The pericardium
‡ The pericardium comprises fibrous and serous components. ‡ The fibrous pericardium is a strong layer which covers the heart. It fuses with the roots of the great vessels above and with the central tendon of the diaphragm below.

‡ Two important sinuses are located between the parietal and visceral layers. .The pericardium ‡ The serous pericardium lines the fibrous pericardium (parietal layer) and is reflected at the vessel roots to cover the heart surface (visceral layer).

the sinus is bounded by the inferior vena cava and the pulmonary veins.The pericardium ‡ Transverse sinus located between the superior vena cava and left atrium posteriorly and the pulmonary trunk and aorta anteriorly. . ‡ Oblique sinus behind the left atrium.


a finger can be passed through the transverse pericardial sinus posterior to the aorta and pulmonary trunk. After the pericardial sac has been opened anteriorly.The pericardium ‡ The transverse pericardial sinus is especially important to cardiac surgeons. .

surgeons can stop or divert the circulation of blood in these large arteries while performing cardiac surgery. inserting the tubes of a coronary bypass machine. and then tightening the ligature.The pericardium ‡ By passing a surgical clamp or placing a ligature around these vessels. .

‡ This manifests itself clinically as shock.The pericardium ‡ Cardiac tamponade (heart compression) is due to critically increased volume of fluid outside the heart but inside the pericardial cavity. This condition is fatal unless pericardial decompression is effected immediately. distended neck veins and muffled/absent heart sounds (Beck s triad). .. e.g. due to stab wounds or from perforation of a weakened area of the heart muscle after heart attack (Haemopericardium).

Pericardiocentesis ‡ Haemopericardium: The normal volume of pericardial fluid. . a condition known as cardiac tamponade. is used to lubricate the apposing surfaces of the serous pericardium during heart movements. ‡ Once the fluid in the cavity exceeds about 250 mL. about 50 mL. the diastolic filling is compromised.

With the positions of the cardiac notches of the lungs and pleura in mind. . ‡ The patient is placed in a supine position with the shoulders raised 60° from the horizontal position. ‡ The needle is inserted in the angle between the xiphoid process and the left costal margin.Pericardiocentesis ‡ This procedure is used in the treatment of cardiac tamponade.

Pericardiocentesis ‡ The tip of the needle is directed upward. toward the left shoulder. and to the left in the left xiphocostal angle. that is. The following structures will be penetrated by the needle: . backward.

Pericardiocentesis ‡ Skin ‡ Subcutaneous tissue ‡ Aponeurosis of the external oblique muscle of the abdomen ‡ Anterior lamina of the aponeurosis of the internal oblique muscle of the abdomen ‡ Rectus abdominis muscle .

‡ Extraperitoneal fat.Pericardiocentesis ‡ Posterior lamina of the aponeurosis of the internal oblique and the transversus abdominis muscles. ‡ Pericardium. ‡ Diaphragm. .

Pericardiocentesis ‡ When pericardial penetration is achieved there is a sudden give. . The needle is connected to a 20-mL syringe with a three-way stopcock to permit aspiration of the fluid.

‡ The needle may enter the pleural cavity.Anatomy of Complications ‡ The needle is advanced too far and enters the myocardium of the right ventricle. . ‡ The needle may pierce the liver. producing a pneumothorax or a hydropneumothorax. ‡ The needle may pierce the anterior descending branch of the left coronary artery.


5in (12mm) from the edge of the sternum. 6th right costal cartilage 0. ‡ 3. 5th left intercostal space 3. ‡ 4. 2nd left costal cartilage 0.Heart surface anatomy ‡ The outline of the heart can be represented on the surface by the irregular quadrangle bounded by the following four points ‡ 1. 3rd right costal cartilage 0.5in (12mm) from the sternum.5in (12mm) from the sternal edge. .5in (9cm) from the midline (corresponding to the apex beat). ‡ 2.


Heart surface anatomy ‡ The left border of the heart (indicated by the curved line joining points 1 and 4) is formed almost entirely by the left ventricle (the auricular appendage of the left atrium superiorly). ‡ The right border (marked by the line joining points 2 and 3) is formed by the right atrium. ‡ The lower border (the horizontal line joining points 3 and 4) corresponds to the right ventricle and the apical part of the left ventricle. .

‡ The second sound (higher-pitched) is produced by the sharp closure of the aortic and pulmonary valves. . one can hear two sounds: lu¯b-du p.Auscultation of Heart Valves ‡ On listening to the heart with a stethoscope. ‡ The first sound (lower-pitched) is produced by the contraction of the ventricles and the closure of the tricuspid and mitral valves.

Auscultation Sites ‡ Pulmonary valve area (P) 2nd intercostal space parasternally on left side. ‡ Mitral valve area (M)5th ICS MCL. ‡ Tricuspid valve area (T) lower sternum or just to right of it. ‡ Aortic valve area (A) 2nd intercostal space parasternally on right side. .

5 in. ‡ The mitral valve is best heard over the apex beat. 3. at the level of the fifth left intercostal space.Auscultation Sites ‡ The tricuspid valve is best heard over the right half of the lower end of the body of the sternum. that is. (9 cm) from the midline. .

