Archive for the ‘ L3-Patho HF ’ Category

L3- Pathology of Heart Failure

Clinical manifestations of heart failure

  • Definition

  • Size of the problem

  • Pathophysiology

  • symptoms

  • Signs

  • Investigations

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    FIGURE 21-24 Unloading of high-pressure baroceptors (circles) in the left ventricle, carotid sinus, and aortic arch generates afferent signals that stimulate cardioregulatory centers in the brain, resulting in the activation of efferent pathways in the sympathetic nervous system. The sympathetic nervous system appears to be the primary integrator of the neurohumoral vasoconstrictor response to arterial underfilling. Activation of renal sympathetic nerves stimulates the release of arginine vasopressin (AVP). Sympathetic activation also causes peripheral and renal vasoconstriction, as does angiotensin II. Angiotensin II constricts blood vessels and stimulates the release of aldosterone from the adrenal gland, and it also increases tubular sodium reabsorption and causes remodeling of cardiac myocytes. Aldosterone may also have direct cardiac effects, in addition to increasing the reabsorption of sodium and the secretion of potassium and hydrogen ions in the collecting duct. The lines designate circulating hormones. (Modified from Schrier RW, Abraham WT: Hormones and hemodynamics in heart failure. N Engl J Med 341:577, 1999.)

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    FIGURE 21-31 The systemic and tissue components of the renin-angiotensin system. Several tissues, including myocardium, vasculature, kidney, and brain, have the capacity to generate angiotensin II independent of the circulating renin-angiotensin system. Angiotensin II produced at the tissue level may play an important role in the pathophysiology of heart failure. ACE = angiotensin-converting enzyme. (Modified from Timmermans PB, Wong PC, Chiu AT, et al: Angiotensin II receptors and angiotensin II receptor antagonists. Pharmacol Rev 45:205, 1993.)

    Symptoms of heart failure

    1. Symptoms of pulmonary venous congestion
    2. Symptoms of systemic venous congestion
    3. Symptoms of low cardiac output
    4. Symptoms of the specific etiology
    5. Symptoms of complications

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    TABLE 7-1 Disorders Causing Dyspnea and Limiting Exercise Performance, Pathophysiology, and Discriminating Measurements

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    TABLE 7-2 American Thoracic Society Scale of Dyspnea

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    TABLE 7-7 A Comparison of Three Methods of Assessing Cardiovascular Disability

    Physical signs of heart failure

    1. General appearance
    2. Complexion
    3. Posture in bed (decubitus)
    4. Nutritional status
    5. Blood pressure
    6. Arterial pulse
    7. Neck veins
    8. Upper limb
    9. Lower limb
    10. Abdominal examination
    11. Chest examination
    12. Local cardiac examination

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    TABLE 7-5 Principal Causes of Generalized Edema: History, Physical Examination, and Laboratory Findings

    The Downward Slope

    GP visit

    Personal data: Mr. Ahmad, 52 years old, from Pakistan

    Past history of throat infection followed by severe malise, a skin rash and swollen, tender joints

    Symptoms:

    1.Breathless on climbing a single flight of stairs (exert ional dyspnea)     .

    2.Waking up in the middle of the night with breathlessness leading him to sleep propped up by several pillow (orthopnea).

    Physical signs:

    1.Pulse: 82/min with occasional irregularity

    2.Bp : 115/90 mmHg

    3.Chest : bilateral basal crepitation

    4.Cardiac examination: pan systolic murmur over the apex radiating to left axilla

