A. The sinoatrial (SA) node is the "pacemaker" of the heart. It is located just beneath the pericardium, at the junction of the SVC and the right atrium. Impulses spread from the SA node throughout the right atrium, to the left atrium, and eventually to the atrioventricular (AV) node.
Figure 5-3. Posteroanterior radiograph of the thorax. Note the location of the pulmonary (P), aortic (A), mitral (M), and tricuspid (T) valves, along with their respective auscultation sites (X). The auscultation sites are located downstream of the blood flow through the valve (arrows). (Adapted with permission from Fleck-enstein P, Tranum-Jensen J: Anatomy in Diagnostic Imaging. Philadelphia, WB Saunders, 1993, p 202.)
branch divides further into a thin anterior division and a thick posterior division. All of the branches terminate in a complex network of Purkinje myocytes.
VIII. NEURAL REGULATION OF THE HEART. The autonomic nervous system only modulates the myogenic heartbeat.
A. The parasympathetic system decreases the heart rate. The cell bodies of preganglionic neurons are located in the dorsal nucleus of the vagus and the nucleus ambiguus of the medulla. The axons of preganglionic neurons run in the vagus nerve (cranial nerve X) and use acetylcholine as a neurotransmitter. The cell bodies of postganglionic neurons are located near the SA and AV nodes. The axons of postganglionic neurons terminate on the SA node and the AV node and use acetylcholine as a neurotransmitter.
B. The sympathetic system increases the heart rate. The cell bodies of the preganglionic neurons are located in the intermediolateral cell column of the spinal cord. The axons of the preganglionic neurons enter the paravertebral ganglia and travel to the stellate and middle cervical ganglia, using acetylcholine as a neurotransmitter. The cell bodies of the postganglionic neurons are located in the stellate and middle cervical ganglia. The axons of the postganglionic neurons are distributed to the myocardium via accompanying blood vessels and use norepinephrine as a neurotransmitter.
IX. CLINICAL CONSIDERATIONS A. Congenital heart malformations
1. Tetralogy of Fallot is caused by abnormal migration of neural crest cells that leads to skewed development of the aorticopulmonary septum. It results in a condition classically characterized by pulmonary stenosis, overriding aorta, interventricular septal defect, and right ventricular hypertrophy. The resultant right-to-left shunting of blood leads to cyanosis.
2. Membranous ventricular septal defect (VSD) is caused by incomplete fusion of the right bulbar ridge, left bulbar ridge, and atrioventricular cushions. This defect results in a condition in which an opening between the right and left ventricles allows left-to-right shunting of blood through the interventricular (IV) foramen. Patients with left-to-right shunting complain of excessive fatigue on exertion. Initially, a membranous ventricular septal defect is associated with left-to-right shunting of blood, increased pulmonary blood flow, and pulmonary hypertension. Later, the pulmonary hypertension causes marked proliferation of the tunica intima and tunica media of the pulmonary muscular arteries and arterioles, thereby narrowing their lumen. Ultimately, pulmonary resistance becomes higher than systemic resistance and causes right-to-left shunting of blood and cyanosis. At this stage, the condition is called the Eisenmenger complex.
3. Patent ductus arteriosus (PDA) occurs when the ductus arteriosus, a connection between the left pulmonary artery and the arch of the aorta, does not close. Normally, the ductus arteriosus closes via smooth muscle contraction within a few hours after birth and forms the ligamentum arteriosum. PDA causes a left-to-right shunting of blood from the aorta back into the pulmonary circulation. A PDA is very common in premature infants and also may result from maternal rubella infection during pregnancy. Prostaglandin E, intrauterine asphyxia, and neonatal asphyxia sustain patency of the ductus arteriosus. Prostaglandin inhibitors (e.g., indomethacin), acetylcholine, histamine, and catecholamines promote closure of the ductus arteriosus.
B. Other disorders (Figure 5-4)
1. Ischemic heart disease. Angina pectoris most commonly is caused by atherosclerotic disease. It results from myocardial ischemia that falls short of inducing cellular necrosis. Clinical findings include: pain that is precipitated by exertion, but relieved by rest; a sensation of pressure or burning in the chest that may last as long as 20 minutes; pain radiating to the arm, jaw, and neck; and tachycardia.
2. Acute myocardial infarction (MI; "heart attack") most commonly is caused by atherosclerotic disease. It results from myocardial ischemia that induces cellular necrosis. Clinical findings include: onset at rest (usually); a sensation of pressure or burning in the chest that lasts longer than 30 minutes; pain radiating to the arm, jaw, and neck; nausea or vomiting; sweating; shortness of breath; and tachycardia. Mis may be silent and without consequence. Complications of MI include congestive heart failure; papillary muscle rupture, indicated by acute onset of congestive heart failure with holosystolic murmur; and life-threatening arrhythmias, common in the first 24 hours after Ml. Electrocardiogram (ECG) findings include: ST segment elevation immediately after the Ml. Later, falling ST segments are observed, and Q waves and inverted T waves appear. Cardiac enzyme levels include elevated total creatine kinase (CK) and CK-2 fraction 6-12 hours after MI; elevated troponin levels 12 hours after MI; and elevated lactate dehydrogenase (LDH) levels, indicated by a reversed LDH 1:LDH2 ratio, 24 hours after MI. Treatments include: sublingual nitroglycerin; beta-blockers to relieve tachycardia and hypertension; streptokinase IV or tissue plasminogen activator to reduce the amount of infarcted tissue, if administered within 6 hours of Ml; atropine to relieve bradycardia; and heparinization and warfarin therapy to prevent ventricular aneurysms, thrombopulmonary embolisms, and deep vein thrombosis.
