Bates Chapter 9: Cardiovascular

Paroxysmal nocturnal dyspnea

describes episode of sudden dyspnea and orthopnea that awaken the Pt fro msleep. - in L. ventricular heart failur or mitral stenosis; may be mimicked by nocturnal asthma attacks

Innocent murmurs - associated findings

none: normal splitting, no ejection sounds, no diastolic murmurs, and no palpable evidence of ventricular enlargement. Occasionally, both an innocent murmur and another kind of murmur are present.

regular, normal heart beats

normal sinus rhythm, second-degree AV block, atrial flutter with a regular ventricular response

S4

not often heard in normal adults, marks atrial contraction. immediately precedes S1 of the next beat and also reflects a pathologic change in ventricular compliance

S2 variations - decreased or absent A2 in the R .second interspace

noted in calcific aortic stenosis because of valve immobility. If A2 is inaudible, no splitting is heard.

S2 and it's 2 components

A2 and P2, caused by closure of the aortic an dpulmonic valves. During expiration these 2 components ar efused into a single sound, during inspiration 2 sounds are heard.

acute aortic dissection

Anterior chest pain, often tearing or ripping, often radiating into the back or neck

S2 variations - fixed splitting

Fixed splitting refers to wide splitting that does not vary with respiration. It occurs in atrial septal defect and right ventricular failure.

Innocent murmurs - mechanism

Innocent murmurs result from turbulent blood flow, probably generated by ventricular ejection of blood into the aorta from teh L. and occasionally the R. ventricle. very common in children and young adults - may also be heard in older people. There is no underlying cardiovascular disease.

Factors influencing arterial pressure

Left ventricular stroke volume Distensibility of the aorta and the large arteries Peripheral vascular resistance, particularly at the arteriolar level Volume of blood in the arterial system.

situs inversus

heart, liver and stomach are all on opposite sides of body

Nephrotic Syndrome Edema

\periorbital puffiness, tight rings

A waves absent

atrial fibrillation

Thrills may accompany loud, harsh, or rumbling murmurs; as in?

aortic stenosis, patent ductus arteriosus, ventricular septal defect, and, less commonly, mitral stenosis. They are palpated more easily in patient positions that accentuate the murmur.

S3 gallop

in older adults, usually indicates a pathologic change in ventricular compliance

aortic insufficiency amplitude pulse

bounding

JVP elevated is specific for?

increased left ventricular end diastolic pressure and low left ventricular ejection fraction, and it increases risk of death from heart failure

mitral valve murmurs heard best where

cardiac apex

crescendo-decrescendo murmur

first rises in intensity than falls midsystolic murmur of aortic stenosis and innocent flow murmurs

S2 variations - increased intensity of A2 in the right second interspace

(where only A2 can usually be heard) occurs in systemic hypertension because of the increased pressure load. It also occurs when the aortic root is dilated, probably because the aortic valve is then closer to the chest wall.

S4 - diastole

- An S4 (atrial sound or atrial gallop) occurs just before S1. It is dull, low in pitch, and heard better with the bell. An S4 is heard occasionally in an apparently normal person, especially in trained athletes and older age groups. More commonly, it is due to increased resistance to ventricular filling following atrial contraction. This increased resistance is related to decreased compliance (increased stiffness) of the ventricular myocardium.63 - Causes of a left-sided S4 include hypertensive heart disease, coronary artery disease, aortic stenosis, and cardiomyopathy. A left-sided S4 is heard best at the apex in the left lateral position; it may sound like "Tennessee." The less common right-sided S4 is heard along the lower left sternal border or below the xiphoid. It often gets louder with inspiration. Causes of a right-sided S4 include pulmonary hypertension and pulmonic stenosis. - An S4 may also be associated with delayed conduction between the atria and ventricles. This delay separates the normally faint atrial sound from the louder S1 and makes it audible. An S4 is never heard in the absence of atrial contraction, which occurs with atrial fibrillation. - Occasionally, a patient has both an S3 and an S4, producing a quadruple rhythm of four heart sounds. At rapid heart rates, the S3 and S4 may merge into one loud extra heart sound, called a summation gallop.

