Iacona- Exam 2: Cardio, Peripheral vasc

Irregular heart sounds

-mitral stenosis: In diastole, left ventricular pressure con- tinues to drop and falls below left atrial pressure. The mitral valve opens. This event is usually silent, but may be audible as a pathologic opening snap (OS) if valve leaflet motion is restricted, as in mitral stenosis. -s3: After the mitral valve opens, there is a period of rapid ventricular filling as blood flows early in diastole from left atrium to left ventricle. In children and young adults, a third heart sound, S3, may arise from rapid deceleration of the col- umn of blood against the ventricular wall. In older adults, an S3, sometimes termed "an S3 gallop," usually indicates a patho- logic change in ventricular compliance. -although not often heard in nor- mal adults, a fourth heart sound, S4, marks atrial contraction. It immediately precedes S1 of the next beat and can also reflect a pathologic change in ventricular compliance.

Myocardial contractility

-refers to ability of heart muscles to shorten after being given a load -Contractility increases when Stimulated by sympathetic action, decreased when blood flow/O delivery to the myocardium is impaired

Afterload

-refers to degree of vascular resistance the left ventricle faces when contracting -Sources of resistance: Tone in walls of aorta, large arteries, and peripheral vascular tree (primarily small arteries/arterioles), as well as volume of blood already in the aorta. ****Pathology increases preload and afterload (called volume and pressure overload), and produces changes in vascular functioning including changes in ventricular impulses (detectable by palpation), and in normal n=heat sounds. May develop murmurs and pathological hearty sounds

Paradoxical pulse

A paradoxical pulse may be detected by a palpable decrease in the pulse amplitude on quiet inspiration. If the sign is less pronounced, a blood pressure cuff is needed. Systolic pressure decreases by >10-12 mm Hg during inspiration. A paradoxical pulse occurs in pericardial tamponade, exacerbations of asthma and COPD, and constrictive pericarditis.

An asymptomatic teenager might have a grade 2/6 midsystolic murmur in the 2nd and 3rd left interspaces. -What could this be/what should you do?

Because this suggests a pulmonic murmur you should assess the RV for hypertrophy by carefully palpating the left parasternal area. Because pulmonic stenosis and atrial septal defects can cause this murmur, auscultate carefully for a split S2, any ejection sounds, and variation with inspira- tion. -Listen to the murmur after the patient sits up. Look for evidence of anemia, hyperthyroidism, or pregnancy that could cause such a murmur by increasing the flow across the aortic or the pulmonic valve. If all your findings are normal, your patient probably has a functional murmur—one with no pathologic significance. Integrating this information allows you to generate a differential diagnosis about the origin of the murmur and pursue further evaluation.

What causes opening/closing of Mitral valve

During diastole, pressure in the blood- filled left atrium slightly exceeds that in the relaxed left ventricle, and blood flows from left atrium to left ventricle across the open mitral valve (Fig. 9-5). Just before the onset of ventricular systole, atrial con- traction produces a slight pressure rise in both chambers. During systole, the left ventricle starts to contract and ventricular pressure rapidly exceeds left atrial pressure, closing the mitral valve (Fig. 9-6). Closure of the mitral valve produces the first heart sound, S1.

Gradation of murmurs

Grade 1 : Very faint, heard only after listener has "tuned in"; may not be heard in all positions Grade 2 : Quiet, but heard immediately after placing the stethoscope on the chest Grade 3 : Moderately loud Grade 4 : Loud, with palpable thrill Grade 5: Very loud, with thrill. May be heard when the stethoscope is partly off the chest Grade 6: Very loud, with thrill. May be heard with stethoscope entirely off the chest *****An identical degree of turbulence would cause a louder murmur in a thin person than in a very muscular or obese person. Emphysematous lungs may diminish the intensity of murmurs.

Surface Projections of the Heart and Great Vessels

-right ventricle (RV) occupies most of the anterior cardiac surface -The inferior border of the RV lies below the junction of the sternum and the xiphoid process. -The RV narrows superiorly and joins the pulmonary artery at the level of the sternal angle, or "base of the heart," a clinical term that refers to the superior aspect of the heart at the right and left 2nd interspaces adjacent to the sternum. -The left ventricle, behind the RV and to the left, forms the left lateral margin of the heart -Its tapered inferior tip is often termed the cardiac apex. clinically important bc produces the apical impulse, identified during palpation of the precordium as the point of maximal impulse (PMI). This impulse locates the left border of the heart and is normally found in the 5th intercostal space at or just medial to the left midclavicular line -In supine patients the diameter of the PMI may be as large as a quarter, approximately 1 to 2.5 cm. ****A PMI >2.5 cm is evidence of left ventricular hypertrophy (LVH) from hypertension or aortic stenosis. -in (COPD), the PMI may be in the xiphoid or epigastric area due to right ventricular hypertrophy. -The aorta curves upward from the left ventricle to the level of the sternal angle, where it arches posteriorly to the left and then down- ward. On the medial border, the superior and inferior venae cavae channel venous blood from the upper and lower portions of the body into the right atrium.

Murmurs during pregnancy

-should be promptly evaluated -Esp concerning if aortic stenosis or pulmonary Hypertension

EKG

-six limb leads in the frontal plane and six chest or precordial leads in the transverse plane -electrical vectors approaching lead cause positive or upward deflection -electrical vectors moving away from lead cause negative or downward deflection -when pos and negative vectors balance, they create isoelectric line ● The small P wave of atrial depolarization (duration up to 80 milliseconds; PR interval 120 to 200 milliseconds) ● The larger QRS complex of ventricular depolarization (up to 100 milliseconds), consisting of one or more of the following: ● the Q wave, a downward deflection from septal depolarization ● the R wave, an upward deflection from ventricular depolarization ● the S wave, a downward deflection following an R wave ● A T wave of ventricular repolarization, or recovery (duration relates to QRS)

Indications to start pharm for hypertension

*Age ≥60 years : Systolic blood pressure ≥150 mm Hg or diastolic blood pressure ≥90 mm Hg (strong recommendation) *Age <60 years : Systolic blood pressure ≥140 mm Hg (expert opinion) Diastolic blood pressure ≥90 mm Hg (strong recom- mendation) *Age >18 years with chronic kidney dis- ease or diabetes : Systolic blood pressure ≥140 mm Hg or diastolic blood pressure ≥90 mm Hg (expert opinion)

assessing the location, diameter, amplitude, and duration of the apical impulse.