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    FIGURE 8-7C A, Palpation of the anterior wall of the right ventricle by applying the tips of three fingers in the third, fourth, and fifth interspaces, and left sternal edge (arrows), during full held exhalation. Patient is supine with the trunk elevated 30 degrees. B, Subxiphoid palpation of the inferior wall of the right ventricle (RV) with the relative position of the abdominal aorta (Ao) shown by the arrow. C, The bell of the stethoscope is applied to the cardiac apex while the patient lies in a partial left lateral decubitus position. The thumb of the examiner’s free left hand is used to palpate the carotid artery for timing purposes. D, The soft, high-frequency early diastolic murmur of aortic regurgitation or pulmonary hypertensive regurgitation is best elicited by applying the stethoscopic diaphragm very firmly to the mid-left sternal edge. The patient leans forward with breath held in full exhalation. E, Palpation of the left ventricular impulse with a fingertip (arrow). The patient’s trunk is 30 degrees above the horizontal. The examiner’s right thumb palpates the carotid pulse for timing purposes. F, Palpation of the liver. The patient is supine with knees flexed to relax the abdomen. The flat of the examiner’s right hand is placed on the right upper quadrant just below the expected inferior margin of the liver; the left hand is applied diametrically opposite. (From Perloff JK: Physical Examination of the Heart and Circulation. 3rd ed. Philadelphia, WB Saunders, 2000.)

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    FIGURE 8-8 Maximal intensity and radiation of six isolated systolic murmurs. HCM = hypertrophic cardiomyopathy; MR = mitral regurgitation; Pulm = pulmonary; VSD = ventricular septal defect. (From Barlow JB: Perspectives on the Mitral Valve. Philadelphia, FA Davis, 1987, p 140.)

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    FIGURE 8-9A A, The basic heart sounds consist of the first heart sound (S1), the second heart sound (S2), the third heart sound (S3), and the fourth heart sound (S4). B, Heart sounds within the auscultatory framework established by S1 and S2. The additional heart sounds are designated as early systolic (ES), midsystolic (MS), late systolic (LS), early diastolic (ED), mid-diastolic (MD), and late diastolic (LD) or presystolic. C, Upper tracing illustrates a low-frequency S4, and the lower tracing illustrates a split S1, the two components of which are of the same quality.

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    FIGURE 8-21 Illustration of great arterial (GA), ventricular (VENT), and atrial pressure pulses with phonocardiogram showing the physiological mechanism of a holosystolic murmur in some forms of mitral regurgitation and in high-pressure tricuspid regurgitation. Ventricular pressure exceeds atrial pressure at the very onset of systole, so regurgitant flow and murmur commence with the first heart sound (S1). The murmur persists up to or slightly beyond the second heart sound (S2) because regurgitation persists to the end of systole (ventricular pressure still exceeds atrial pressure). V = atrial v wave.

    Medical emergency

    Symptoms:

    Sudden severe breathlessness, and began to cough up pin frothy sputum (cardiac asthma; acute pulmonary edema)

    Physical signs:

    1.Mr Ahmad was breathing rapidly with extreme difficulty (severe dyspnea)

    2.His lips and finger-tips were cyanosed (central cyanosis)

    3.Both ankles were swollen (bilateral edema of both L.L)

    4.Palpable liver (enlarged congested pulsating liver)

    5.Pulse: 120/min with marked  irregularity

    6. Chest : bilateral basal crepitation over the lower 2/3 of the chest

    7.Cardiac examination: pan systolic murmur over the apex radiating to left axilla

    INVETIGATIONS

    ECG:

    Atrial fibrillation (AF)

    Chest x-ray:

    cardiomegally, mainly left side of the heart with central congestion of both lung fields (cardiogenic pulmonary edema)

    Biochemical test:

    normal cardiac troponin T level

    Echocardiography:

    1.Thickened, rigid mitral valve leaflets

    2.Severe mitral regurgitation

    3.Dilated LV with depressed systolic function (low ejection fraction EF)

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    FIGURE 9-4 Top, Electrode connections for recording the three bipolar limb leads I, II, and III. R, L, and F indicate locations of electrodes on the right arm, the left arm, and the left foot, respectively. Bottom, Electrode locations and electrical connections for recording a unipolar precordial lead. Left, The positions of the exploring electrode (V) for the six precordial leads. Right, Connections to form the Wilson central terminal for recording a precordial (V) lead. (From Goldberger AL: Clinical Electrocardiography: A Simplified Approach. 6th ed. St Louis, CV Mosby, 1999.)

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    FIGURE 9-11 The waves and intervals of a normal electrocardiogram. (From Goldberger AL: Clinical Electrocardiography: A Simplified Approach. 6th ed. St Louis, CV Mosby, 1999.)