Mitral stenosis - diastolic - associated findings

- S1 is accentuated and may be palpable at teh apex - an opening snap often follows S2 and initates the urmur - if pulmonary hypertension develops, P2 is accentuated, and the R. ventricular impulse becomes palpable - mitral regurg and aortic valve disease may be associated w/ mitral stenosis

Aortic regurg. - diastolic - associated findings

- an ejection sound may be present - an S3 or S4, if present, suggests severe regurgitation - Progressive changes in the apical impulse include increased amplitude, displacement laterally and downward, widened diameter, and increased duration. - The pulse pressure increases, and arterial pulses are often large and bounding. A midsystolic flow murmur or an Austin Flint murmur suggests large regurgitant flow.

S1 variations - accentuated S1

-S1 is accentuated in (1) tachycardia, rhythms with a short PR interval, and high cardiac output states (e.g., exercise, anemia, hyperthyroidism) and (2) mitral stenosis. In these conditions, the mitral valve is still open wide at the onset of ventricular systole and then closes quickly.

S1 variations - normal

-S1 is softer than S2 at the base (right and left 2nd interspaces). -S1 is often but not always louder than S2 at the apex.

carotid pulsations

-palpable -a more vigorous thrust with a single outward component -pulsations not eliminated by this pressure -height of pulsations unchanged by position -height of pulsations not affected by inspiration

Internal Jugular Palpations

-rarely palpable -soft, biphasic, undulating quality, usually w/ 2 elevations and 2 troughs per heart beat -pulsations eliminated by light pressur eon the vein(s) just above the sternal end of the clavicle -height of pulsations changes w/ position, dropping as the patient becomes more upriht -height of pulsations usually falls with inspirations

pulmonic valve murmurs herad best where?

2nd and 3rd L. interspaces close to teh sternum, but also at higher or lower levels

pulmonary hypertension

A prominent pulsation here often accompanies dilatation or increased flow in the pulmonary artery. A palpable S2 suggests increased pressure in the pulmonary artery

angina pectoris

Classic exertional pain, pressure, or discomfort in the chest, shoulder, back, neck, or arm in angina pectoris, seen in 50% of patients with acute myocardial infarction; atypical descriptors also are common, such as cramping, grinding, pricking; rarely, tooth or jaw pain.17,18 Annual incidence of exertional angina is 1 per 1000 in the population 30 years or older.

Pathological murmurs - aortic stenosis - associated findings

A2 decreases as aortic stenosis worsens. A2 may be delayed and merge with P2 → single S2 on expiration or paradoxical S2 split. Carotid upstroke may be delayed, with slow rise and small amplitude. Hypertrophied left ventricle may → sustained apical impulse and an S4 from decreased compliance.

S1 and it's 2 components

earlier mitral and later tricuspid sound. mitral i smuch louder heard throughout the precordium and is loudest at the cardiac apez. softer tricuspid component is heard best at the lower left sternal border (can hear S1 split here). S1 does not vary with respiration

irregular, rhythmic or sporadic heart beat

early beats, atrial or nodal prematures contraction OR ventricular premature contractions. sinus arythmia.

ascites and liver failure edema

enlarged waistline

Patent Ductus arteriosus - systolic and diastolic

Timing: continuous murmur in both systole and diastole, often with a silent interval late in diastole. loudest in late systole, obscures S2 and fades in diastole Location: L. 2nd interspace Radiation: toward the L. clavicle Intensity: usually loud, sometimes associated w/ a thrill quality: harsh, machinery-like pitch: medium

Stenotic Valve

abnormally narrowed valvular orifice that obstructs blood flow

Left Lateral Decubitous brings out what?

accentuates left sided S3 and S4 and mitral murmurs, especially mitral stenosis

Early Systolic Ejection Sounds

Early systolic ejection sounds occur shortly after S1, coincident with opening of the aortic and pulmonic valves. They are relatively high in pitch, have a sharp, clicking quality, and are heard better with the diaphragm of the stethoscope. An ejection sound indicates cardiovascular disease. Listen for an aortic ejection sound at both the base and apex. It may be louder at the apex and usually does not vary with respiration. An aortic ejection sound may accompany a dilated aorta, or aortic valve disease from congenital stenosis or a bicuspid valve. A pulmonic ejection sound is heard best in the 2nd and 3rd left interspaces. When S1, usually relatively soft in this area, appears to be loud, you may be hearing a pulmonic ejection sound. Its intensity often decreases with inspiration. Causes include dilatation of the pulmonary artery, pulmonary hypertension, and pulmonic stenosis.