*Location. -Initially try to assess location with the patient supine, because the left lateral decubitus position displaces the apical impulse to the left. Locate two points: the interspaces, usually the 5th or possibly the 4th, which give the vertical loca- tion; and the distance in centimeters from the midclavicular line (or mid- sternal line), which gives the horizontal location. For the midclavicular line, use a ruler to mark the midpoint between the ster- noclavicular and acromioclavicular joints so that other clinicians can reproduce your findings. *****Pregnancy or a high left diaphragm may shift the apical impulse upward and to the left. *****Lateral displacement toward the axillary line from ventricular dilatation is seen in heart failure, cardiomyopathy, and ischemic heart disease; and also in thoracic deformities and mediastinal shift. ******Lateral displacement from the midcla- vicular line makes increased left ven- tricular volume and a low left ventricular EF 5 and 10 times more *Diameter. -Palpate the diameter of the apical impulse. In the supine patient, it usually measures less than 2.5 cm, about the size of a quarter, and occupies only one interspace. It may feel larger in the left lateral decubitus position. ******In the left lateral decubitus position, a diffuse PMI with a diameter >3 cm sig- nals left ventricular enlargement;131 a diameter of >4 cm makes left ventric- ular overload almost 5 times more likely *Amplitude. -Estimate the amplitude of the impulse. Is the PMI brisk and tapping, diffuse, or sustained? These are three important descriptors in clinical practice. Normally, the amplitude of the PMI is small and feels brisk and tapping. Some young adults have an increased amplitude, or hyperkinetic impulse, especially when excited or after exercise; the duration, however, is normal. ******A hyperkinetic high-amplitude impulse may occur in hyperthyroid- ism, severe anemia, pressure over- load of the left ventricle from hypertension or aortic stenosis, or volume overload of the left ventricle from aortic regurgitation. *Duration. -Duration is the most useful characteristic of the apical impulse for identifying hypertrophy of the left ventricle. To assess duration, auscultate the heart sounds as you palpate the apical impulse, or watch the movement of your stethoscope as you listen at the apex. Estimate the proportion of systole occupied by the apical impulse. Normally, it lasts through the first two thirds of systole, or often less, but does not continue to the second heart sound. ******A sustained high-amplitude impulse significantly increases the likelihood of LVH from the pressure overload seen in hypertension. If such an impulse is displaced laterally, consider volume overload. *******A diffuse sustained low-amplitude (hypokinetic) impulse is seen in heart failure and dilated cardiomyopathy.

bisferans pulse

-A bisferiens pulse is an increased arterial pulse with a double systolic peak, detected during moderate compression of the artery. Causes include pure aortic regurgitation, combined aortic stenosis and regurgitation, and, though less commonly palpable, hypertrophic cardiomyopathy.

Heart Murmurs

-Abnormal sounds distinguished by their pitch and their longer duration. -They are attributed to turbulent blood flow and are usually diagnostic of valvular heart disease. At times, they may also represent "innocent" flow murmurs, especially in young adults. -A stenotic valve has an abnormally narrowed valvular orifice that obstructs blood flow, as in aortic stenosis, and causes a characteristic murmur. So does a valve that fails to fully close, as in aortic regurgitation. Such a valve allows blood to leak backward in a retrograde direction and produces a regurgitant murmur. -location and timing with the murmur's shape, maximal intensity, direction of radiation, grade of intensity, pitch, and quality should be identified, remember, LIPS R QT

Hypertension and CVD

-About one third of U.S. adults over the age of 20 years have hypertension (defined as a blood pressure ≥140/90 mm Hg) -Primary (essential) hypertension is the most common cause of hypertension: risk factors include age, genetics, black race, obesity and weight gain, exces- sive salt intake, physical inactivity, and excessive alcohol use. -Secondary hypertension accounts for less than 5% of hypertension cases. Causes include sleep apnea, chronic kidney disease, renal artery stenosis, medications, thyroid disease, parathyroid disease, Cushing syndrome, hy- peraldosteronism, pheochromocytoma, and coarctation of the aorta -While the prevalence of hypertension is similar between men and women, prevalence in blacks is substantially higher than in whites. -Most hypertensive adults know of their diagnosis, though only about 75% are taking medications, only half reach BP goals

Edema

-Accumulation of excessive fluids in extra vascular interstitial space -Can have up t 110% weight gain before pitting edema becomes noticeable -Focus on location, timing, and setting of the dema -Ask if worse in morning or night, do shoes/socks get tight? -Are your eyelids puffy/swollen in the morning, have you have to let out your belt, are your rings suddenly tight on your fingers. Consider asking the patient to weigh themselves each morning If they retain fluidto detect ascites ****Causes are frequently cardiac (r/l vent dysfunction, pulm hypertension), or pulm obstructive diseases. Can also be nutritional (hypoalbuminemia), or positional (Dependent edema occurs in the lowest body Parts ), anascara is severe generalized edema extending to the sacrum and abdomen *****Ascites from liver failure: -Look for periorbital puffiness and tight rings of nephrotic syndrome and an enlarged waistline

Arterial pulses/BP

-Arterial pulse is caused by: Contraction of the left ventricle causes blood to be ejected into the aorta and then move systemically, as the waves move through the body, it makes the pulse -BP cuff measures the peaks of BP in systole and the lowest troughs in diastole -Differences btw systolic and diastolic is referred to as the pulse pressure -Factors affecting BP: *Left ventricular stroke volume *Distensibility of aorta and large arteries *peripheral vascular resistance, particularly at arteriolar level *Volume of blood in the arterial system ***Changes in any of these factors alter systolic, diastolic, or both pressures -BP levels fluctuate a lot throughout the day w: physical activity, emotional state, pain, noise, environmental temp, coffee, tobacco, drugs, and time o day ****Pulses in the arms and legs are unsuitable for timing events in the cardiac system bc there's a large gap btw peripheral pulses and ventricular contraction

What leads to aortic valve opening/closing in cardiac cycle

-As left ventricular pressure continues to rise, it quickly exceeds the pressure in the aorta and forces the aortic valve open (Fig. 9-7). In some pathologic conditions, an early systolic ejection sound (Ej) accompanies the opening of the aortic valve. Normally, maximal left ventricular pressure corresponds to systolic blood pressure. -As the left ventricle ejects most of its blood, ventricular pressure begins to fall. When left ventricular pressure drops below aortic pressure, the aortic valve closes (Fig. 9-8). Aortic valve closure produces the second heart sound, S2, and another diastole begins.

IDing systole and diastole

-As you auscultating the chest, also palpate the right carotid artery in the lower third of the neck w index and middle fingers S1 is just before the upstroke and S2 is right after -Note intensities, interval btw S1 and 2 is systole, and the one between S2 and 1 is diastole

Carotid Artery Thrills and Bruits.

