B4M1C4: Cardiovascular System Flashcards
What are the anatomical valve areas?
● Tricuspid valve
● Mitral valve
● Pulmonary valve
● Aortic valve
What is on the right half of sternum opposite the 4th ICS?
Tricuspid valve
What is on the left half of the sternum opposite 4th LCC (left Costal Cartilage)?
Mitral valve
What is on the Medial end of 3rd LCC (Left Costal Cartilage) and adjoining part of sternum?
Pulmonary valve
What is on the Left half of the sternum opposite the 3rd ICS?
Aortic valve
Where are the different heart sounds are best heard?
○ Mitral area - at and around the cardiac apex (over the apex of the left ventricles)
○ Tricuspid area - at or near the lower left sternal border (over the right ventricle)
○ Pulmonic area - 2nd and 3rd left interspaces close to the sternum (upward along the pulmonary areas)
○ Aortic area - 2nd right interspace (upward along the
aorta).
● It’s a low slightly prolonged “lub”, caused by vibration set up by the sudden closure of the mitral and tricuspid at the start of the ventricular systole.
● Normally heard over the entire precordium
● S1 is usually louder than S2 at the cardiac apex (left 5th ICS near the midclavicular line)
● It is usually fainter than S2 at the base of the heart.
● It marks the beginning of the ventricular systole.
First heart sound (S1)
● It’s a shorter, high-pitched “dup”, caused by vibrations associated with the closure of the aortic and pulmonary valves just after the end of ventricular systole.
● The aortic valve component (A2) precedes the pulmonic component (P2).
● A2 is best heard in the medial end of the 2nd right ICS while P2 is best heard in the medial end of the 2nd left ICS.
● It is usually louder than S1 at the base of the heart.
Second heart sound (S2)
Soft, low-pitched heard about one-third of the way through diastole in many normal young individuals. It coincides with the period of rapid ventricular filling and is probably due to vibrations set up by an in-rush of blood.
Third heart sound (S3)
Sometimes heard immediately before (S1) when atrial pressure is high.
It is due to ventricular filling and is rarely heard in normal adults.
Fourth heart sound (S4)
The atrial pressure changes are transmitted to the great veins, producing three characteristic waves in the record of Jugular pressure:
○ a wave
○ c wave
○ v wave
due to atrial systole
a wave
occurs when the ventricle begins to contract; caused partly by slight backflow of blood into the atria at the onset of ventricular contraction but mainly by bulging of the AV valve backward toward the atria because of increased pressure in the ventricle
c wave
occurs toward the end of ventricular contraction; it results from slow flow of blood into the atria from the veins while the AV valves are closed during ventricular contraction
v wave
What is characterized principally by deforming fibrotic valvular disease, particularly mitral stenosis, of which it is virtually the only cause?
Chronic rheumatic heart disease
What is the most common cause of heart disease in children in developing countries and is the major cause of mortality and morbidity in adults as well?
CHRONIC RHEUMATIC HEART DISEASE
CHRONIC RHEUMATIC HEART DISEASE most commonly affects what gender?
More commonly affects females, sometimes up to twice as frequently as males.
KEY PATHOLOGIC FEATURE OF CHRONIC RHEUMATIC HEART DISEASE
● Organization of the acute inflammation and subsequent deforming fibrosis, particularly the valvular leaflets become thickened and retracted, causing permanent deformity.
● The mitral valve is virtually always deformed.
● The cardinal anatomic changes of the mitral (or tricuspid) valve are leaflet thickening; commissural fusion; and shortening, thickening, and fusion of the tendinous cords.
● Microscopically, there is diffuse fibrosis, and often neovascularization that obliterates the originally layered and avascular leaflet architecture. Aschoff bodies are replaced by fibrosis scars.