Right Ventricular Impulse - hyperkinetic: example, locatiom, diameter, amplitude, duration

Example: anxiety, hyperthyroidism, severe anemia Location: 3rd, 4th or 5th ICS Diameter: not useful Amplitude: slightly more forceful Duration: normal

Left Ventricular Impulse - volume overload: example, location, diameter, amplitude, duration

Example: aortic or mitral regurg. Location: displaced to the left and possibly downward Diameter: > 2cm. Amplitude: diffuse duration: often slightly sustained

Right Ventricular Impulse - Volume overload: examples, location, diameter, amplitude, duration

Example: atrial septal defect Location: left sternal border, extending towrad the left cardiac border, also subxiphoid Diameter: not useful Amplitude: slightly to markedly more forceful Duration: normal to slightly sustained

Right Ventricular Impulse - pressure overload: example, location, diameter, amplitude, duration

Example: pulmonic stenosis, pulmonary HTN Locaiton: 3rd,4th and 5th ICS, also subxiphoid Diameter: not useful Amplitude: more forceful Duration: sustained

Left Ventricular Impulse - hyperkinetic : examples, locations, diameter, amplitude, duration

Examples: anxiety, hyperthyroidism, severe anemia Location: normal Diameter: approx. 2 cm, through increased amplitude may make it seem larger Amplitude: more forceful tapping Duration: <2/3 systole

Left Ventricular Impulse - pressure overload : examples, location, diameter, amplitude, duration

Examples: aortic stenosis, hypertension Location: normal Diameter: >2cm amplitude: more forceful tapping duration: sustained (up to S2)

Sinus node

acts as cardiac pace maker. R. atrium near the junction of the vena cava. automatically discharges impulse about 60-100/min. travels to AV node

pathological murmurs - pulmonic stenosis - associated findings

In severe stenosis, S2 is widely split, and P2 is diminished or inaudible. An early pulmonic ejection sound is common. May hear a right-sided S4. Right ventricular impulse often increased in amplitude and sustained.

S2 variations - physiologic splitting

Listen for physiologic splitting of S2 in the 2nd or 3rd left interspace. The pulmonic component of S2 is usually too faint to be heard at the apex or aortic area, where S2 is a single sound derived from aortic valve closure alone. Normal splitting is accentuated by inspiration and usually disappears on expiration. In some patients, especially younger ones, S2 may not become single on expiration. It may merge when the patient sits up.

pathological murmurs- hypertrophic cardiomyopathy

Location: 3rd and 4th left interspaces radiation: down the L. sternal border to the apex, possibly to the base, but not to the neck Intensity: variable Pitch: medium quality: harsh aids: decreases with squating, inceases with valsalva and standing

Ventricular septal defect

Location: 3rd, 4th, 5th left interspaces Radiation: often wide intensity: often very loud, with a thrill pitch: high, holosystolic qualitiy: often harsh. Associated findings:S2 may be obscured by the loud murmur. findings vary with the severity of the defect and with associated lesions. Mechanism: a ventricular septal defect is a conjenital abnormality in which blood flows from the relatively high-pressure L. ventricle into the low-pressure R. ventricle through a hole. The defect may be accompanied by other abnormalities, but an uncomplicated lesion is described here.

Mitral Regurgitation

Location: Apex Radiation: To the L. axilla, less often to the L. sternal border Intensity: soft to loud; if loud, associated w/ an apical thrill Pitch: medium to high Quality: harsh, holosystolic aids: unlike tricuspid regurgitation, it does not become louder in inspiration associated findings: S1 normal (75%), loud (12%), soft (12%). An apical S3 reflects volume overload of the left ventricle. The apical impulse is increased in amplitude (diffuse), laterally displaced, and may be sustained. Mechanism: when the mitral valve fails to close fully in systole, blood regurgitates from the left ventricle to left atrium, causing a murmur. This leakage ceates volume overload on th eleft ventricle, with subsequent dilation. Several structural abnormalities cause this condition, and findings may vary accordingly.