-As you palpate the carotid artery, you may detect vibrations, or thrills, like the throat vibrations of a cat when it purrs. Proceed to auscultation. -Auscultate both the carotid arteries to listen for a bruit, a murmur-like sound arising from turbulent arterial blood flow. Ask the patient to stop breathing for ∼15 seconds, then listen with the DIAPHRAGM of the stethoscope (Hears higher pitches better).Note that higher-grade stenoses may have lower frequency or even absent sounds, more amenable to detection with the bell. -Place the diaphragm near the upper end of the thyroid cartilage below the angle of the jaw, which overlies the bifurca- tion of the common carotid artery into the external and internal carotid arteries. A bruit in this location is less likely to be confused with a transmitted murmur from the heart or subclavian or vertebral artery bruits. ****Although usually caused by atherosclerotic luminal stenosis, bruits are also caused by a tortuous carotid artery, external carotid arterial disease, aortic stenosis, the hypervascularity of hyper- thyroidism, and external compression from thoracic outlet syndrome. Bruits do not correlate with clinically significant underlying disease -Listen for bruits in older patients and patients with suspected cerebrovascular disease

Palpation -General chest wall/heaves, thrills, lifts

-Begin with general palpation of the chest wall. -Heaves, Lifts, Thrills; S1 and S2, S3 and S4. *palpate in the 2nd right interspace, the 2nd left interspace, along the sternal border, and at the apex for heaves, lifts, thrills, impulses from the RV, and the four heart sounds. ■ To palpate heaves and lifts, use your palm and/or hold your fingerpads flat or obliquely against the chest. Heaves and lifts are sustained impulses that rhythmically lift your fingers, usually produced by an enlarged right or left ventricle or atrium and occasionally by ventricular aneurysms. ■ For thrills, press the ball of your hand (the padded area of your palm near the wrist) firmly on the chest to check for a buzzing or vibratory sensation caused by underlying turbulent flow. If present, auscultate the same area for murmurs. Conversely, once a murmur is detected, it is easier to palpate a thrill in the position that accentuates the murmur, such as the leaning forrward position after detecting aortic regurgitation. ****The presence of a thrill changes the grading of the murmur, ■ Palpate impulses from the RV in the right ventricular area, normally at the lower left sternal border and in the subxiphoid area *****Palpation is less useful in patients with a thickened chest wall or increased AP diameter. ■ To palpate S1 and S2, using firm pressure, place your right hand on the chest wall. With your left index and middle fingers, palpate the carotid upstroke to identify S1 and S2 just before and just after the upstroke. With practice, you will succeed in palpating S1 and S2. For S3 and S4, apply lighter pressure at the cardiac apex to detect the presence of any extra movements.

Continuous murmurs

-Begins in systole and extends into all or part of diastole (but is not necessarily uniform throughout) Congenital patent ductus arteriosus and AV fistulas, common in dialysis patients, produce continuous murmurs that are nonvalvular in origin. Venous hums and pericardial friction rubs also have both systolic and diastolic com- ponents.

Palpable S3 and 4

-By inspection and palpation may be able to see -With patient in left lateral decubitus, palpatethe apical beat as the patient EXHALES and holds breath ****A brief early to middiastolic impulse represents a palpable S3, an outward movement just before S1 signifies a palpable S4

Shortness of breath

-Can be dyspnea, orthopedist, PND -Dyspnea is uncomfortably awareness of breathing, common in pateienst with cardiac/pulmonary probs. *****Sudden dyspnea occurs in PE, spontaneous pneumo and anxiety. -orthopnea: dyspnea that occurs when patient is supine and improves with sitting up, classically quantified by the number of pillows used for sleeping. *****Orthopnea and PND occur in left ventricular heart failure, mitral stenosis, and COPD -PND: Episodes of sudden dyspnea/orthopnea that awaken the patient from sleep, usually 1-2 hours after going to bed. Feels like they need to stand up or go to the window for air. May be associated wheezing/coughing. Episode usually subsides, but then recourses around the same tim next night. *****PND may be mimicked by nocturnal asthma attacks

Cardiac Inspection

-Careful inspection of the anterior chest may reveal the location of the apical impulse or PMI, or less commonly, the ventricular movements of a left-sided S3 or S4. Shine a tangential light across the chest wall over the cardiac apex to make these move- ments more visible. Plan to further characterize these movements as you proceed to palpation.

Common/concerning symptoms of heart

-Chest pain -Palpations -SOB: dyspnea, orthopedist, PND -Swelling (Edema) -fainting (syncope) -Keep in mind these sorts of symptoms can be cardiac or pulmonicin origin -Also important to quantify a patients baseline level of activity. Ex ISSN have chest pain, does it occur when climbing stairs? How many flights/ etc -When did symptoms appear/change?

Heart murmurs

-Distinguished from other sounds by their pitch -Attributed to turbulent blood flow, and usually indicate valvular pathology, at times, can be innocent, esp in young adults -Can have a stenotic or regurgitant valve. See other quiz for more details

Changes over lifetime

-Easier to palpate the PMIin kids/lung adults, but harder when get older and AP diameter gets larger, impulse gets hard to find. -For same reason, splitting of S2 may be harder to hear, as pulmonic part gets harder to hear -Almost everyone has a heart murmur at some point, usually innocent, may originate in heart or in large vessels -Jugular venous hum 9common in children), can still be heard in young adulthood -Cervical systolic murmur/bruit, may be innocent in children, but becomes sus for atherosclerotic disease in adult

The carotid pulse

-Examine carotid pulse, including upstroke, amplitude/contour, and presence/absence of thrills or bruits -carotid pulse gives info about the cardiac function, esp aortic valve stenosis and regurgitation How to assess amplitude/contour: *Patient supine w head of bed elevated to 30. Inspect neck for carotid pulsation (Just medial to SCM), *Palpate right lower carotid (lower third of the neck, says you can palpate with thumbs), palpate just medial to SCM muscle (around cricoid cage). Do not palpate the carotid sinus (which is up near the top of the thyroid cartilage) *NEVER palpate both at once, may cause syncope! *Slowly increase pressure until you feel max pulsation, then slowly decrease pressure until can best sense contour and arterial pressure ****Pressure on the carotid sinus can induce bradycardia/cause drop in BP

Oscillation point of JPV

-Find the highest point of oscillation in the eternal jug vein -usually measured in vertical distance above the angle of Louis, patient is at 60 degrees on bed, but usual height for measurement is 30 - Position patients head to the left, then right, identifying the external on each side, then focus on the one on the right. JVP is the highest oscillation point (meniscus), (If patient is hypovolemic (septic), expect oscillation to b weakened, can help to lower the bed So patient lies flat, if hypervolemic, expect her opposite and raise bed to 60 or 90 degrees) -If JVP is >3cm above the sternal angle, it is abnormal Steps for measuring: 1. Make the patient comfortable. Raise the head slightly on a pillow to relax the SCM muscles. 2. Raise the head of the bed or examining table to about 30°. Turn the patient's head slightly away from the side you are inspecting. 3. Use tangential lighting and examine both sides of the neck. Identify the exter- nal jugular vein on each side, then find the internal jugular venous pulsations. 4. If necessary, raise or lower the head of the bed until you can see the oscillation point or meniscus of the internal jugular venous pulsations in the lower half of the neck. 5. Focus on the right internal jugular vein. Look for pulsations in the supraster- nal notch, between the attachments of the SCM muscle on the sternum and clavicle, or just posterior to the SCM. Distinguish the pulsations of the internal jugular vein from those of the carotid artery (see box below). 6. Identify the highest point of pulsation in the right jugular vein. Extend a long rectangular object or card horizontally from this point and a centimeter ruler vertically from the sternal angle, making an exact right angle. Mea- sure the vertical distance in centimeters above the sternal angle where the horizontal object crosses the ruler and add to this distance 5 cm, the distance from the sternal angle to the center of the right atrium. The sum is the JVP. -JVP measured at >3 cm above the sternal angle, or more than 8 cm in total distance above the right atrium, is considered elevated above normal.

