diastolic filling

Normal contour: two outward deflections (a and v waves) and two inward deflections (x' and y descents); a third outward deflection ("c" wave) is usually too small to visiualize

"a" wave - atrial contraction, largest, after p wave in ECG, but before the 1st heart sound, so pre-systolic in timing

"c" wave - bulging of the tricuspid valve into the right atrium during ventricular isovolumetric contraction, begins with first heart sound

x' descent - composite of an early x descent produced by right atrial relaxation and a later x descent produced by pulling of the tricuspid valve cusps during right ventricular ejection; occurs during ventricular systole and ends just prior the second heart sound; systolic collapse of venous pulse collides with carotid pulse

v wave - build up of venous return in right atrium when tricuspid valve is closed during isovolemic ventricular relaxation; begins just prior to 2nd heart sound and ends right after it;

y descent - fall in right atrial pressure when tricuspid valve opens during the filling phase of ventricular diastole; just after 2nd heart sound, producing a diastolic collapse of the venous pulse

tricuspid stenosis:

•giant "a" waves, due to obstruction to right artrial emptying, pre-systolic in timing, since rt. atrial contraction precedes rt. ventricular contraction

atrial fibrilation: absent "a" waves, complete cessation of atrial contraction

•slow y descent: occuring shortly after the 2nd heart sound indicates an obstruction to right atrial emptying

3rd degree heart block: intermittent cannon "a" waves, right atrial contraction occurs with right ventricular contraction; since tricuspid valve is closed, full force of atrial contraction shot upward into jugular veins, systolic in timing, aterial pulse is regular;

right ventricular hypertrophy: giant "a" waves (obstruction to rt. atrial empyting)

tricuspid regurgitation: giant "v" waves, rt. ventricular volume is ejected into rt. atrium, v-wave occurs syndronously with carotid pulse; systolic pulsation of jugular pulse; ear lobes and eyeballs may pulsate synchronously with each giant v wave

pulmonary stenosis: giant "a" waves, obstruction to rt. ventricular emptying

right ventricular demand pacemakers: cannon "a" waves, regular arterial pulse = > atrioventricular dissociation

apical impulse - begins with the first heart sound, moves outward during the first third of systole, and occurs prior to the carotid pulsation in mid-systole

normally the size of a dime

confined to a single intercostal space (5th)

medial to midclavicular line

access patient in supine and in the left lateral decubitus position

aortic stenosis - anacrotic pulse (pulsus tardus et parvus, slow-rising)

aortic regurgitation - waterhammer pulse (rapid and sudden systolic expansion)

mitral regurgitation - hyperkinetic pulse (strong and abrupt character)

idiopathic hypertrophic subaortic stenosis - pulsus bisferiens (two palpable beats during systole of each cycle)

severe aortic regurgitation - pulsus bisferiens

Normal apical impulse

size: dime (1 cm)

location: medial to the midclavicular line, confined to a single intercostal space (5th intercostal space)

duration: begins with first heart sound, moves outward during the first third of systole, and occurs prior to the carotid pulsation in mid-systole

In a state of pressure overload (e.g. in aortic stenosis or essential hypertension), the left ventricle becomes hypertrophic concentrically; the wall thickness greatly increases as new sarcomeres are added in-parallel to existing sarcomeres (not nec. in prorportion to chamber radius)

In a state of volume overload (e.g. in chornic mitral regurgitation or chornic atrial regurgitation), the ventricle becomes dilated; the ventricle responds by adding new sarcomeres in-series with existing sarcomeres (i.e. the sarcomeres lengthen rather than thicken); while maintaining normal sarcomere lengths,  the heart can expand to receive a greater volume of blood; wall thickness increases in proportion to the increase in chamber radius

aortic stenosis - high pressure (presusre overloading state) => left ventricular hypertrophy, sustained apical impulse

no more than 3cm in diameter, 1-2 intercostal spaces, medial to or at midclavicular line, simultaneous with the carotid pulse (which is delayed), and may not retract until after second heart sound

tricuspid stenosis - normal or diminished apical impulse

chronic aortic regurgitation - high volumes (volume overloading) => left ventricular dilation, hyperdynamic apical impulse, downward to the left