Pathological Murmurs- aortic stenosis

Location: R. 2nd interspace radiation: foten to the carotids, down the L. sternal border, even to he apex Intensity: sometimes soft but often loud, with a thrill Pitch: medium, harsh; crescendo-dcrescendo may b ehigher at the apex Quality: often harsh; may be more musical at the apex aids: heard best with he patient sitting and leraning forward

Left ventricular PMI: location, diameter, amplitude, duration

Location: in the 4th or 5th interspace, ~7-10 cm lateral to the midsternal line, depending on the diameter of the chest Diameter: discrete, or ≤2 cm Amplitude: brisk and tapping Duration: ≤2/3 of systole

Tricuspid Regurgitation

Location: lower left sternal border Radiation: to teh right of the sternum, to the xiphoid area, and perhaps to the left midclavicular line, but not into the axilla. intensity: variable Pitch: medium Quality: blowing, holosystolic Aids: unlike mitral regurgitation, the intensity may increase slightly with inspiration Associated findings: the right ventricular impulse is increased in amplitude an dmay be sustained. An S3 may be audible along the lower left sternal border. The jugular venous pressure is often elevated, with large V waves in the jugular vein Mechanism: When the tricuspid valve fails to close fully in systole, blood regurgitates from right ventricle to right trium, producing a murmur. The most common cause is R. ventricular failure and dilation, withresulting enlargemnt of the tricuspid orifice. Either [pulmonary hypertension or L. ventricular failure is the usual initiating cause.

Mitral Stenosis - diastolic

Location: usually limited to the apex radiation: little or none intensity: grade 1 to 4 pitch: descrescendo low-pitched rumble. use the bell Aids: Placing the bell exactly on the apical impulse, turning the patient into a left lateral position, and mild exercise all help to make the murmur audible. It is heard better in exhalation.

Aortic Regurgitation - diastolic

Location:2nd to 4th L. interspaces Radiation: if loud to the apex, perhaps to the R. sternal border Intensity: Grade 1-3 Pitch: high, use the diapharm Quality: blwoing decrescendo; may be mistaken for breath sounds Aids: the murmur is heard best with the patient sitting, leanign forward, wit breath held after exhalation

pathological murmurs- hypertrophic cardiomyopathy - mechanism

Massive ventricular hypertrophy is associated with unusually rapid ejection of blood from the left ventricle during systole. Outflow tract obstruction of flow may coexist. Accompanying distortion of the mitral valve may cause mitral regurgitation.

PQRST

P wave - atrial depolarization (80 ms) QRS - ventricular depolarization Q wave - donward deflection from septal depolarization R wave - upward deflection from ventricular depolarization S wave - downward deflection following anR wave T wave - ventricular repolarization, or recovery

S2 variations - paradoxical or reversed splitting

Paradoxical or reversed splitting refers to splitting that appears on expiration and disappears on inspiration. Closure of the aortic valve is abnormally delayed so that A2 follows P2 in expiration. Normal inspiratory delay of P2 makes the split disappear. The most common cause of paradoxical splitting is left bundle branch block.

pathological murmurs - pulmonic stenosis - mechanism

Pulmonic valve stenosis impairs flow across the valve, increasing right ventricular afterload. Congenital and usually found in children. In an atrial septal defect, the systolic murmur from pathologically increased flow across the pulmonic valve may mimic pulmonic stenosis.

pathological mumurs- hypertrophic cardiomyopathy - associated findings

S3 may be present. An S4 is often present at the apex (unlike mitral regurgitation). The apical impulse may be sustained and have two palpable components. The carotid pulse rises quickly, unlike the pulse in aortic stenosis.

rhythms - atrial or nodal premature contractions (supraventricular)

Rhythm. A beat of atrial or nodal origin comes earlier than the next expected normal beat. A pause follows, and then the rhythm resumes. Heart Sounds. S1 may differ in intensity from the S1 of normal beats, and S2 may be decreased.

rhythms - ventricular premature contractions

Rhythm. A beat of ventricular origin comes earlier than the next expected normal beat. A pause follows, and the rhythm resumes. Heart Sounds. S1 may differ in intensity from the S1 of the normal beats, and S2 may be decreased. Both sounds are likely to be split.

rhythms - sinus arrhythmia

Rhythm. The heart varies cyclically, usually speeding up with inspiration and slowing down with expiration. Heart Sounds. Normal, although S1 may vary with the heart rate.

rhythms - atrial fibrillation and atrial flutter w/ varying AV block

Rhythm. The ventricular rhythm is totally irregular, although short runs of the irregular ventricular rhythm may seem regular. Heart Sounds. S1 varies in intensity.