3. Cor pulmonale (pulmonary hypertensive heart disease) is right ventricular dilation caused by pulmonary hypertension. Acute cor pulmonale is right ventricular dilation that follows a large thrombopulmonary embolism. Chronic cor pulmonale is right ventricular hypertrophy followed by dilation that is caused by prolonged obstruction of pulmonary vasculature (e.g., emphysema).
4. Calcific valve disease occurs when valves become thickened and distorted by fibrous scarring and calcium nodules. It most commonly affects the aortic valve. Calcific valve disease renders the valve cusps immobile and impairs blood flow from the left ventricle during systole, thereby leading to heart failure.
Figure 5-4. (>A) Gross specimen of a myocardial infarction. The left ventricular myocardium is thickened as a result of persistent hypertension. Note the discoloration of the left ventricular wall and part of the interventricular septum as a result of the infarction (arrows). L = left ventricle; R = right ventricle. (B) Gross specimen of chronic cor pulmonale. Note the dilated right ventricle (R) with hypertrophied trabeculae. The left ventricle (L) has been compressed by the right ventricular enlargement. (C) Gross specimen of calcific valve disease. Note the congenitally malformed bicuspid (rather than the standard tricuspid) aortic valve, which is thickened and distorted by calcium nodules (CN). (U) Gross specimen of rheumatic heart disease. Note the "fish mouth" or "button-hole" stenosis (arrows) of the mitral valve caused by fibrotic thickening and the row of vegetation along the line of closure. (£) Gross specimen of infective endocarditis. Note the large, friable vegetations (arrows) on the mitral valve. (A adapted and C reprinted with permission from Stevens A, Lowe J: Human Histology, 2nd ed. St. Louis, Mosby, 1997, pp 152, 155; B adapted and D and E reprinted with permission from Cotran RS, Kumor V, Robbins SL: Robbins' Pathologic Basis of Disease, 5th ed. Philadelphia, WB Saunders, 1994, pp 543, 550, 552.)
5. Rheumatic heart disease results from rheumatic fever. Acute rheumatic fever typically follows pharyngitis caused by group A ß-hemolytic streptococci. Anti-streptococcal antibodies made by the patient cross-react with host connective tissue (e.g., heart valves), leading to rheumatic heart disease. The mitral valve most commonly is affected. The valve leaflets become red and swollen, fibrosis develops, and a row of small, wart-like vegetations (verrucae) appears along the line of closure. Rheumatic heart disease leads to "fish mouth," or "button-hole," stenosis of the mitral valve. Finally, Aschoff bodies, which are pathognomonic lesions consisting of perivascular, fibrinoid, necrosis-surrounded inflammatory cells (giant Aschoff cells) develop.
6. Infective endocarditis is the colonization of heart valves with bacteria.
a. Acute bacterial endocarditis most commonly is caused by Staphylococcus aureus (50%) and Streptococcus species (35%) and typically is seen on previously normal heart valves. Clinical findings include: Janeway lesions (erythematous, nontender lesions on the palms and soles), splinter hemorrhages in the nail beds, high fever with chills, hematuria, petechiae, and splenomegaly. Large, friable vegetations on the heart valves may lead to systemic septic emboli or perforation of the heart valve, causing valvular incompetence.
b. Subacute bacterial endocarditis is caused by Staphylococcus epidermidis, Streptococcus viridans, Enterococcus species, or gram-negative bacilli. It typically is seen on previously abnormal heart valves. Clinical findings include: Roth spots (retinal hemorrhages), Osier nodes (erythematous, tender lesions on the fingers and toes), fatigue, low-grade fever without chills, anemia, hematuria, and splenomegaly.
7. Wolff-Parkinson-White syndrome is a congenital disorder in which there is an accessory conduction pathway between the atria and the ventricles. Usually, this condition is asymptomatic. A re-entry loop may develop in which impulses travel to the ventricles via the normal conduction pathway, but return to the atria via the accessory conduction pathway, causing supraventricular tachycardia.
X. CROSS-SECTIONAL ANATOMY. Note the anteroposterior position of the various structures. A bullet or knife wound at a specific vertebral level would penetrate specific anatomic structures in an anteroposterior direction.
