Heart Sounds: S1 and Variations

Heart Sounds: S1 Sounds and Variations

• Accentuated S1 occurs when S1 is louder than S2
• The mitral valve is wide open and closes quickly
• Hyperkinetic states can cause accentuated S1 due to increased blood velocity from fever, anemia, or hyperthyroidism
• Mitral stenosis where leaflets are mobile, can result in accentuated S1 due to increased ventricular pressure being needed to close the valve
• Diminished S1 occurs when S1 is softer than S2
• The mitral valve is not fully open during ventricular contraction and valve closing
• Delayed conduction, as in a first-degree heart block, allows the mitral valve to drift closed before ventricular contraction closes it; this can cause diminished S1
• Mitral insufficiency from extreme calcification may result in diminished S1
• Delayed or diminished ventricular contraction also causes diminished S1
• Split S1 occurs when S1 splits
• The left and right ventricles contract at different times during asynchronous ventricular contractions
• Split S1 may become softer with inspiration and is normal in children, young adults, and pregnant women
• Conduction delays cardiac impulse, in bundle branch block can cause Split S1
• Ventricular ectopy, where the impulse starts in one ventricle and spreads to the second, can cause Split S1
• Varying S1 occurs when the mitral valve is in different positions when contraction occurs
• Rhythms with independently beating atria and ventricles can cause Varying S1
• Totally irregular rhythms such as atrial fibrillation can cause Varying S1

Heart Sounds: S2 Sounds and Variations

• A split S2, referred to as A2 and P2, results from delayed closure of the pulmonic valve during inspiration.
• S2 is normally a crisp, distinct sound
• Accentuated S2 occurs when S2 is louder than S1
• It occurs if the aortic or pulmonic valve has a higher closing pressure
• Increased pressure in the aorta from exercise or excitement
• Booming S2 is heard in systemic hypertension
• Increased pressure in the pulmonary vasculature due to mitral stenosis or congestive heart failure
• Calcification of the semilunar valve
• Diminished S2 occurs when S2 is softer than S1
• It occurs if the aortic or pulmonic valve have decreased mobility
• Still mobile as in pulmonic or aortic stenosis
• Decreased systemic blood pressure weakens the valves, such as in shock
• Aortic or pulmonic stenosis, where the valves are thickened and calcified, causes diminished S2
• Normal Physiologic Split S2 is best heard over the second or third left intercostal space
• is heard only during inspiration
• disappears during expiration in adults
• Splitting that does not disappear during expiration is suggestive of heart disease
• Wide Split S2 involves an increased splitting that persists throughout the respiratory cycle and widens on expiration
• It occurs in delayed electrical activation of the right ventricle
• Right bundle branch block delays pulmonic valve closing
• Fixed Split S2 is wide splitting that does not vary with respiration
• It occurs with delayed closure in one or both valves
• An atrial septal defect or right ventricular failure delays pulmonic valve closure
• Reversed Split S2, known as a paradoxical split, appears on expiration and disappears on inspiration
• It occurs when aortic valve closure is abnormally delayed, causing A2 to follow P2 in expiration
• A left bundle branch block can cause this
• Accentuated A2 is loud over the right second intercostal space
• Increased pressure as in systemic hypertension
• Aortic root dilation due to the closer position of the aortic valve to the chest wall
• Diminished A2 is soft or absent over the right second intercostal space
• Immobility of the aortic valve in calcific aortic stenosis
• Accentuated P2 appears has P2 louder than or equal to A2
• A wide split S2 is heard at the apex, indicating accentuated P2
• Pulmonary hypertension, dilated pulmonary artery, and atrial septal defect
• Diminished P2 occurs when P2 is soft or absent
• Increased anteroposterior diameter of the chest (barrel chest)
• Aging, pulmonic stenosis, or COPD

Jugular Venous Pressure

• A Wave: Rise in atrial pressure during atrial contraction
• X Descent: Right atrial relaxation and descent of atrial floor during ventricular systole
• V Wave: Right atrial filling, increased volume, increased pressure
• Y Descent: Right atrial emptying into right ventricle, decreased atrial pressure