4-5 cm diameter; down and to the left (lateral to midclavicular line); synchronously with the carotid pulse; which peaks during the first half of systole; difficult to obliterate with applied pressure

mitral stenosis - left parasternal impulse

essential hypertension - high pressure (presusre overloading state) => left ventricular hypertrophy, sustained apical impulse

pulmonic hypertension - parasternal impulse (pressure overloading of rt. ventricle)

tricuspid regurgitation - hyperdynamic, paraxiphoid, or LLSB pulse (volume overloading)

pulmonic regurgitation - hyperdynamic impulse, paraxiphoid or LLSB pulse (volume overloading)

mitral regurgitation - high volumes (volume overloading) => left ventricular dilation, hyperdynamic apical impulse, downward to the left

ventricular septal defect (VSD) - hyperdynamic apical impulse displaced down and to the left

pulmonic stenosis - left parasternal sustained impulse

Pressure overloading: Pulmonic hypertension or Pulmonic stenosis - outward, parasternal impulse, that occurs at the same time as apical impulse

Volume overloading: pulmonic insufficiency, tricuspid insufficiency, ASD, hyperdynamic high amplitude impulse along the LLSB or beneath the xiphoid

aortic valve - 2RICS (aortic band)

pulmonic valve - 2LICS (3rd LICS)

tricuspid valve - 4th and 5th LICS

Mitral valve - apex

left ventricular area - apex

right ventricular area - 4LICS

wide splitting of S1 -

delayed closure of tricuspid valve - RBBB

tricuspid valve is held open longer by inc. rt. atrial volume and rt. atrial pressure - ASD

Long P-R - decreased intensity, mitral valve is almost closed at onset of ventricular contraction (1st degree heart block);

short P-R - increased intensity, mitral valve is open (anomalous AV conduction)

increased ventricular contractility - increased intensity; since hyperkinetic states (anemia, pregnancy, anxiety, hyperthyroidism)

decreased ventricular contractility - decreased in intensity (CHF)

3rd degree heart block - varies in intensity, since there's an atrioventricular dissociation (atrial and ventricle not contracting in sync)

mitral stenosis - increased intensity - mitral valve wide open

atrial fibrillation - variable intensity (rhythm is irregularly irregular)

ventricular demand pacemaker - varies in intensity, since atrioventricular dissociation

Aortic and pulmonic valve closure, in that order. Both the LV and RV pressure drops below the aortic and pulmonic arterial pressure, respectively; hence valve closure.

physiologic splitting of S2 - widens during inspiration, and narrows during expiration.

Inspiration - decrease in intrathoracic pressure and venous return increases => inc. right ventricle filling => right ventricle ejection => delayed closure of pulmonary valve; (2) expansion of lungs during inspiration decreases the resisatnace to blood flow in the pulmonary circulation, bringing blood forward through the pulmonary valve via inertia

expiration - inc. in intrathoracic pressure and venous return decreases => dec. right ventricular filling and rt. ventricular ejection; pulmonic valve closes earlier

s4 - atrial contraction against a ventricle w/ decreased compliance  => more forceful atrial contraction

ventricular hypertrophy - systemic hypertension, aortic stenosis, pulmonary htn, pulmonary stenosis

myocardial infarction => decreased ventricular compliance

s4 - increases with inspiration (right-sided)

decreases with inspiration (left-sided)

decreases with standing (left-sided)

atrial fibrillation excludes s4

mitral valve opening under high pressure

or

tricuspid valve

ejection sound - when aortic or pulmonic valve has reached its elastic limit or when blood is forcefully ejected to a great vessel

occurs with aortic stenosis, pulmonic stenosis (valvular), pulmonary htn (vascular)

if accompanied by a murmur, then it's always pathologic

Mid-systolic clicks are sufficient to diagnose MVP or TVP.

Mechanism: sudden tensing of the chordae tendineae as the AV valve leaflets ballon into the atria during mitrla and tricuspid valve prolapse (regurgitant flow)

diaphragm - used for listening to higher pitched sounds (100-400 Hz)

bell - used for listening to lower pitched sounds (20-70 Hz). Mitral stenosis, s3 and s4 are best hearsd with the bell

How to tell difference between split s1 and S1+ ES and S4 + S1?