Valve lesions and etiologies:
Mitral stenosis
Rheumatic fever
Congenital
Severe mitral annular calcification
SLE, RA
Mitral regurgitation
Acute
Endocarditis
Papillary muscle rupture (post-MI)
Trauma
Chordal rupture/leaflet flail (MVP, IE)
Chronic
Myxomatous (MVP)
Rheumatic fever
Endocarditis (healed)
Mitral annular calcification
Congenital (cleft, AV canal)
HOCM with SAM
Ischemic (LV remodeling)
Dilated cardiomyopathy
Radiation
Aortic stenosis
Congenital (bicuspid, unicuspid)
Degenerative calcification
Rheumatic fever
Radiation
Aortic regurgitation
Valvular
Congenital (bicuspid)
Endocarditis
Rheumatic fever
Myxomatous (prolapse)
Traumatic
Syphilis
Ankylosing spondylitis
Root disease
Aortic dissection
Cystic medial degeneration
Marfan’s syndrome
Bicuspid aortic valve
Nonsyndromic familial aneurysm
Aortitis
Hypertension
Tricuspid stenosis
Rheumatic
Congenital
Tricuspid regurgitation
Primary
Rheumatic
Endocarditis
Myxomatous (TVP)
Carcinoid
Radiation
Congenital (Ebstein’s)
Trauma
Papillary muscle injury (post-MI)
Secondary
RV and tricuspid annular dilatation
Multiple causes of RV enlargement
(e.g., long-standing pulmonary HTN)
Chronic RV apical pacing
Pulmonic stenosis
Valve disease
Congenital
Postvalvotomy
Endocarditis
Annular enlargement
Pulmonary hypertension
Idiopathic dilation
Marfan’s syndrome
Rheumatic fever is the leading cause of this condition.
MITRAL STENOSIS
Other less common etiologies of obstruction to left atrial outflow: congenital mortal valve stenosis, cor triatriatum, mitral annular calcification with extension into the leaflets, systemic lupus erythematosus, rheumatoid arthritis, left atrial myxoma, and infective endocarditis with large vegetations.
Pure or predominant Mitral Stenosis occurs in approximately 40% of all patients with:
rheumatic heart disease and a history of rheumatic fever
In rheumatic MS, the valve leaflets were diffusely thickened by fibrous tissue and/or calcific deposits. The mitral commissures fuse, the chordae tendineae fuse and shorten, the valvular cusps become rigid, and these changes, in turn, lead to narrowing at the apex of the funnel-shaped (“fish-mouth”) valve.
Calcification of the stenotic mitral valve immobilizes the leaflets and narrows the orifice further.
PATHOPHYSIOLOGY OF MITRAL STENOSIS
● In normal adults the mitral valve orifice is 4-6 cm2.
● In the presence of significant obstruction i.e., when the orifice is less than approximately 2 cm2, blood can flow from the LA to the left ventricle (LV) only if propelled by an abnormally elevated left atrioventricular pressure, the hallmark of MS.
● When the mitral valve opening is reduced to 1 cm2, a LA pressure of approximately 25 mmHg is required to maintain a normal cardiac output (CO).
● The elevated pulmonary venous and pulmonary arterial (PA) wedge pressures reduced pulmonary compliance, contributing to exertional dyspnea.
An increase in heart rate shortens diastole proportionately more than systole and diminishes the time available for flow across the mitral valve.
Therefore, at any given level of CO, tachycardia augments the transvalvular gradient and elevates further the LA pressure. The LV diastolic pressure is normal in isolated MS. LV dysfunction, as reflected in reduced LV ejection fraction (EF), occurs in about one-fourth of patients with severe chronic MS. In severe MS and whenever the pulmonary vascular resistance is significantly increased, the pulmonary arterial pressure (PAP) is elevated even when the patient is at rest. Further elevations of LA, pulmonary arterial wedge, and pulmonary arterial pressure occur during exercise.
The hemodynamic response to mitral obstruction ranges from a normal CO and a high left atrioventricular pressure gradient to a markedly reduced CO and low transvalvular pressure gradient. The clinical and hemodynamic features of MS are influenced by the level of pulmonary arterial pressure. Pulmonary hypertension results from:
○ Passive backward transmission of the elevated LA pressure.
○ Pulmonary arteriolar constriction which presumably is triggered by LA and pulmonary venous hypertension (reactive pulmonary hypertension).
○ Interstitial edema in the walls of the small pulmonary vessels.
○ Organic obliterative changes in the pulmonary vascular bed. Severe pulmonary hypertension results in tricuspid regurgitation (TR) and pulmonary incompetence as well as right-sided heart failure.