S1 variations - diminished S1

S1 is diminished in first-degree heart block (delayed conduction from atria to ventricles). Here the mitral valve has had time after atrial contraction to float back into an almost closed position before ventricular contraction shuts it. It closes more quietly. S1 is also diminished (1) when the mitral valve is calcified and relatively immobile, as in mitral regurgitation and (2) when left ventricular contractility is markedly reduced, as in congestive heart failure or coronary heart disease.

S1 variations - Split S1

S1 may be split normally along the lower left sternal border where the tricuspid component, often too faint to be heard, becomes audible. This split may sometimes be heard at the apex, but consider also an S4, an aortic ejection sound, and an early systolic click. Abnormal splitting of both heart sounds may be heard in right bundle branch block and in premature ventricular contractions.

S1 Variations - varying S1

S1 varies in intensity (1) in complete heart block, when atria and ventricles are beating independently of each other and (2) in any totally irregular rhythm (e.g., atrial fibrillation). In these situations, the mitral valve is in varying positions before being shut by ventricular contraction. Its closure sound, therefore, varies in loudness.

Pathological murmurs - aortic stenosis - mechanism

Significant aortic valve stenosis impairs blood flow across the valve, causing turbulence, and increases left ventricular afterload. Causes are congenital, rheumatic, and degenerative; findings may differ with each cause. Other conditions mimic aortic stenosis without obstructing flow: aortic sclerosis, a stiffening of aortic valve leaflets associated with aging; a bicuspid aortic valve, a congenital condition that may not be recognized until adulthood; a dilated aorta, as in arteriosclerosis, syphilis, or Marfan's syndrome; pathologically increased flow across the aortic valve during systole can accompany aortic regurgitation.

Systolic Clicks

Systolic clicks are usually caused by mitral valve prolapse—an abnormal systolic ballooning of part of the mitral valve into the left atrium. The clicks are usually mid- or late systolic. Prolapse of the mitral valve is a common cardiac condition, affecting about 5% of the general population. There is equal prevalence in men and women. The click is usually single, but you may hear more than one, usually at or medial to the apex, but also at the lower left sternal border. It is high-pitched, so listen with the diaphragm. The click is often followed by a late systolic murmur from mitral regurgitation—a flow of blood from left ventricle to left atrium. The murmur usually crescendos up to S2. Auscultatory findings are notably variable. Most patients have only a click, some have only a murmur, and some have both. Systolic clicks may also be of extracardial or mediastinal origin. Findings vary from time to time and often change with body position. Several positions are recommended to identify the syndrome: supine, seated, squatting, and standing. Squatting delays the click and murmur; standing moves them closer to S1.

Jugular Venous Pulsations

The first elevation, the presystolic a wave, reflects the slight rise in atrial pressure that accompanies atrial contraction. It occurs just before S1 and before the carotid pulse. The following trough, the x descent, starts with atrial relaxation. It continues as the right ventricle, contracting during systole, pulls the floor of the atrium downward. During ventricular systole, blood continues to flow into the right atrium from the venae cavae. The tricuspid valve is closed, the chamber begins to fill, and right atrial pressure begins to rise again, creating the second elevation, the v wave. When the tricuspid valve opens early in diastole, blood in the right atrium flows passively into the right ventricle, and right atrial pressure falls again, creating the second trough, or y descent. To remember these four oscillations in an oversimplified way, think of the following sequence: atrial contraction, atrial relaxation, atrial filling, and atrial emptying. (You can think of the a wave as atrial contraction and the v wave as venous filling.)

Aortic regurg- diastolic- mechanism

The leaflets of the aortic valve fail to close completely during diastole, and blood regurgitates from the aorta back into the left ventricle. Volume overload on the left ventricle results. Two other murmurs may be associated: (1) a midsystolic murmur from the resulting increased forward flow across the aortic valve and (2) a mitral diastolic (Austin Flint) murmur, attributed to diastolic impingement of the regurgitant flow on the anterior leaflet of the mitral valve.