Split S1 is louder at apex;

if you hear splitting at the 2nd intercostal spaces, think S1+ ES

if you only hear it with the bell, then it's S4 + S1

How to tell difference bet. split s2, S2+OS, and S2+S3?

split s2 - louder at the 2nd intercostal spaces

S2+OS - it's louder at the apex, and widens on standing

s2+ s3 - can only be heard with bell

squatting - increases size of ventricle chambers, increases venous return, filling, inc. left ventricular afterload (everything inc. except HOCM and MVP)

aortic regurg - inc

aortic stenosis - inc

mitral regurg - inc

tricuspid regurg - inc

tricuspid stenosis - inc.

IHSS - dec

MVP - dec

standing - decreases venous return and vent filling - all sounds decrease except HOCM and MVP/TVP

aortic regurg - dec

aortic stenosis - dec

mitral regurg - dec

tricuspid regurg - dec

tricuspid stenosis - dec

IHSS - inc.

MVP - inc.

inspiration - increases venous return on right side,all right sided sounds louder (for expiration, left sided sounds)

aortic regurg - dec

aortic stenosis - dec

mitral regurg - dec

tricuspid regurg - inc

IHSS - dec

MVP - dec

valsalva - pt. forcibly exhales against a closed glottis - rt/lf ventricular filling decrease; all left sided dec. except

aortic regurg. - dec

aortic stenosis - dec

mitral regurg - dec.

tricuspid regurg - dec

tricuspid stenosis - dec

IHSS - inc

MVP - inc

handgrip - increases lf. ventricular afterload, increasing all left sided regurg murmurs

aortic regurg - inc

aortic stenosis - dec

mitral regurg - inc

tricuspid regurg - dec

tricuspid stenosis - dec.

IHSS - dec.

MVP - dec

amyl nitrate - lowers peripheral vascular resistance (afterload) - inc. all left. sided stenotic murmurs

aortic regurg - dec

aortic stenosis - inc.

mitral regurg - dec

mitral stenosis - inc.

tricuspid regurg - dec.

tricuspid stenosis - dec.

IHSS - dec.

MVP - dec.

mitral stenosis is only audible from left lateral decubitus position

aortic regurgitation is accentuated when pt. leans forward and holds breath in forced exhilation

midsystolic murmurs show postextrasystolic potentiation, since the murmur intensity increasees because the beat following the pause is more forceful than normal beats and pause increases ventricular filling and stroke volume

holosystolic murmurs - do not show postextrasystolic potentiation because the increased force of contraction and large stroke volume are distributed between two openings: the normal aortic valve and the regurgitant mitral valve

IHSS - increases with valsalva and standing (makes left ventricle cavity smaller)

mechanism: anterior leaflet of mitral valve contacts the hypertrophied interventricular septum

decreases with squatting  or passive leg elevation (makes left ventricle cavity larger)

wide pulse pressure - abnormally large stroke volume raises systolic blood pressure and the regurgitant volume reduces the diastolic blood pressure pulse pressure > 80; diastolic blood pressure < 50;

bounding (water-hammer) pulse

pulsus bisferiens - ejection of large stroke volume into the aorta creates a ventrui effect that draws the walls of the aorta together and transiently obstructs forward flow;

to-and-fro pulsation of blood (Quincke's pulse) in the proximal nail bed when presssure is applied to the distal nail bed

bobbing of the head with each heart beat (DeMusset's sign) blanching of the face (lighthouse sign), pulsation of the uvula (muller's sign) and pulsation of the retinal arterioles (Becker's sign)  - large systolic stroke volume and rapid diastolic run-off that characterize severe aortic regurgitation.

to-and-fro bruit audible over femoral artery (Duroziez's sign); stroke volume

dullness to percussion, increased tactile frmitus and egophony at the lower tip fo the left scapula- due to lung compression by the dilated left ventricle(Ewart's sign)

Hill's sign - foot-arm BP difference > 60;