Summary: MS impedes LV filling, thereby increasing LA pressure. The elevated LA pressure is transmitted back to the lungs and eventually leads to RV failure.
What is the hallmark of Mitral stenosis?
abnormally elevated left atrioventricular pressure
SYMPTOMATOLOGY OF MITRAL STENOSIS
● In temperate climates, the latent period between the initial attack of rheumatic carditis and the development of symptoms is generally about two decades; most patients begin to experience disability in the fourth decade of life.
● Exertional dyspnea, orthopnea, paroxysmal dyspnea and hemoptysis
● Hemoptysis occurs most frequently in patients who have elevated LA pressures without markedly elevated pulmonary vascular resistance.
● Recurrent pulmonary emboli, sometimes with infarction,are an important cause of morbidity and mortality rates late in the course of MS.
PHYSICAL FINDINGS IN MITRAL STENOSIS
Inspection and Palpation
● Malar flush with pinched and blue facies
● Jugular pulse reveals a prominent A wave due to vigorous right atrial systole
● Diastolic thrill at the cardiac apex, particularly with the patient in the left lateral recumbent position.
● Systemic arterial pressure is usually normal or slightly low.
● An RV tap along the left sternal border signifies an enlarged RV.
Auscultation
● Opening snap (OS) of the mitral valve most readily audible in expiration at, or just medial to the cardiac apex; maybe easily heard along the left sternal edge or at the base of the heart.
● Loud S1 (accentuated and snapping) and slightly delayed
● The Pulmonic component of the second heart sound (P2) is often accentuated, and the two components of the second
heart sound (S2) are closely split.
● Pansystolic murmur audible along the left sternal border, usually louder during inspiration and diminishes during forced expiration (Carvallo’s sign).
● Graham Steell Murmur, a high-pitched diastolic, decrescendo-blowing murmur along the left sternal border, results from dilation of the pulmonary valve ring and occurs patients with mitral valve disease and severe pulmonary hypertension.
● Low-pitched, rumbling, diastolic murmur, best heard at the apex,’ with the patient in the left lateral recumbent position; accentuated by mild exercise carried out just before auscultation.
Pansystolic murmur audible along the left sternal border, usually louder during inspiration and diminishes during forced expiration. What is the sign called?
Carvallo’s sign
What is a high-pitched diastolic, decrescendo-blowing murmur along the left sternal border, results from dilation of the pulmonary valve ring and occurs in patients with mitral valve disease and severe pulmonary hypertension?
Graham Steell Murmur
DIFFERENTIAL DIAGNOSIS FOR MITRAL STENOSIS
Mitral Regurgitation
● Prominent diastolic murmur at the apex which commences slightly later than in patients with MS
● Clear-cut evidence of LV enlargement
● Opening snap and increased P2 are absent
● S1 is soft or absent
● Apical pansystolic murmur of at least grade III/VI intensity
● Presence of S3
Primary Pulmonary Hypertension
● Occurs most frequently in young women
● Opening snap and diastolic rumbling murmur are absent
● Pulmonary artery wedge and LA pressures are normal
Atrial Septal Defect
● Absence of LA enlargement and of Kerley B line
● Fixed splitting of S2
● Grade 2 or 3 mid-systolic murmur at the mid to upper left sternal border
Aortic Regurgitation
● Apical mid-diastolic murmur (Austin Flint Murmur) which is not intensified in presystolic and becomes softer with the administration of amyl nitrate.
LABORATORY EXAMINATIONS AND FINDINGS
Electrocardiogram (ECG)
● Sinus rhythm
● Tall and peaked P wave in lead Il and upright in lead V1
● Right atrial enlargement
● Right axis deviation and RV hypertrophy in the presence of severe pulmonary hypertension
● QRS complex is usually normal
Roentgenogram
● Earliest changes are straightening of the left border of the cardiac silhouette, prominence of the main pulmonary arteries, dilatation of the upper lobe pulmonary veins, and backward displacement of the esophagus by an enlarged LA.
● Kerley B lines are fine, dense, opaque, horizontal lines that are most prominent in the lower and midlung fields
Echocardiogram with Doppler (2D Echo w/ Doppler)
● The most sensitive and specific noninvasive methods for diagnosing MS.