Opening Snap - diastole

The opening snap is a very early diastolic sound usually produced by the opening of a stenotic mitral valve. It is heard best just medial to the apex and along the lower left sternal border. When it is loud, an opening snap radiates to the apex and to the pulmonic area, where it may be mistaken for the pulmonic component of a split S2. Its high pitch and snapping quality help to distinguish it from an S2. It is heard better with the diaphragm.

Persistent splliting results from?

delayed closure of the pulmonic valve or early closure of the aortic valve

Pericardial friction rub - systolic and diastolic

Timing: may have three short components, each associated w/ friction from cardiac movement in the pericardial sac: (1) atrial systole, (2) ventricular systole, and (3) ventricular diastole. Usually the first two components are preent; all three make diagnosis easy; only one (usually systolic) invites confusion w/ a murmur location: variable but usually herad best in the 3rd interspace to the L. of the sternum Radiation: little Intensity: variable, may increase when the patient leans forward, exhales, and holds breath (in contrast to pleural rub) Quality: scartchy, scraping Pitch: high - use diaphragm

aortic valve murmurs heard best where?

anywhere from the R 2nd intercostal space to the apex

S2 variations - increased intensity of P2

When P2 is equal to or louder than A2, suspect pulmonary hypertension. Other causes include a dilated pulmonary artery and an atrial septal defect. When a split S2 is heard widely, even at the apex and the right base, P2 is accentuated.

Mitral stenosis - diastolic - mechanism

When the leaflets of the mitral valve thicken, stiffen, and become distorted from the effects of rheumatic fever, the mitral valve fails to open sufficiently in diastole. The resulting murmur has two components: (1) middiastolic (during rapid ventricular filling) and (2) presystolic (during atrial contraction). The latter disappears if atrial fibrillation develops, leaving only a middiastolic rumble.

S2 variations - pathologic Splitting (involves splitting during expiration and suggests heart disease)

Wide splitting of S2 refers to an increase in the usual splitting that persists throughout the respiratory cycle. Wide splitting can be caused by delayed closure of the pulmonic valve (as in pulmonic stenosis or right bundle branch block). As illustrated here, right bundle branch block also causes splitting of S1 into its mitral and tricuspid components. Wide splitting can also be caused by early closure of the aortic valve, as in mitral regurgitation.

S3 - diastole

You will detect physiologic S3 frequently in children and in young adults to the age of 35 or 40. It is common during the last trimester of pregnancy. Occurring early in diastole during rapid ventricular filling, it is later than an opening snap, dull and low in pitch, and heard best at the apex in the left lateral decubitus position. The bell of the stethoscope should be used with very light pressure. A pathologic S3 or ventricular gallop sounds just like a physiologic S3. An S3 in a person over age 40 (possibly a little older in women) is almost certainly pathologic, arising from altered left ventricular compliance at the end of the rapid filling phase of diastole.62 Causes include decreased myocardial contractility, congestive heart failure, and volume overloading of a ventricle, as in mitral or tricuspid regurgitation. A left-sided S3 is heard typically at the apex in the left lateral decubitus position. A right-sided S3 is usually heard along the lower left sternal border or below the xiphoid with the patient supine, and is louder on inspiration. The term gallop comes from the cadence of three heart sounds, especially at rapid heart rates, and sounds like "Kentucky."

Left ventricular hypertrophy, or enlargement

a pmi greater than 2.5 cm

Dependent Edema

appears in the lowest body parts: the feet and lower legs when sitting, or the sacrum when bedridden. Causes may be cardiac (congestive heart failure), nutritional (hypoalbuminemia), or positional.

functional murmurs

are short, early, midsystolic murmurs that decrease in intensity with maneuvers that reduce left ventricular volume, such as standing, sitting up, and straining during the Valsalva maneuver.

tricuspid valve murmurs herad best where

at base or near the lower left sternal border

irregular, total heart beat

atrial fibrillation, atrial flutter w/ varying block

midsystolic murmur

beings after S1 and stops before S2. brief gaps are audible bt the murmur and the heart sounds. typically arise from blood fow across the semilunar valves

Sitting up, leaning forward and exhale complete w/out inhalation emphasizes what?

brings out aortic murmurs. You may easily miss the soft diastolic murmur of aortic regurgitation unless you listen at this position.