For each of the valvular lesions below describe the following: pulse contour, pulse pressure, JVP, apical impulse, splitting of the second heart sound; murmur in terms of quality, timing, radiation, effect of inspiration, effect of physical and pharmacologic maneuvers; associated sounds:

aortic stenosis

For each of the valvular lesions below describe the following: pulse contour, pulse pressure, JVP, apical impulse, splitting of the second heart sound; murmur in terms of quality, timing, radiation, effect of inspiration, effect of physical and pharmacologic maneuvers; associated sounds:

aortic regurgitation

For each of the valvular lesions below describe the following: pulse contour, pulse pressure, JVP, apical impulse, splitting of the second heart sound; murmur in terms of quality, timing, radiation, effect of inspiration, effect of physical and pharmacologic maneuvers; associated sounds:

mitral regurgitation

For each of the valvular lesions below describe the following: pulse contour, pulse pressure, JVP, apical impulse, splitting of the second heart sound; murmur in terms of quality, timing, radiation, effect of inspiration, effect of physical and pharmacologic maneuvers; associated sounds:

mitral stenosis

For each of the valvular lesions below describe the following: pulse contour, pulse pressure, JVP, apical impulse, splitting of the second heart sound; murmur in terms of quality, timing, radiation, effect of inspiration, effect of physical and pharmacologic maneuvers; associated sounds:

tricuspid regurgitation

For each of the valvular lesions below describe the following: pulse contour, pulse pressure, JVP, apical impulse, splitting of the second heart sound; murmur in terms of quality, timing, radiation, effect of inspiration, effect of physical and pharmacologic maneuvers; associated sounds:

tricuspid stenosis

For each of the valvular lesions below describe the following: pulse contour, pulse pressure, JVP, apical impulse, splitting of the second heart sound; murmur in terms of quality, timing, radiation, effect of inspiration, effect of physical and pharmacologic maneuvers; associated sounds:

pulmonary stenosis

For each of the valvular lesions below describe the following: pulse contour, pulse pressure, JVP, apical impulse, splitting of the second heart sound; murmur in terms of quality, timing, radiation, effect of inspiration, effect of physical and pharmacologic maneuvers; associated sounds:

IHSS

For each of the valvular lesions below describe the following: pulse contour, pulse pressure, JVP, apical impulse, splitting of the second heart sound; murmur in terms of quality, timing, radiation, effect of inspiration, effect of physical and pharmacologic maneuvers; associated sounds:

mitral valve prolapse

For each of the valvular lesions below describe the following: pulse contour, pulse pressure, JVP, apical impulse, splitting of the second heart sound; murmur in terms of quality, timing, radiation, effect of inspiration, effect of physical and pharmacologic maneuvers; associated sounds:

ventricular septal defect

For each of the valvular lesions below describe the following: pulse contour, pulse pressure, JVP, apical impulse, splitting of the second heart sound; murmur in terms of quality, timing, radiation, effect of inspiration, effect of physical and pharmacologic maneuvers; associated sounds:

atrial septal defect

Austin flint murmur - regurgitant flow impinges upon the anterior leaflet of the mitral valve and partially closes it

decreases with administration of amyl nitrate as opp. to mitral stenosis

3rd heart sound => AF murmur

mid-to-late diastolic rumbling murmur

pulmonary regurgitation increases with inspiration

and also does not cause the peripheral mnaifestations in aortic regurgitation

crescendo affect (presystolic accentuation) - last part of atrial systole and the first part of ventricular systole; LV pressure begins to rise, partially closing the stenotic mitral valve, creating a functional stenosis + anatomic stneosis => presystolic accentuation

disappears with atrial fibrillation

mitral stenosis - rumbling murmur, amyl nitrate increases the intensity, increased S1, sustained left parasternal impulse (right ventricular hypertrophy), normal apical impulse

tricuspid stenosis - intensity increases with inspiration, giant "a' waves, slow y descent

systolic component - pulmonic valve

diastolic component - tricuspid valve

increased forward flow across both valves

cervical venous hum - continuous murmur that is best hear in the neck; turbulent flow in the internal jugular vein caused by compression of the jugular and transverse process of the atlas

heard in children, increased in intensity when patient turns head 30-60 degrees away from side being examines

diminished when compression fo jugular veins

midsystolic, vibratory or buzzing quality, changes with position

periodic vibrations across the left ventricular outflow tract and aortic valve

3rd LICS adjacent to sterum

loudest in recumbent, diminishes when standing

grade 3/6

systolic - ventricular contraction

early diastolic -passive ventricular filling

late diastolic - atrial contraction