Blood pressure/HR- Phys exam

-General appearance, patients color, resp rate, and level of anxiety can clue to many issues -BP: After letting patient rest for 5 in quiet, calm setting w feet on the floor, get appropriate sized cuff, put arm at heart level (usually 4th intercostal, midsternum, support the pt Arm), make sure the bladder of the cuff is over the brachial artery ****If arm is above heart, pressure will appear low, if below it will appear high -Inflate about 30-40mm above the point where radial pulse disappears -As you release, listen for korotkoff sounds (at least 2 consecutive beats), this is systolic. Diastolic comes when the sounds disappear *****Clinical measurements may be somewhat unreliable, repetition and averaging of tests may help Heart rate: Palpate at radial, or listen at PMI

Paradoxical pulse

-Greater than normal drop in systolic BP during inspiration -If the pulse varies in amplitude with respiration or you suspect cardiac tamponade (because of jugular venous distention, dyspnea, tachycardia, muffled heart tones, and hypotension), use a blood pressure cuff to check -As the patient breathes quietly, lower the cuff pressure to the systolic level. Note the pressure level at which the first sounds can be heard. Then drop the pressure very slowly until sounds can be heard throughout the respiratory cycle. Again note the pressure level. The difference between these two levels is normally no greater than 3 or 4 mm Hg. *****The pressure when Korotkoff sounds are first heard is the highest systolic pressure during the respiratory cycle. The pressure when sounds are heard throughout the cycle is the lowest sys- tolic pressure. A difference between these levels of ≥10 mm Hg to 12 mm Hg constitutes a paradoxical pulse **** found most commonly in acute asthma and obstructive pulmonary disease. It also occurs in pericardial tam- ponade and at times in constrictive peri- carditis and acute pulmonary embolism.

Location and Timing of Cardiac Findings.

-Identify both the anatomical location of impulses, heart sounds, and murmurs and where they fall in the cardiac cycle. Remember to integrate your findings with the characteristics of the patient's JVP and carotid upstroke. -Timing of sounds is often possible through auscultation alone, but aided by inspection and palpation as well. In most patients with normal or slow heart rates, it is easy to identify the paired heart sounds of S1 and S2 that mark the onset of systole and diastole. The relatively long diastolic interval after S2 separates one pair from the next -The relative intensity of S1 and S2 is also helpful. S1 is usually louder than S2 at the apex; S2 is usually louder than S1 at the base."Inching" your stethoscope also helps clarify the timing of S1 and S2. -At times, the intensities of S1 and S2 may be abnormal, or at rapid heart rates the duration of diastole may shorten, making it difficult to distinguish systole from diastole. Palpation of the carotid artery during auscultation is an invaluable aid to the timing of sounds and murmurs. Since the carotid upstroke always occurs in systole immediately after S1, sounds or murmurs coinciding with the upstroke are systolic; sounds or murmurs following the carotid upstroke are diastolic. *****For example, S1 is diminished in first- degree heart block; S2 is diminished in aortic stenosis.

Feeling pulse at brachial artery

-In patients with carotid obstruction, kinking, or thrills, assess the pulse in the brachial artery, applying the techniques described previously for determining amplitude and contour. -The patient's arm should rest with the elbow extended, palm up. Cup your hand under the patient's elbow or support the forearm. You may need to flex the elbow to a varying degree to get optimal muscular relaxation. Use the index and middle fingers or thumb of your opposite hand for palpation. Feel for the pulse just medial to the biceps tendon

Distinguishing Jugular Venous Pulsations from Carotid Pulsations.

-Internal jugular pulsation: *Rarely palpable *Soft biphasic undulating quality, usu- ally with two elevations and charac- teristic inward deflection (x descent) *Pulsations eliminated by light pressure on the vein(s) just above the sternal end of the clavicle *Height of pulsations changes with position, normally dropping as the patient becomes more upright *Height of pulsations usually falls with inspiration -Carotid pulsations: *Palpable *A more vigorous thrust with a single outward component *Pulsations not eliminated by pressure on veins at sternal end of clavicle *Height of pulsations unchanged by position *Height of pulsations not affected by inspiration

Isometric handgrips

-Isometric handgrip increases the systolic murmurs of mitral regurgitation, pulmonic stenosis, and ventricular septal defect, and also The diastolic murmur of aortic Regurgitation and mitral stenosis

Standing/Squatting

-May help to 1, identify a prolapsed mitral valve and 2, distinguish hypertrophic cardiomyopathy from aortic stenosis -Standing venous return to heart decreases, arterial pressure, stroke volume, and volume of blood in left vent all decline. Squatting does the opposite -Listen to patient's heart in both positions: *When squatting, the intensity of a hypertrophic cardiomyopathy decreases, and the intensity of an aortic stenosis increases, and the sounds of a prolapsed mitral decrease, also associated with delay of clicks *When standing, the intensity of a hypertrophic cardiomyopathy increases, and aortic stenosis decreases, and the sounds of any mitral prolapse increase, also associated with earlier clicks and lengthened murmur

Chest pain

-Most common syymptom of coronary heart disease (CHD) - CHD is Leading killer of men and women. 1 in 7 U.S deaths. highest for AA -When examining always be considering life threatening: Angina pectoralis, MI, dissecting aorta, aortic aneurysm, PE -Men and women w MI present with angina, but Women (Esp over 65) can also be more atypical w pain in upper back, neck, jaw, SOB, paroxysmal nocturnal dyspnea, N/V, and fatigue -Innapropriate discharge from ER results in 25% mortality rate -Ask open ended and then pointed: ask to point to the pain, describe OLD CARTS, and any associated symptoms

Systolic murmurs

-Murmurs that coincide with carotid upstroke -Systolic murmurs usually point to valvular disease, but may also be physiological flow arising from normal valves -Can be midsystolic or pansystolic, early sys are rare. Midsystolic may be harmless physiological murmurs (usually sound of blood flow across the semilunars) and decrease in intensity with maneuvers that lessen left ventricular volume (like Valsalva) -Late systolic murmurs is the murmur o mitral regurgitation, and is often preceded by a systolic click —-Systolic murmurs include: innocent, physiological, aortic stenosis, hypertrophic cardiomyopathy, pulmonic stenosis (all midsystolic), mitral regurgitation, tricuspid regurgitation, and ventricular septal defect