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    FIGURE 9-12 Normal electrocardiogram recorded from a 48-year-old woman. The vertical lines of the grid represent time, with lines spaced at 40 msec intervals. Horizontal lines represent voltage amplitude, with lines spaced at 0.1 mV intervals. Every fifth line in each direction is typically darkened. The heart rate is approximately 72 beats/min; the PR interval, QRS, and QTc durations measure about 140, 84, and 400 msec, respectively; and the mean QRS axis is approximately +35 degrees.

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    FIGURE 32-15A Atrial fibrillation produced by “focal” mechanisms. A, A rapid, regular atrial tachycardia (left side of figure) at a cycle length (CL) of 200 milliseconds degenerates into atrial fibrillation (right side of figure) characterized by rapid, irregular atrial depolarizations. B, A premature atrial complex (marked by the asterisk) induces atrial fibrillation (right side of figure). Elimination of these focal triggers for atrial fibrillation can eliminate the atrial fibrillation.

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    FIGURE 12-3A Frontal projection of the heart and great vessels. A, Left and right heart borders in the frontal projection. B, A line drawing in the frontal projection demonstrates the relationship of the cardiac valves, rings, and sulci to the mediastinal borders. A = ascending aorta; AA = aortic arch; Az = azygous vein; LA = left atrial appendage; LB = left lower border of pulmonary artery; LV = left ventricle; PA = main pulmonary artery; RA = right atrium; S = superior vena cava; SC = subclavian artery.

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    FIGURE 12-15 Patient with acute pulmonary edema. Note engorged hila bilaterally, with typical pattern of pulmonary edema on the right. Also note intraaortic counterpulsation balloon with radiopaque tip at the top of the descending aorta (arrow) and the balloon expanded in the aorta below it (large arrow).

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    FIGURE 11-11 Schematic of the transducer orientation used for acquiring parasternal views. The scanning plane of the ultrasound beam is superimposed on a schematic of the heart. Plane 1 represents a parasternal long-axis view in which the right ventricular outflow tract, proximal portion of the aorta and aortic valve, anterior ventricular septum, cavity of the left ventricle containing the mitral valve, and inferoposterior wall of the left ventricle can be visualized. Scanning plane 1 results in an ultrasound image, as noted in Figure 11-12. Scanning plane 2 is obtained by rotating the transducer 90 degrees and can be used to obtain a family of short-axis views of the heart (see Fig. 11-14). (From Feigenbaum H: Echocardiography. 4th ed. Malvern, PA, Lea & Febiger, 1986.)

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    FIGURE 11-12 Parasternal long-axis view of the left ventricle in diastole (top) and systole (bottom). Chambers and cardiac structures are as noted. This view corresponds to plane 1 of Figure 11-11. Ao = aorta; LA = left atrium; LV = left ventricle; MV = mitral valve; RV = right ventricular outflow tract.

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    FIGURE 11-56 Four panels depicting varying degrees of mitral regurgitation; the two top panels are apical four-chamber transthoracic views showing, on the left, mild mitral regurgitation and, on the right, moderate to severe mitral regurgitation. On the left, note the relatively narrow jet directed from the tips of the mitral valve toward the posterior left atrial wall. On the right, note the larger jet, filling approximately 40 percent of the left atrial cavity. The two bottom panels are transesophageal echocardiograms. On the left, note the mitral regurgitation occurring in two discrete jets and, on the right, the highly eccentric jet, which courses along the extreme lateral wall of the left atrium. LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle.

    TREATMENT

    MEDICAL

    1. Diuretics: furosemide
    2. Oxygen
    3. Inotropic & anti arrhythmic: Digoxin
    4. Angiotensin converting enzyme inhibitor:Ramipril
    5. Beta blocker: Carvedilol nVasodilator:Glyceryl trinitrate
    6. Antiplatelet: aspirin
    7. Anticoagulant: Warafarin

    SURGICAL

    1.Mitral valve replacement

    PREVENTION

    1.Infective endocarditis

    2.Rheumatic fever (primary, secondary and tertiary)