Heart and Vascular Abnormalities: Definitions

• Chest Pain
• Caused by cardiac, pulmonary, muscular, or GI origin
• Angina manifests as squeezing, steady, severe pain with pressure around the heart
• Angina pain may radiate to the left shoulder, down the left arm, or to the jaw
• Angina accompanied by diaphoresis and worsened by activity indicates angina
• Palpitations
• Caused by abnormalities in the heart’s conduction system or attempts to increase cardiac output
• May cause anxiety
• Fatigue
• Results from compromised cardiac output
• Worsens in the evening as the day progresses when related to decreased cardiac output
• Dyspnea
• Results from congestive heart failure, pulmonary disorders, coronary artery disease, myocardial ischemia, and myocardial infarction
• May occur at rest, during sleep, or with varying degrees of exertion
• Nocturia
• Related to heart failure and hypertension which lead to fluid retention and altered kidney function
• Increasein renal perfusion during periods of rest of recumbency
• Decreased frequency may be related to decreased CO
• Dizziness
• Caused by decreased blood flow to the brain due to myocardial damage
• Other factors: inner ear syndromes, decreased cerebral circulation, and hypotension
• Increases fall risk
• Edema
• Occurs as a result of heart failure
• Congenital or Acquired Defects affect the heart’s ability to pump and decrease oxygen supply to the tissues
• Rheumatic Fever
• Precursor for rheumatic carditis, which occurs in at least 40% of patients
• Rheumatic carditis results from group A beta-hemolytic streptococci exposure
• Inflammation of all heart layers leads to impaired contraction and valvular function
• Previous Heart Surgery may alter heart sounds
• Surgery and cardiac balloon interventions indicate prior cardiac compromise
• Dyslipidemia
• Greatest risk factor for coronary artery disease
• Elevated cholesterol linked to atherosclerosis
• Jugular Vein Distension (JVD) indicates increased central venous pressure
• May be caused by right ventricular failure, pulmonary hypertension, pulmonary emboli, or cardiac tamponade
• COPD clients: JVD only during expiration
• Clients with severe constrictive pericarditis: inspiratory increase in venous pressure (Kussmaul’s sign)
• Bruit is a blowing or swishing sound from turbulent blood flow in a narrowed vessel
• Indicates occlusive arterial disease
• Bruit cannot be heard with ⅔ occlusion
• Pulse Irregularity can indicate arterial constriction or occlusion in one carotid artery if there is Inequality
• Weak pulse: hypovolemia, shock, or decreased cardiac output
• Bounding or Firm pulse: hypervolemia or increased cardiac output
• Delayed upstroke indicates aortic stenosis
• Variations in strength from beat to beat or with respiration
• Thrills may indicate narrowing of the artery, severe aortic stenosis, systemic hypertension, pulmonic stenosis and pulmonic hypertension in the second to third left intercostal space
• Loss of elasticity indicates arteriosclerosis
• Feels similar to a purring cat/pulsation in 3 anatomical areas other than the mitral area is usually associated with a grade IV or higher murmur
• Lift/Heaves/Pulsations are abnormal when not at the apical pulsation
• May result from an enlarged ventricle due to overload due to right ventricular hypertrophy caused by valvular disease, pulmonic hypertension or chronic lung disease
• Diffuse lifting left during systole at the left lower sternal border
• No Apical Impulse may be impossible to palpate with pulmonary emphysema
• Accentuated Apical Impulse is a sign of pressure overload
• There is increased force and duration
• Commonly associated with aortic stenosis or systemic hypertension
• Displaced Apical Impulse
• If the apical impulse is >1-2 cm, displaced, more forceful, or of longer duration, suspect cardiac enlargement
• Volume overload and/or ventricular hypertrophy and dilatation associated with mitral regurgitation, aortic regurgitation, or left-to-right shunts
• Bradycardia & Tachycardia
• Bradycardia is considered values under 60 bpm, Tachycardia is defined as values over 100bpm
• May result in decreased cardiac output
• Irregular rhythms, such as premature atrial or ventricular contractions, atrial fibrillation, atrial flutter with varying block, should be further evaluated
• May predispose the client to decreased cardiac output, heart failure, or emboli
• Pulse Deficit is the difference between apical and peripheral/radial pulses
• May indicate atrial fibrillation, atrial flutter, premature ventricular contractions, and varying degrees of heart block
• Ejection Sounds or Clicks (during Systole)
• High-frequency sounds heard just after S1 due to a functioning but diseased valve
• A mid-systolic click is associated with mitral valve prolapse
• Aortic Ejection Click is heard during systole at the second right intercostal
• Occurs with the opening of the aortic valve and does not change with respiration
• Pulmonic Ejection Click is heard at the second left intercostal
• Becomes softer with inspiration
• Midsystolic Click is heard in middle or late systole
• It can be heard over the mitral or apical area
• It is the result of mitral valve leaflet prolapse during left ventricular emptying, A late systolic murmur typically indicates mild mitral regurgitation
• Opening Snap
• Occurs early in diastole
• Heard with the opening of a stenotic or stiff mitral valve
• It is heard throughout the whole precordium and does not vary with respirations
• Has a higher pitch than S3 and mistaken for a split S2 or S3
• Pathologic S3 (Ventricular Gallop) is heard toward the left side of the precordium, may be revealed when the client assumes the left lateral position
• Result of vibrations caused by blood hitting the ventricular wall during rapid ventricular filling
• Associated with coronary artery disease, hypertensive heart disease, cardiomyopathy, aortic stenosis, myocardial failure, volume overload of ventricle - may be earliest sign of heart failure