Splitting of S2 heart sounds

-Nite that right sided cardiac event happen slightly after and slightly softer than left sided bc of pressure differences. -This is what causes the the s2 split, as right sided closure of pulmonic can happen later than the aortic. A2 happens before P2 -Inspiration exaggerates split bc inhaling increases filling time of the right heart, making preexisting time difference btw closure even greater, or creating the split where you couldn't hear it before. -Walls of veins also contain less smooth muscle than the arteries, causing the venous system, and therefore right sided, pressure to be lower than the arterial and left sided circulation. This also contributes to later closure of P2 -During expiration the 2 components usually fuse to make the normal S2 -when auscultating fra split, A2 is going to be louder, and can be heard through the precordium, P2 is going to be heard best at the 2nd and 3rd left ICS close to the sternum, its here that you should search for any splitting

Blood Pressure Classification for Adults

-Normal: <120/<80 -Prehypertension: 120-139/80-89 -Hypertension Stage 1: *Age 18-60: 140-159/90-99 *Age 60+ : 150-159/90-99 -Hypertension stage 2: >160/>100 If renal disease/diabetes/age >60: <140/<90

S2 split

-Note that right-sided cardiac events usually occur slightly later than those on the left. -Instead of a hearing a single heart sound for S2, you may hear two discernible components, the first from left-sided aortic valve closure, or A2, and the second from right-sided closure of the pulmonic valve, or P2. -During inspira- tion, the right heart filling time is increased, which increases right ventricular stroke volume and the duration of right ventricular ejection compared with the neighboring left ventricle. This delays the closure of the pulmonic valve, P2, splitting S2 into its two audible components. During expiration, these two com- ponents fuse into a single sound, S2 -Of the two components of the S2, A2 is normally louder, reflecting the high pressure in the aorta. It is heard throughout the precordium. In contrast, P2 is relatively soft, reflecting the lower pressure in the pulmonary artery. -It is heard best in its own area, the 2nd and 3rd left interspaces close to the sternum. It is here that you should search for the splitting of S2.!!!!!!!

Identifying JVD

-One of most important/frequently used. JVP closely parallels pressure in the right atrium (Central venous pressure, related to blood volume in venous system). *****JVP accurately predicts the elevations in fluid volum in heart failure, but prognostic value is unclear -Best measured using the pulsation of the right internal jugular, which is directly in light with right atrium/Vena cava. Right external may also be used, but not s direct to heart/sup VC. This test is also not useful for kids under 12, as the pulsation is not usually visible -pressure changes in the right atrialdue to filling, contracting, and emptying is visible and named by wave forms. Most visible wave form is the downward motion of X. This inward movement is the way to distinguish the jugular from the carotid (which has an outward dominance). -Observing JV pulsation can tell you about the volume status, right and left ventricular functioning, latency of tricuspid and pulmonary valves, pressure in the precordium and arrhythmia caused by junction along rhythms and AV blocks ****Ex. JVP falls with loss of blood or decreased venous vascular tone an increases with right and left heart failure , pulm hypertension, tricuspid stenosis, AV dissociation, increased venous vascular tone, and pericardial compression/tamponade

Jugular venous pulsations (Waves)

-Oscillations in the right internal jugular vein, and often in the external jugular vein, reflect changing pressures in the right atrium. Careful inspection of these waveforms reveals two quick peaks and two troughs. Considerable practice and experience are required to discern these fluctuations. ■ The first elevation, the presystolic a wave, reflects the slight rise in atrial pressure that accompanies atrial contraction. It occurs just prior to S1 and before the carotid upstroke. ■ The following trough, the x descent, starts with atrial relaxation. It continues as the RV, contracting during systole, pulls the floor of the atrium downward, and ends just before S2. 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 pas- sively into the RV, and right atrial pressure falls again, creating the second trough, or y descent. *****A simplified way to remember the three peaks is: a for atrial contraction, c for carotid transmission (although this may represent closure of the tricuspid Valve) and v for venous filling. -To the naked eye, the two descents, x and y, are the most visible events in the cycle of atrial contraction, atrial re- laxation, atrial filling, and atrial emptying again followed by atrial contrac- tion. Of the two, the sudden collapse of the x descent late in systole is more prominent, occurring just before S2. The y descent follows S2 early in diastole. -Observe the amplitude and timing of the jugular venous pulsations. To time them, feel the left carotid artery with your right thumb or listen to the heart simultaneously. The a wave just precedes S1 and the carotid pulse, the x descent can be seen as a systolic collapse, the v wave almost coincides with S2, and the y descent follows early in diastole. Look for absent or unusually prominent waves.

Percussion of heart

-Palpation has replaced percussion for determining heart size, but if you cant palpate the PMI, percussion my be your only option, but it really has limited correlation to actual size -Starting well to the left of the heart, palpate down to the 3rd, 4th, 5th, and possibly 6th interspaces ****A markedly dilated failing heart may have a hypokinetic apical impulse displaces the heart to the left. A large pericardial effusion may make the impulse undetectable

Dyslipidemia CVD Risk Factor

-Persons with clinical atherosclerotic CVD include "those with an acute coronary syndrome and those with a history of MI, stable or unstable, angina, coronary of other arterial revascular- ization, or stroke, transient ischemic attack, or peripheral arterial disease ... of atherosclerotic origin. -Use the CVD risk calculators to establish 10-year risk. -Recommendations for beginning statins: ■ For patients with clinical CVD (secondary prevention) or LDL cholesterol levels >190 mg/dL (primary prevention)—prescribe high-intensity statin therapy. ■ For patients with diabetes and/or LDL cholesterol levels from 70 to 189mg/ dL—determine the 10-year risk of atherosclerotic CVD with the new risk calculator (see above). Although the evidence for initiating statins for pri- mary prevention is stronger for adults with 10-year risks above 7.5%, statins can also be considered for risk levels between 5% and <7.5%.