Apical impulse displaced laterally from?

cardiac enlargement in congestive heart failure, cardiomyopathy, ischemic heart disease. Displacement in deformities of the thorax and mediastinal shift.

aortic stenosis

causes a characteristic murmur

decreased pulsation causes include?

decreased stroke volume and local factors in the artery such as atherosclerotic narrowing or occlusion.

atrial septal

defecta marked increase in amplitude with little or no change in duration occurs in chronic volume overload or the R. vetnricle as from an atrial septal defect

aortic stenosis

delayed carotid upstroke

crescendo murmur

grows louder. presystolic murmur of mitral stenosis

decrescendo murmur

grows softer. early sdiastolic murmur of aortic regurgitation

dextrocardia

heart situated on teh right side of chest. usually associated w/ congenital heart disease

increased amplitude may also reflect what?

hyperthyroidism, severe anemia, pressure overload of the left ventricle (as in aortic stenosis), or volume overload of the left ventricle (as in mitral regurgitation).

Hypovolemic/hypervolemic patients and their JVP

hypovolemic -JVP with be low, so lower the head of the bed to see JVP hypervolemic- JVP high so raise the head of the bed

pressure overload of the R ventricle. as in pulmonic stenosis or pulmonary hypertension

impulse ith increased amplitude and duration

A waves (prominant) in increased resistance to R. atrial contractions in what?

increased resistance to right atrial contraction, as in tricuspid stenosis; also in first-degree atrioventricular block, supraventricular tachycardia, junctional rhythms, pulmonary hypertension, and pulmonic stenosis.

orthopnea

is dyspnea that occurs when Pt is lying down and improves when Pt sits up. - left ventricular heart failure or mitral stenosis; also in obstructive lung disease

acute coronar syndrome

is increasingly used to refer to any of the clinical syndromes caused by acute myocardial ischemia, including unstable angina, non-ST elevation myocardial infarction, and ST elevation infarction.

sustained, high-amplitude impulse that is normally located suggests?

left ventriular hypertrophy from pressure overload, if displaced laterally consider volume overload

What is the reason for unilateral distention of the external jugular vein

local kinking or obstruction

Atrioventricular node

located low in the atrial septum. delayed impulse before going to bundle of His and ventricular myocardium. muscular contractions follow.

pathological murmurs - pulmoni stenosis

location: 2nd and 3rd L. interspaces radiation: if loud, toward the L. shoulder and neck intensity: soft to loud; if loud, associated w/ a thrill pitch: medium; crescendo-decrescendo quality: often harsh

Physiologic murmurs

location: 2nd and 4th intercostal spaces b/t the L. sternal border and the apex Radiation: little intensity: grade 1 to 2, possibly a 3 pitch: soft to medium quality: variable aids: usually decreases or disappears on sitting

innocent murmurs

location: 2nd and 4th intercostal spaces b/t the L. sternal border and the apex Radiation: little intensity: grade 1 to 2, possibly a 3 pitch: soft to medium quality: variable aids: usually decreases or disappears on sitting

Aging may change the heart how?

locations of the apical impulse; pitch of heart sounds and murmurs; stiffness of the arteries; blood pressure.

S3

may arise from rapid deceleration of the column of blood against the ventricular wall, common in children and young adults

Pansystolic (holosystolic) murmurs

pathological, arising from blood flow from a chamber with high pressure to one of lower pressure, through a valve or other structure that hsould be closed. the murmur begins immediately with s1 and continues up to S2.

valsalva maneuver

person strains down against a closed glottis. hypertrophic cariomyopathy murmur is only systolic murmur that increased in intenity with this

Physiologic murmurs - associated findings

possible signs of a likely cause

Unilateral pulsatile bulge

produced by a tortuous and kinked carotid artery

S2 - the second heart sound

produced by aortic valve closure, then another diastole begins

sudden dyspnea in?

pulmonary embolus, spontaneous pneumothorax, anxiety

P2 (loud) suggests

pulmonary hypertension

myocardial contractility

refers to the ability of the cardiac muscle, when given a load, to shorten. Contractility increases when stimulated by action of the sympathetic nervous system and decreases when blood flow or oxygen delivery to the myocardium is impaired.