• Auscultated in children but disappears upon standing or sitting up, people with high cardiac output and in women in third trimester of pregnancy is considered normal
• Rhythm of the word “Kentucky”
• Pathologic S4 (Atrial Gallop) is heard toward the right side of the precordium
• Noncompliance during atrial contraction, heard late in diastole before S1
• Result of vibrations from blood flowing rapidly into the ventricles after atrial contraction
• May be caused by coronary artery disease, pulmonary hypertension, aortic and pulmonic stenosis, AMI
• May be revealed when the client assumes the left lateral position
• NORMAL: Trained athletes, older clients after exercise
• Rhythm of the word "Tennessee"
• Summation Gallop creates a quadruple rhythm
• Opening snaps occur early in diastole and indicate mitral valve stenosis
• Diastolic filling time is shortened, moving S3 and S4 closer together, resulting in one prolonger sound
• Associated with severe congestive heart disease
• Cardiomyopathy includes forceful or stronger pulsations in the mitral area, cardiac enlargement
• Friction Rub is heard during the systolic pause
• May also be heard during the diastolic pause
• Can be caused by inflammation of the pericardial sac
• High-pitched, scratchy, scraping sound which may increase with exhalation and when patient leans forward
• 3 components: Atrial systole, ventricular systole, ventricular diastole
• Commonly heard during the first week after a myocardial infarction
• Patent Ductus Arteriosus is a congenital anomaly that leaves an open channel between the aorta and pulmonary artery
• Classified as a continuous murmur, it is heard in both systole and diastole; loudest in late systole, obscures S2
• Medium pitch and harsh, machinery-like sound
• Venous Hum is common in children and is a benign sound caused by turbulence of blood in JV
• Low-pitched sound, described as humming or roaring continuous murmur, loudest in late diastole
• Abnormal Heart Rhythms
• Premature Atrial or Junctional Contractions: Beats occur earlier than the next expected beat are followed by a pause and rhythm resumes with the next beat
• Premature Ventricular Contractions: Beats occur earlier than the next expected beat, followed by a pulse; thythm resumes with the next beat
• Sinus Arrhythmia: Heart Rate speeds up and slows down in a cycle, becoming faster with inhalation and slower with expiration
• Atrial Fibrillation and Atrial Flutter with Varying Ventricular Response: Ventricular contraction occurs irregularly with short runs of irregular rhythm possibly appearing regularly
• Arterial Pulse and Pressure Waves
• Anacrotic Limb: Initial upstroke that occurs as blood is rapidly ejected from the ventricle through the open aortic valve into the aorta
• Systolic Peak: Anacrotic limb ends here, the waveform’s highest point
• Dicrotic Limb: Falling arterial pressure as blood travels into peripheral vessels and the waveform turns downward
• Dicrotic Notch: Ventricular pressure is less than in the aortic root, resulting in aortic valve closure and a small notch
• End Diastole: Lowest point and closing of the aortic notch, the beginning of diastole
• Heart Murmurs -- Midsystolic Murmurs
  • Innocent Murmur -Not associated with any physical abnormality -Occurs when ejection of blood into the aorta is turbulent -In children and young adults, and older adults with no evidence of CVD is common -Usually disappears when the patient sits
  • Physiologic Murmur -Caused by temporary increase in blood flow -Can occur with anemia, pregnancy, fever, and hyperthyroidism
  • Pulmonic Stenosis -Results from impeded flow across the pulmonic valve and increased right ventricular afterload -A congenital anomaly in children
  • Aortic Stenosis -May be mimicked by atrial septal and there are pathologic changes in flow across the valve -Stenosis of aortic valve impedes blood flow across the valve and increases left ventricular afterload -Can result from congenital anomaly, rheumatic disease, or a degenerative process -Aortic sclerosis, bicuspid aortic valve, a dilated aorta, or a mimicking condition such as aortic regurgitation may mimic this sound
  • Hypertrophic Cardiomyopathy -Unusual rapid ejection of blood from the left ventricle during systole -Results from massive hypertrophy of ventricular muscle with coexisting obstruction to blood flow -Mitral regurgitation may happen if there is accompanying distortion of the mitral valve -- Pansystolic Murmurs (occurs the whole duration of ventricular systole)
  • Mitral Regurgitation -Mitral valve fails to close fully in systole -Blood moves from the left ventricle into the left atrium -Volume overload occurs causing dilatation and hypertrophy -Heard best in the left lateral decubitus position, does not become louder with inspiration
  • Tricuspid Regurgitation -Blood flows from the right ventricle back to the right atrium during tricuspid valve malfunction or failure to completely close -Commonly caused by right ventricular failure with dilatation secondary to pulmonary hypertension or left ventricular failure -Right ventricular impulse is prolonged; evident JVD with S3 -May increase with respiration
  • Ventricular Septal Defect -Congenital anomaly causes blood to flow from the left ventricle to the right ventricle, through a hole in the septum -Loud murmur that obscures A2 -Increases with exercise -- Diastolic Murmurs (Early decrescendo: incompetent SL valve (aortic valve); Rumbling in mid- to late diastole: mitral valve) -Aortic Regurgitation -Leaflets of aortic valve fail to close -Blood flows from the aorta back into left ventricle which can cause LV volume overload -Possible Ejection Sound -Hold breath, exhale, and lean forwards while sitting -Mitral Stenosis -Diseased mitral valve -Thick and stiff -Loud during mid diastole