Cardiac exam

-Positioning the Patient. *Supine, with the head elevated 30°: After examining the JVP and carotid pulse, inspect and palpate the precordium: the 2nd right and left interspaces; the RV; and the LV, including the apical impulse (diameter, location, amplitude, duration). *Left lateral decubitus: Palpate the apical impulse to assess its diameter. Lis- ten at the apex with the bell of the stethoscope. ****Low-pitched extra sounds such as an S3, opening snap, diastolic rumble of mitral stenosis *Supine, with the head elevated 30°: Listen at the 2nd right and left interspaces, down the left sternal border to the 4th and 5th interspaces, and across to the apex the six listening areas with the diaphragm, then the bell. As indicated, listen at the lower right sternal border for right-sided murmurs and sounds, often accentuated with inspiration, with the diaphragm and bell. *Sitting, leaning forward, after full exhalation: Listen down the left sternal border and at the apex with the diaphragm. ******Soft decrescendo higher-pitched diastolic murmur of aortic regurgitation

Leaning forward position

-Primarily for hearing aortic regurgitation (Crescendo-decrescendo) -Have patient sit up, lean forward, exhale completely and hold -Use the DIAPHRAGM to listen along the left sternal border and at the apex

JV pressure/pulsations

-Reflects the right atrial pressure, which then equals the central venous pressure, and right ventricular end-diastolic pressure -Best estimated from the right internal jugular which has most direct contact with the right atrium. (Remember that the JV lies deep to the sternonucleo muscle, so you more watch more the transmitted pulsation than see the actual jugular) -Jugular venous pulsation: caused by Changes pressures in the right atrium during diastole ad systole which produces the emptying/filling of the pulsation seen on the skin * Atria contraction: produces alpha wave in jugular just before systole/S1 * Atrial relaxation: calls x wave, little descent of the jugular (after the a wave) * Right ventricular systole: causes v wave (another elevation) *Blood passively empties into the RV during early and middle diastole: thee y wave (is another descent)

Screening for CVD

-Responsible for 1 in 3 deaths, primary and secondary prevention both very important -Health promo, Need to: *Understand epidemiological data for CVD *ID modifiable cardiovascular risk factors *help patient reduce risks w behavior/lifestyle changes & pharm tx -Early screening also important bc heart disease has a long asymptomatic latent period, begin screening as early as 20 years -The absence of clinically manifest CVD and the simultaneous presence of optimal levels of seven health metrics, including four health behaviors (lean body mass index <25 kg/m2, not smoking, being physically active, and fol- lowing a healthy diet), and three health factors (untreated total cholesterol <200 mg/dL, untreated blood pressure <120/<80 mm Hg, and fasting blood glucose <100 mg/dL). ****Approximately 13% of U.S. adults meet five or more criteria, 5% meet six or more criteria, and virtually none meet seven criteria at ideal level -Steps: Step 1: Screen for Global Risk Factors. Step 2: Calculate 10-Year and Lifetime CVD Risk Using an Online Calculator. Step 3: Track Individual Risk Factors—Hypertension, Diabetes, Dyslipidemias, Metabolic Syndrome, Smoking, Family History, and Obesity

Pulses alternans

-Rhythm of the pulse remains regular, but the force of the arterial pulse alternates bc of alternating strong and weak vent contractions -Almost always indicates severe left vent dysfunction -usually besT felt by applying light pressure on the Randal or femoral arteries, use BP cuff to confirm finding, and when deflating lower to just below the systolic, will hear the strong systolic beats and then the softer diastolic, will start to hear alternating beats of loud and soft or a sudden doubling of the pulse as the pressure declines ***** Placing patient in upright position may accentuate sounds

Other Risk Factors fo CVD: Smoking, Family History, and Obesity.

-Risk factors such as smoking, family history, and obesity contribute substantially to the population of CVD -Smoking increases the risk of CHD and stroke by two- to fourfold compared to nonsmokers or past smokers who quit >10 years previ- ously. -Among adults, 13% report a family his- tory of heart attack or angina before age 50 years. -Obesity, or BMI over 30 kg/m , contributed to 112,000 excess adult deaths compared to those of normal weight, and was associated with 13% of CVD deaths in 2004.

Splitting of S1

-SPLITTING DOESNT VARY WITH INSPIRATION -Mitral sound is louder and happens first, tricuspid is softer and happens slightly slower sometimes, causing the split. Again, this is bc of varying pressures on the right and left sides. -The mitral sound is heard throughout the precordium and is best heard at the apex -Tricuspid sound is best heard at the lower left sternal borders, and it is hear that you would hear splitting bc sound isn't overshadowed by the mitral sound

Diastolic Murmurs

-Susually represent valvular heart disease -May be early systolic, mid, or late -Early decrescendo diastolic usually represent regurgitant flow across incompetent semilunar valves -Mid and late diastolic "rumbling" represents turbulent flow over the AV valves -Less common than systolic -Murmurs include: Aortic regurgitation, mitral stenosis

systole and diastole

-Systole is the period of ventricular contraction. Normally, maximal left ventricular pressure corresponds to systolic blood pressure. *pressure in the left ventricle rises. Ventricle ejects much of its blood into the aorta, the pressure levels off and starts to fall *Diastole is the period of ventricular relaxation. Ventricular pressure falls further to below 5 mm Hg, and blood flows from atrium to ventricle. Late in diastole, ventricular pressure rises slightly during inflow of blood from atrial contraction. -S1 and S2 define the duration of systole and diastole. Closure of the mitral valve produces the first heart sound, S1. Aortic valve closure produces the second heart sound, S2. -Right heart sounds occur at pressures that are usually lower than those on the left, and are usually less audible. They also happen slightly later bc of the lowered pressure

Left sternal border in the 3rd, 4th, or 5th interspace

-THIS IS HOW YOU FEEL THE RV AREA -With patient at 30 degrees ask patient to exhale and briefly stop breathing, the place the tips of your curved fingers into the left 3rd, 4th, and 5th interspaces to palpate for th systolic pulse of the right ventricle -If there is an impulse, record the location, amplitude, and location. In really thin people may feel a little tap, especially when they're anxious ****A sustainedleft parasternal movement beginning at S1 points to pressure overload from pulmonary hypertension and pulmonic stenosis or the chronic ventricular overload of an atrial septal defect. A sustained movement later in systole can be seen in mitral regurg -In patient with increased AP diameter, ask patient to inhale and hold breath and palpate at the epigastric or subxiphoid area for the RV, with hand flattened, press index finger just under the rib cage and up toward the left shoulder ****This might be the case in COPD bc hyperinflation of the lungs may prevent palpation of a hypertrophied RV in th left preternatural area, they can be palpated high in the epigastrum instead

Palpating The Apical impulse (Left vent area)

-The Apical Impulse or Point of Maximal Impulse. *The apical impulse represents the brief early pulsation of the left ventricle as it moves anteriorly during contraction and contacts the chest wall. In most examinations the apical impulse is the PMI; however, pathologic conditions such as right ventricular hypertrophy, a dilated pulmonary artery, or an aortic aneurysm may produce a pulsation that is more prominent than the apex beat. *****In dextrocardia, a rare congenital transposition of the heart, the heart is situated in the right chest cavity and generates a right-sided apical impulse. Use percussion to help locate the heart border, the liver, and stomach. In full situs inversus, the heart, trilobed lung, stomach, and spleen are on the right, and the liver and gallbladder are on the left. -If you cannot identify the apical impulse with the patient supine, ask the patient to roll partly onto the left side into the left lateral decubitus position. Palpate again, using the palmar surfaces of several fingers. If you cannot find the apical impulse, ask the patient to exhale fully and stop breathing for a few seconds. When examining a woman, it may be helpful to displace the left breast upward or laterally as necessary, or ask her to do this for you. *****The apex beat is palpable in 25% to 40% of adults in the supine position and in 50% to 73% of adults in the left lateral decubitus position, especially those who are thin. Obesity, very muscular chest wall, or an increased AP diameter of the chest may obscure detection. -Now assess the location, diameter, amplitude, and duration of the apical impulse. You may wish to have the patient breathe out and briefly stop breathing to check your findings.