● Thickened mitral leaflets with dowing motion in diastole, an elevated mitral gradient and reduced orifice area.
Cardiac Catheterization and Angiocardiography
● Left heart catheterization is useful in clarifying the picture when there is a discrepancy between clinical and echocardiographic findings.
● Helpful in assessing associated lesions such as aortic stenosis and aortic regurgitation.
Coronary Angiography
● Advisable preoperatively to detect patients with critical coronary obstructions that should be bypassed at the time of operation.
Treatment of Mitral Stenosis
Medical Management
● Penicillin prophylaxis of group A β-hemolytic streptococcal infection for secondary prevention of rheumatic fever is important for at risk-patients with rheumatic MS
● For symptomatic patients:
○ Restriction of sodium intake and small doses of oral diuretics
○ Beta blockers, nondihydropyridine calcium channel blockers (DILTIAZEM or VERAPAMIL) and digitalis glycosides are useful in slowing the ventricular rate of patients with AF (atrial fibrillation)
○ Warfarin to an international normalized ratio (INR) of 2 - 3 should be administered indefinitely to patients with MS, who have AF or a history of thromboembolism.
○ If MS is not severe enough to warrant percutaneous commissurotomy, reversion to sinus rhythm pharmacologically or using electrical countershock is indicated.
Surgical Management
● Mitral valvotomy is indicated in symptomatic (New York Heart Association (NYHA) Functional Class ll-IV) patients with isolated MS, whose effective orifice (valve area) is <~1 cm2/m2 body surface area or <1.5 cm3 in normal-sized adults.
● Two techniques:
○ Percutaneous mitral balloon valvotomy (PMBV) is the procedure of choice for patients with relatively pliable leaflets with little or no commissural calcium, subvalvular structure not significantly scarred or thickened, and no left atrial thrombus
○ Surgical valvotomy
● Successful valvotomy is defined by 50% reduction in the mean mitral valve gradient and a doubling of the mitral valve area.
● Valvotomy is not recommended for patients who are entirely asymptomatic and/or who have mild stenosis (mitral valve area>1.5cm2)
● Indications for mitral valve replacement (MVR):
○ MS patients with significant associated MR (mitral regurgitation)
○ Patients whose valve has been severely distorted by previous transcatheter or operative manipulation
○ Patients in whom the surgeon does not find it possible to improve valve function significantly with valvotomy
○ Patients with severe M - i.e., an orifice area ≤ 1cm3 and are in NYHA class II (New York Heart Association), i.e., symptomatic with ordinary activity despite optimal medical therapy.
May result from an abnormality or disease process that affects any one or more of the five functional components of the mitral valve apparatus:
○ Leaflets
○ Annulus
○ Chordae tendineae
○ Papillary muscles
○ Subjacent myocardium
MITRAL REGURGITATION
ETIOLOGY OF MITRAL REGURGITATION
Acute
● Acute myocardial infarction (MI) with papillary muscle rupture
● Blunt chest wall trauma
● Infective endocarditis
● Rupture of chordae tendineae
Chronic Rheumatic Heart Disease
● Rheumatic fever
● Mitral valve prolapse (MVP)
● Extensive mitral annular calcification
● Congenital valve defects (atrioventricular cushion defect and cleft anterior mitral valve leaflet)
● Hypertrophic obstructive cardiomyopathy (HOCM)
● Dilated cardiomyopathy
● Ischemia (ventricular remodeling)
PATHOPHYSIOLOGY OF MITRAL REGURGITATION
● The resistance of LV emptying is reduced.
● As a consequence, the LV is decomposed into the LA during ejection, and with the reduction in LV size, there is a rapid decline in LV tension.
● The initial compensation is more complete LV emptying.
● However, LV volume increases progressively as the severity of the regurgitation increases and as LV function deteriorates. This increase in LV volume is often accompanied by a depressed forward cardiac output (CO).
● The regurgitation volume varies directly with LV systolic pressure and the size of the regurgitation orifice; the latter in turn, is influenced profoundly by the extent of LV dilatation.
● Summary:
○ A portion of LV stroke volume is pumped back into the LA in systole causing increased LA pressure and decreased cardiac output.