Peripheral Vascular System

Abnormalities and Definitions

• Chronic Arterial Occlusive Disease: Leg pain awakens client, marking an advanced stage of disease
• Diabetes: Lack of pain signals neuropathy in this abnormality
• Varicose Veins
• Hereditary
• Develop from increased venous pressure and pooling
• Risk factors: prolonged standing
• Distended, bulging, and tortuous appearance, varying by severity
• Common in the anterior lateral thigh and lower leg, the posterior lateral calf, or anus (hemorrhoids)
• Result from incompetent valves, weak vein walls, or obstruction above
• Peripheral Edema (Swelling)
• Results from obstructed lymphatic flow or venous insufficiency due to incompetent valves or decreased osmotic pressure
• May occur with deep vein thrombosis
• Reduces tissue perfusion and wound oxygenation if leg or foot ulcers are present
• Enlarged Lymph Nodes suggest possible local or systemic infection
• Lymphatic tissue loss occurs with aging, resulting in smaller, fewer nodes
• Impotence occurs with decreased blood flow or vessel occlusion
• Associated with aortoiliac occlusion
• Aortoiliac Occlusion (Leriche’s Syndrome) is characterized by a blockage/narrowing of the lower aorta, reducing pelvic/lower extremity blood flow
• Triad of claudication, impotence, and decreased femoral pulses
• Men may struggle to achieve or maintain an erection
• Deep Vein Thrombosis is a deep leg vein blood clot, typically developing in the lower leg or thigh