Valsalva maneuver

-The normal systolic blood pressure response follows four phases: (1) tran- sient increase during onset of the "strain" phase when the patient bears down, due to increased intrathoracic pressure; (2) sharp decrease to below baseline as the "strain" phase is maintained, due to decreased venous return; (3) further acute drop of both blood pressure and left ventricular volume during the "release" phase, due to decreased intrathoracic pressure; and (4) "overshoot" increased blood pressure, due to reflex sympathetic activation and increased stroke volume. -To distinguish the murmur of hypertrophic cardiomyopathy, ask the supine patient to "bear down, like straining during a bowel movement." Alternatively, place one hand on the patient's midabdomen and ask the patient to strain against it. With your other hand, place your stethoscope on the patient's chest and listen at the lower left sternal border. ******The murmur of hypertrophic cardiomy- opathy is the only systolic murmur that increases during the "strain phase" of the Valsalva maneuver due to increased outflow tract obstruction -The Valsalva maneuver can also identify heart failure and pulmonary hyperten- sion. Inflate the blood pressure cuff to 15 mm Hg greater than the systolic blood pressure and ask the patient to perform the Valsalva maneuver for 10 seconds, then resume normal respiration. Keep the cuff pressure locked at 15 mm Hg above the baseline systolic pressure during the entire maneuver and for 30 seconds afterward. Listen for Korotkoff sounds over the brachial artery throughout. Typically, only phases 2 and 4 are significant, since phases 1 and 3 are too short for clinical detection. In healthy patients, phase 2, the "strain" phase, is silent; Korotkoff sounds are heard after straining is released during phase 4. *****In patients with severe heart failure, blood pressure remains elevated and there are Korotkoff sounds during the phase 2 strain phase, but not during phase 4 release, termed "the square wave" response. This response is highly correlated with volume overload and elevated left ventricular end-diastolic pressure and pulmonary capillary wedge pressure, in some studies outperforms brain neuropeptide

Auscultation of heart (general)

-The outlined areas are not always were murmurs from those valves are best heard. In patients with cardiac dilatation/hypertrophy/anomalies of great vessels, and dextrocardia, these areas wont apply either -6 spots: APTM 22345 -Use the diaphragm to ascultate high pitched sounds like S1, S2, the murmurs of aortic and mitral regurgitation, andpericardial friction rubs, midsystolic clicks, ejection sounds, and OS, Listen throughout precordium with diaphragm with pressure -Use the bell to ascultate low pitched sounds like S3, 4, murmur of mitral stenosis. Listen w bell around PMI and along lower left sternal border

Large bounding pulses

-The pulse pressure is increased, and the pulse feels strong and bounding. The rise and fall may feel rapid, the peak brief. Causes include (1) increased stroke volume, decreased peripheral resistance, or both, as in fever, anemia, hyperthyroidism, aortic regurgitation, arteriovenous fistulas, and patent ductus arteriosus; (2) increased stroke volume because of slow heart rates, as in bradycardia and complete heart block; and (3) decreased compliance (increased stiffness) of the aortic walls, as in aging or atherosclerosis.

A 60-year-old woman with angina might have a harsh 3/6 midsystolic cre- scendo-decrescendo murmur in the right 2nd interspace radiating to the neck -What is this consistent with?

-These findings are consistent with aortic stenosis but could arise from aortic sclerosis (leaflets are scle- rotic but not stenotic), a dilated aorta, or increased flow across a normal valve. Assess any delay in the carotid upstroke and the intensity of A2 for evi- dence of aortic stenosis. Check the api- cal impulse for LVH. Listen for aortic regurgitation as the patient leans for- ward and exhales.

Right second interspace

-This is aortic area -Search for pulsations/palpable heart sounds ****Pulsations here suggest dilated or aneurysm all aorta. A palpable S2 can accompany systemic hypertension.

The Left second interspace

-This is the pulmonic area!!! -This interspace overlies the pulmonary artery -As the patient holds expiration, inspect and palpate for pulm artery pulsations/transmitted heart sounds ****Prominent pulsation here often accompanies dilation or increased flow in the pulm artery. Palpable S2 points to increased pulmonary artery pressure from pulmonary hypertension

Transient arterial occlusion

-Transient compression of both arms by bilateral blood pressure cuff inflation to 20 mm Hg greater than peak systolic blood pressure augments the murmurs of mitral regurgitation, aortic regurgitation, and Ventricular septal defect

Syncope

-Transient loss of consciousness followed by recovery -MCC I neurocardiogenic (includes vasovagal)

Palpitations

-Unpleasant awareness of heartbeat -Patient may describe as skipping, fluttering, pounding, or stopping of the heart -May be irregular, rapidly slow/accelerate, or come from increased forcefulness of cardiac contraction -Common in anxious/hyperthyroidism, do not always mean heart disease (ex. Most sirs dysrythmias, like V tach do not have palpitations) -can have patient show the beat by tapping it out, also ask how long it lasted, if there was any sudden acceleration/deceleration, sudden start/stop, regular or irregular, etc. -ECG may be indicated ****Clues in history may include: transient skips and flip flops (possible premature contraction), rapid regular beating of sudden onse/offset (possible paroxysmal superventricular tach), and a rapid regular rate of <120, especially if starting and stopping (possibly sinus tach)

Left lateral decubitus

-Used to hear mitral stenosis, or to exaggerate S3/4 (Mitral stenosis is the major one though), listen with the bell at the apical impulse -Brings the left ventricle closer to the chest wall

Special populations at risk for CVD

-Women *Leading cause of death for women *Increased rates blamed on obesity, Men and women still get diabetes in equal amounts *>65 women have more hypertension and is less controlled *2/33rdsof American women are overweight/obese *Have a higher lifetime risk of stroke than men *Women have unique risk factors for stroke: pregnancy, hormone therapy, early menopause, and preeclampsia. Women are more likely than men to have risk factors of atrial fibrillation, migraine with aura, obesity, and metabolic syndrome. Atrial fibrillation, which increases stroke risk fivefold in women, is often asymptomatic and undetected. -African Americans: *The high prevalence of high cholesterol, obesity, and diabetes in Mexican Americans places them at similar risk to blacks. *While the prevalence of hypertension is similar between men and women, prevalence in blacks is substantially higher than in whites.