afterload

refers to the degree of vascular resistance to ventricular contraction. Sources of resistance to left ventricular contraction include the tone in the walls of the aorta, the large arteries, and the peripheral vascular tree (primarily the small arteries and arterioles), as well as the volume of blood already in the aorta.

preload

refers to the load that stretches the cardiac muscle before contraction. The volume of blood in the right ventricle at the end of diastole, then, constitutes its preload for the next beat. Right ventricular preload is increased by increasing venous return to the right heart. Physiologic causes include inspiration and the increased volume of blood flow from exercising muscles. The increased blood volume in a dilated right ventricle of congestive heart failure also increases preload. Causes of decreased right ventricular preload include exhalation, decreased left ventricular output, and pooling of blood in the capillary bed or the venous system.

Jugular Venous Pressure (JVP)

reflects the R. atrial pressure, which in turn equas central venous pressure and right venticular end-diastolic presure. best to use R. internal jugular vein. Falls with loss of blood, increased with R. of L. heart failure, pulmonary hypertension, tricustpid stenosis and pericardial compression or tamponade.

P2

relatively soft, heard best in 2nd and 3rd L. interspaces close to the sternum.

hypokinetic (sustained low amplitude)

result from dilated cardiomyopathy

pulsus alternans

rhythm or th epulse remains regular, but the force of the arterial pulse alternates b/c strong and weak venticular contractions.

Increased IJP suggests what?

right-sided congestive heart failure or, less commonly, constrictive pericarditis, tricuspid stenosis, or superior vena cava obstruction

early decrescendo diastolic murmurs

signify regurgitant flow through an incompetent semilunar valve, more commonly the aortic

regular, slow heart beat

sinus bradycardia, second degree AV block, complete heart block

Regular, fast heart beats

sinus tachycardia, supraventricular tachycardia, atrial flutter w/ a regualr ventricular response, ventricular tachycardia

cardiogenic shock amplitude pulse

small, thready, or weake amplitude of pulse

middiastolic murmur

starts a short time after S2, fade away or merge into a late diastolic murmur. reflect turbulent flow across the atrioventricular valves

early diastolic murmur

starts immediately after S2, w/out discernible gap, then usually fades into a silence before the next S1. accopmanies regurgitant flow across incompetent semilunar valves

late systolic murmur

starts in mid or late systole and persists up to S2. Murmur of mitral valve prolapse and is often preceded by a systolic click.

late disatolic murmur

starts late in diastole and typically continues up to S1.

pansystolic (holosystolic) murmur

starts with S1 and stops at S2, w/out a gap b/t murmur and heart sounds. often occur with regurgitant flow across the atrioventricular valves

rumbling diastolic murmurs in mid- or late diastole

suggest stenosis of an atrioventricular valve, usually the mitral

S2 palpable

suggests systemic hypertension. pulsation here suggest a dilated or aneuysmal aorta

Venous hum - systolic and diastolic

timing: continuous murmur w/out a silent interval. loudest in diastole location: above the medial third of the clavicles, especially on teh right radiation: 1st and 2nd interspaces intensity: soft to moderate. can be obliterated by pressure on the jugular veins quality: humming, roaring pitch: low (heard better with the bell)

V wave large

tricuspid egurgitation, constrictive pericarditis

Physiologic murmurs - mechanism

turbulence due to a temporary incrase in blood flow in predisposing conditions such as anemia, pregnancy, fever, and hyperthyroidism

dyspnea

uncomfortable awareness of breathing that is inappropriate gien level of exertion

S2 variations - decreased or absent P2

usually from the increased anteroposterior diameter of the chest associated with aging. It can also result from pulmonic stenosis. If P2 is inaudible, no splitting is heard.

aortic regurgiation or insufficiency

valve that fails to fully close

regurgitant murmur

vavle that allows blood to lek backward in a retrograde direction

obstructive lung disease and JVP

venous pressure may appear elevated on expiration only; the veins collapse on inspiration. does not indicate CHF

During Systole

ventricular contraction. aortic valve is open, allowing ejection of blood from the L ventricle into the aorta. mitral valve is closed, preventing blood from regurgitating back into the l. atrium

during diastole

ventricular relaxation. aortic valve is closed, preventing regurgitation of blood fro the aorta bak into the left venticle. mitral valve is open, allowing blood to flow from the l. atrium into the relaxed l. ventrcle