A. At T2-3, where three branches of the aortic arch originate (Figure 5-5)
B. At about T5—6, through the ascending aorta and pulmonary trunk (Figure 5-6)
C. At about T7—8, through the four chambers of the heart (Figure 5-7)
1. Manubrium of sternum
2. First rib
3. Sternal end of clavicle
4. Right brachiocephalic vein
7. Left subclavian artery
10. Brachiocephalic trunk
11. Axillary fat with lymph nodes and vessels
12. Latissimus dorsi and teres major (arms elevated)
13. Left internal jugular vein
14. Left common carotid artery
AOA: Aortic arch AZ: Azygous vein BC: Brachiocephalic artery BV: Left brachiocephalic vein C: Spinal cord
CC2: Second costal cartilage CJ: Costochondral junction E:Esophagus
ES: Erector spinae IS: Infraspinatus L: Lung
LC: Left common carotid artery
LS: Left subclavian artery
PM: Pectoralis major
PMi: Pectoralis minor SA: Serratus anterior SP: Scapula SS: Subscapularis SVC: Superior vena cava T: Trachea TZ: Trapezius
Figure 5-5. (A) CT scan (labeled and unlabeled) at about T2—3. Note the relations of the brachiocephalic trunk, left common carotid artery, and left subclavian artery. The inset shows the level of the cross-section. (B) MRI scan at about T2—3. The line diagram shows the level of the cross-section. (A reprinted with permission from Fleckenstein P, Tranum-Jensen J: Anatomy in Diagnostic Imaging. Philadelphia, WB Saunders, 1993, p 209; B adapted with permission from Barrett CP, Anderson LD, Holder LE, et al: Primer of Sectional Anatomy with MRI and CT Correlation, 2nd ed. Baltimore, Williams & Wilkins, 1994, pp 53, 54.)
AA: Ascending aorta AZ: Azygous vein C: Spinal cord DA: Descending aorta E: Esophagus ES: Erector spinae
HA: Hemiazygous vein IT: Internal thoracic artery LB: Left main bronchus LD: Latissimus dorsi PM: Pectoralis major PMi: Pectoralis minor
PT: Pulmonary trunk RB: Right main bronchus RPA: Right pulmonary artery SA: Serratus anterior ST: Sternum
SVC: Superior vena cava
1. Anterior mediastinum
2. Ascending aorta
3. Superior caval vein
4. Right superior pulmonary vein and apical branches of right pulmonary artery
5. Right intermediate bronchus
6. Azygous vein
9. Pulmonary trunk
10. Right pulmonary artery
11. Left superior pulmonary vein
12. Left superior lobar bronchus
13. Left pulmonary artery
14. Left principal bronchus
Figure 5-6. (A) CT scan (labeled and unlabeled) at about T5—6. Note the position of the ascending aorta and the pulmonary trunk. The inset shows the level of the cross-section. (B) MRI scan at about T5—6. The line diagram shows the level of the cross-section. (A reprinted with permission from Fleckenstein P, Tranum-Jensen J: Anatomy in Diagnostic Imaging. Philadelphia, WB Saunders, 1993, p 214; B reprinted with permission from Barrett CP, Anderson LD, Holder LE, et al: Primer of Sectional Anatomy with MRI and CT Correlation, 2nd ed. Baltimore, Williams & Wilkins, 1994, pp 59, 60.)
1. Right ventricle 5. Esophagus 9. Serratus anterior
2. Right atrium 6. Thoracic aorta 10. Latissimus dorsi
3. Left ventricle 7. Nipple 11. Inferior angle of scapula
4. Left atrium 8. Body of mammary gland
Az: Azygous vein
C: Spinal cord
CA1: Right coronary artery
CA2: Left anterior descending artery
DA: Descending aorta
EF: Epicardial fat
ES: Erector spinae
FP: Fibrous pericardium HAZ: Hemiazygous vein IT: Internal thoracic artery IVC: Inferior vena cava IVS: Interventricular septum LA: Left atrium LD: Latissimus dorsi LI: Liver
LV: Left ventricle MV: Mitral valve PF: Pericardial fat RA: Right atrium RV: Right ventricle SA: Serratus anterior ST: Sternum
Figure 5-7. (A) CT scan (labeled and unlabeled) at about T7—8. Note the position of the four chambers of the heart. The inset shows the level of the cross-section. (B) MRI scan at about T7— 8. The line diagram shows the level of the cross-section. It is important to know the arrangement of the heart chambers in an anteroposterior direction. A typical clinical vignette question may ask about a patient who is shot through the sternum. In what order would the bullet pass through the chambers of the heart before it exits the back? (A reprinted with permission from Fleckenstein P, Tranum-Jensen J: Anatomy in Diagnostic Imaging. Philadelphia, WB Saunders, 1993, p 219; B reprinted with permission from Barrett CP, Anderson LD, Holder LE, et al: Primer of Sectional Anatomy with MRI and CT Correlation, 2nd ed. Philadelphia, Williams & Wilkins, 1994, pp 69, 70.)
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