Diabetes and CVD

-dramatic increase in obesity coupled with physical inactivity has created an epidemic of diabetes. -There are striking disparities in the age-adjusted diabetes prevalences among adults: 7% to 9% of whites and Asian Americans compared to ∼13% of Hispanics and blacks, rising to 16% of American Indian/Alaska Natives. -only 25% of those affected are treated and controlled, and diabetes is associated with a two-fold increased risk of CVD

S1 split

-earlier mitral and a later tricuspid sound. -The mitral sound—the principal component of S1—is much louder, again reflecting the higher pressures on the left side of the heart. -mitral S1 can be heard throughout the precordium and is loudest at the cardiac apex!!!!!!! -softer tricuspid component is heard best at the lower left sternal border; it is here that you may hear a split S1!!!!!! -The earlier louder mitral component may mask the tricuspid sound, however, and splitting is not always detectable. Splitting of S1 does not vary with respiration.

Murmur Right 2nd interspace to the apex

Aortic valve murmur

Cardiac pumping terms

Cardiac output: volume of blood ejected from each ventricle during 1 minute. product of heart rate and stroke volume. Stroke volume: (the volume of blood ejected with each heartbeat) depends in turn on preload, myocardial contractility, and afterload.

Murmur at and around the cardiac apex

Mitral valve

Preload

Preload refers to the load that stretches the cardiac muscle before contraction. The volume of blood in the RV at the end of diastole constitutes its preload for the next beat -Right vent preload is increased by increasing venous return to the right heart, this may be caused by increased flow in inspiration or during exercise -Can have path causes too: Increase in load from dilated right ventricle in heart failure -Causes of lessened right ventricular preload: exhalation, decreased left vent output, and pooling ofblood in capillary bed/venous system ****Pathology increases preload and afterload (called volume and pressure overload), and produces changes in vascular functioning including changes in ventricular impulses (detectable by palpation), and in normal n=heat sounds. May develop murmurs and pathological hearty sounds

Murmur at Left 2nd and 3rd interspaces close to the sternum, but also at higher or lower levels

Pulmonic valve

Auscultation sounds

S1: Note its intensity and any apparent splitting. Normal splitting is detectable along the lower left sternal border. S2: Note it's intensity Split S2: Listen for splitting of this sound in the 2nd and 3rd left interspaces. Ask the patient to breathe quietly, and then slightly more deeply than normal. Does S2 split into its two components, as it normally does? If not, ask the patient to (1) breathe a little more deeply, or (2) sit up. Listen again. A thick chest wall may make the pulmonic component of S2 inaudible. *Width of split. How wide is the split? It is normally quite narrow. *Timing of split. When in the respiratory cycle do you hear the split? It is normally heard late in inspiration. *Does the split disappear as it should, during exhala- tion? If not, listen again with the patient sitting up. *Intensity of A2 and P2. Compare the intensity of the two components, A2 and P2; A2 is usually louder. *******When either A2 or P2 is absent, as in aortic or pulmonic valve disease, S2 is persistently single. *******Expiratory splitting suggests a valvu- lar abnormality *******Persistent splitting results from delayed closure of the pulmonic valve or early closure of the aortic valve. A loud P2 points to pulmonary hypertension. Extra Sounds in Systole: Such as ejection sounds or systolic clicks Note their location, timing, intensity, and pitch, and variations with respiration Extra Sounds in Diastole: Such as S3, S4, or an opening snap Note the location, timing, intensity, and pitch, and variations with respiration. An S3 or S4 in athletes is a normal finding. Systolic and Diastolic Murmurs: Murmurs are differentiated from S1, S2, and extra sounds by their longer duration. ****The systolic click of mitral valve pro- lapse is the most common extra sound.

Pulses Alternans

The pulse is completely regular, but has alternating strong and weak beats (unlike bigeminy). If there is only a slight difference between the strong and weak beats, detection requires use of a blood pressure cuff (see p. 381). Pulsus alternans indicates left ventricular failure and is usually accompanied by a left-sided S3.

Small weak pulses

The pulse pressure is diminished, and the pulse feels weak and small. The upstroke may feel slowed, the peak prolonged. Causes include (1) decreased stroke volume, as in heart failure, hypovolemia, and severe aortic stenosis; and (2) increased peripheral resistance, as in exposure to cold and severe heart failure.

Bigeminal pulse

This disorder may mimic pulsus alternans. A bigeminal pulse is caused by a normal beat alternating with a premature contraction. The stroke volume of the premature beat is diminished in relation to that of the normal beats, and the pulse varies in amplitude accordingly.

Murmur At or near the lower left sternal border

Tricuspid valve

Hearts conduction system

a group of special- ized cardiac cells located in the right atrium near the junction of the vena cava. The sinus node acts as the cardiac pacemaker and automatically discharges an impulse about 60 to 90 times a minute. This impulse travels through both atria to the AV node, a specialized group of cells located low in the atrial septum. Here, the impulse is delayed before passing down the bundle of His and its branches to the ventricular myocardium. Muscu- lar contraction follows: first the atria, then the ven- tricles. The normal conduction system is diagrammed

Assessment characteristics of Carotid pulse

● The amplitude of the pulse: This correlates reasonably well with the pulse pres- sure. ****The carotid pulse is small, thready, or weak in cardiogenic shock; the pulse is bounding in aortic regurgitation ● The contour of the pulse wave: namely the speed of the upstroke, the duration of its summit, and the speed of the downstroke. The normal upstroke is brisk; it is smooth, rapid, and follows S1 almost immediately. The summit is smooth, rounded, and roughly midsystolic. The downstroke is less abrupt than the upstroke. *****The carotid upstroke is delayed in aortic stenosis ● Any variations in amplitude, either from beat to beat or with respiration. *****Pulsus alternans and a bigeminal pulse vary beat to beat; a paradoxical pulse varies with respiration, described below. ● The timing of the carotid upstroke in relation to S1 and S2. Note that the normal carotid upstroke follows S1 and precedes S2. This relationship is very helpful in correctly identifying S1 and S2, especially when the heart rate is increased and the duration of diastole, normally longer than systole, is short- ened and approaches the duration of systole.

IDing heart murmurs

● Time the murmur—is it in systole or diastole? What is its duration? ● Locate where on the precordium the murmur is loudest—at the base, along the sternal border, at the apex? Does it radiate? ● Conduct any necessary maneuvers, such as having the patient lean forward and exhale or turn to the left lateral decubitus position. ● Determine the shape of the murmur—for example, is it crescendo or decre- scendo, is it holosystolic? ● Grade the intensity of the murmur from 1 to 6, and determine its pitch and quality. ● Identify associated features such as the quality of S1 and S2, the presence of extra sounds such as S3, S4, or an OS, or the presence of additional murmurs. ● Be sure you are listening in a quiet room!