Additional DVT Information

• Thigh clots are more dangerous since they have increased potential to reach the lung
• Cause is unknown
• Indicated by a positive Homans’ sign (calf pain and tenderness)
• Risk factors: -- Conditions increasing blood clotting -- Low deep vein blood flow -- Cancer/vascular conditions -- Prolonged sitting -- Pregnancy (>6 weeks postpartum) -- Age (>60 yo) -- Overweight -- Oral contraceptives -- Hormone therapy -- Postmenopausal hormone replacement -- Central venous catheter
• Pharmaceutical interventions -- Cilostazol (Pletal): Increases blood flow -- Clopidogrel (Plavix): Increases blood flow -- Aspirin: Prevents blood clotting, used to reduce cardiovascular risks -- Pentoxifylline (Trental): Reduces blood viscosity, improving tissue blood flow and decreasing hypoxia -- Xenaderm (Trypsin): Topical medication that improves wound oxygenation through increase blood flow and healing promotion
• Post-Thrombotic Syndrome may result in tissue damage
• Lymphedema results from blocked lymphatic circulation
• May be caused by breast surgery
• Usually affects one extremity, causing induration and non-pitting edema
• May indicate venous obstruction
• Raynaud’s Disease is a vascular disorder caused by vasoconstriction or vasospasm of the fingers or toes
• Characterized by rapid color changes (pallor, cyanosis, redness), swelling, pain, numbness, tingling, burning, throbbing, coldness
• Commonly occurs bilaterally
• Capillary Refill Time >2 Seconds may suggest vasoconstriction, decreased cardiac output, shock, arterial occlusion, or hyperthermia
• Buerger’s Disease causes inflammation and blockages in small and medium-sized blood vessels, primarily in the hands and feet, leading to reduced blood flow and the potential for tissue damage and gangrene
• Risk factors include smoking or tobacco use
• Scleroderma may be indicated by decreased radial pulse
• Known as systemic sclerosis
• Diseases involving hardening and tightening of the skin
• Hyperkinetic State is indicated by increased radial pulse volume,4+ or bounding pulse
• Partial/Complete Arterial Occlusion is indicated by diminished (1+/2+) or absent pulse (0)
• Compartment Syndrome occurs by Compression of pulses by external sources
• Arteriosclerosis can be indicated by the lack of resilience or inelasticity of the artery wall
• Bilateral Edema is suggested by the absence of visible veins, tendons, or bony prominences
• Usually indicates systemic problems (e.g. congestive heart failure), local problems (e.g. abnormal or blocked lymph vessels) or prolonged sitting (orthostatic edema).
• Unilateral Edema
• Characterized by a 1 cm difference in measurement at the ankles, or a 2 cm difference at the calf, and a swollen extremity
• Usually caused by venous stasis due to insufficiency or an obstruction and may be caused by Lymphedema
• Muscular Atrophy is indicated by a difference in measurement between legs
• Usually from disuse due to stroke or from being in a cast for a prolonged time
• Superficial Vein Thrombophlebitis is marked by redness, thickening, and tenderness along the vein
• Inflammation of a superficial vein
• Stages of Lymphedema
• Stage 0 has no observable signs or symptoms
• Impaired, sub-clinical lymph drainage
• May be present over long periods prior to advancing
• Stage I presents with swelling
• Affected area pits with pressure
• Elevation relieves swelling
• Skin texture is smooth
• Spontaneously reversible -Stage II Skin: Skin is firmer, tighter/shinier -Pitting May or May Not Occur -Spontaneously Irreversible -Hair loss or nail changes may be experienced in an affected extremity -Assistance is needed to reduce edema
• Stage III -Irreversible -Skin Folds Develop -Potenital risk of cellulitis, infections, or ulcerations -An affected area may ooze fluid -An affected area is non pitting with a permanent eczema -Skin is firm and thick -Hyperkeratosis, fat deposits, and acanthosis are present
• Arterial and Venous Insufficiency
• Arterial Insufficiency: Cold, pale, and clammy skin, Thin/shiny skin with loss of lower leg hair, ulcers is usually painful at the tips of toes, toe webs, heel, or outer pressure points
• Venous Insufficiency: Warm with Brown Pigmentation warm skin, achey in lower leg or medial ankle.
• ABI
• 1-1.2 is normal
• 0.8 - 1.0 Mild Insufficiency
• 0.5 - 0.8 -Moderate insuffiency
• Less than 0.5 Severe Insuffiency -Less than 0.3 Limb Threatening
• Types of Edema
• Lymphedema -Nonpitting and blocked lump Vessels
• No skin ulceration or pigmentation
• Usually Bilateral -Chronic Venous Insufficiency -Usually Unilateral -Skin Ulceration and Pigmentation May Be Present

Assessment

• HA Honsoc Review
• Starts with assessment and IPPA format; IF ABDOMEN: IAPP
• Head to Neck Assessment: --Larger head is normal with infants or Paget's
• Acromegaly or microcephaly. -Marrasmus is sunken. -- Temporal Artery Should Be Non-Tender -- Palpability -- If there is the TMJ Presenting, If pressing could indicate to brady cardia -- Could Indicate a condition if TMJ is Limited TMJ ASSESSMENT -Smooth is Normal -No Clicking is normal -Neck Assessment -Should be able to move Normal .
• Lymph node assessment less then 1cm and more is abnormal
• Vocal Femitus on Thrax and Lungs Assessment Note: Fremitus is symmetric, if not possible
• if not possible to palpitate speaker to speak Lounder. NOTE: During inhalation, diaphragm goes down; During exhalation, diaphragm goes up