‡ The aortic valve is best heard over the medial end of the second right intercostal space.Auscultation Sites ‡ The pulmonary valve is heard best over the medial end of the second left intercostal space. .

followed by loss of flexibility and shrinkage. Later. ‡ Narrowing (stenosis) and valvular incompetence (regurgitation) result. fibrous thickening occurs.Valvular Disease of the Heart ‡ Inflammation of a valve can cause the edges of the valve cusps to stick together. . and the heart ceases to function as an efficient pump.

a rippling effect is set up. lu¯b-du p. ‡ Should the valve orifices become narrowed or the valve cusps distorted and shrunken by disease. .Valvular Heart Murmurs ‡ Apart from the sounds of the valves closing. the blood passes through the normal heart silently. leading to turbulence and vibrations that are heard as heart murmurs.

although protected by the thoracic cage.Cardiac Injuries Cardiac Contusion ‡ The heart. . can be squeezed between the sternum and the vertebral column.

‡ The severity of the pain is often unrelated to the seriousness of the cause. . musculoskeletal chest wall pain. and other non life-threatening causes. ‡ Myocardial pain may mimic oesophagitis.Chest Pain ‡ May be caused by disease in the thoracic and abdominal walls or in many different chest or abdominal viscera.

‡ Visceral Pain Visceral pain is diffuse and poorly localized.Somatic pain ‡ Pain arising from the chest or abdominal walls is intense and discretely localized. ‡ Somatic pain arises in sensory nerve endings in these structures and is conducted to the central nervous system by somatic segmental spinal nerves. .

.‡ It is conducted to the central nervous system along afferent autonomic nerves.

Referred Pain ‡ Visceral pain frequently is referred to skin areas that are innervated by the same segment of the spinal cord as is the painful viscus. . ‡ One theory is that the nerve fibers from the viscus and the dermatome ascend in the central nervous system along a common pathway and the cerebral cortex is incapable of distinguishing between the sites of origin.

Referred Pain ‡ Another theory is that under normal conditions the viscus does not give rise to painful stimuli. whereas the skin area repeatedly receives noxious stimuli. .

the sinoatrial (SA) and AV nodes.Arterial Supply of the Heart ‡ Right coronary artery: arises from the ascending aorta and runs in the coronary (AV) sulcus. the right marginal artery. and the posterior interventricular artery. ‡ Important branches are the SA nodal artery. the right ventricle. ‡ The right coronary artery primarily supplies the right atrium. .

the anterior interventricular (descending) artery and the circumflex artery. . It divides into two branches.‡ left coronary artery: arises from the ascending aorta. ‡ The left coronary artery supplies most of the left ventricle. and the interventricular septum. the left atrium.


It joins the coronary sinus. It is the main tributary of the coronary sinus. ‡ Middle cardiac vein: lies in the posterior interventricular sulcus. ‡ The venae cordis minimae and anterior cardiac veins open directly to the chambers of the heart.The venous drainage of the heart ‡ Coronary sinus: is the main vein of the coronary circulation. ‡ Great cardiac vein: lies in the anterior interventricular sulcus. it lies in the posterior coronary sulcus. . It drains to an opening in the right atrium.

The venous drainage of the heart .

they are essentially functional end arteries. ‡ A sudden block of one of the large branches of either coronary artery will usually lead to necrosis of the cardiac muscle (myocardial infarction). ‡ Most cases of coronary artery blockage are caused by an acute thrombosis on top of a chronic atherosclerotic narrowing of the lumen. . have numerous anastomoses at the arteriolar level.Coronary Artery Disease ‡ Coronary arteries .

‡ Arteriosclerotic disease of the coronary arteries may present in three ways, depending on the rate of narrowing of the lumina of the arteries: ‡ (1) General degeneration and fibrosis of the myocardium occur over many years and are caused by a gradual narrowing of the coronary arteries. ‡ (2) Angina pectoris is cardiac pain that occurs on exertion and is relieved by rest. In this condition, the coronary arteries are so narrowed that myocardial ischemia occurs on exertion but not at rest.

‡ (3) Myocardial infarction occurs when coronary flow is suddenly reduced or stopped and the cardiac muscle undergoes necrosis. Myocardial infarction is the major cause of death in industrialized nations. ‡ Because coronary bypass surgery, coronary angioplasty, and coronary artery stenting are now commonly accepted methods of treating coronary artery disease, it is incumbent on the student to be prepared to interpret still- and motion-picture angiograms that have been carried out before treatment.

Myocardial Infarction and Papillary Muscle Rupture
‡ Rarely, in acute myocardial infarction involving the left ventricle, a papillary muscle may rupture. ‡ Rupture of the posteromedial papillary muscle is more common since it is supplied by a single artery, the right coronary artery. ‡ The anterolateral papillary muscle is less likely to rupture since it has a dual blood supply from the anterior interventricular and circumflex branches of the left coronary artery.

Development of the heart .

Embryological derivatives of adult heart .

a number of changes occur in the circulatory system because of the cessation of placental blood flow and start of lung respiration.Foetal Circulation ‡ Foetal circulation involves three shunts: ductus venous. and foramen ovale ‡ After birth. . ductus arteriosus.

Changes After Birth Remnant in Adult ‡ Closure of right and left umbilical arteries forms Medial umbilical ligaments. ‡ Closure of left umbilical vein forms Ligamentum teres ‡ Closure of ductus venosus forms Ligamentum venosum ‡ Closure of foramen ovale forms Fossa ovale ‡ Closure of ductus arteriosus forms Ligamentum arteriosum .


a small opening persists. .Congenital Anomalies ‡ Atrial Septal Defects (ASD): After birth. the foramen ovale becomes completely closed as the result of the fusion of the septum primum with the septum secundum. ‡ In 25% of hearts. but this is usually of such a minor nature that it has no clinical significance.

Atrial Septal Defects (ASD) ‡ Secundum-type ASDs are caused by excessive resorbtion of the SP. This results in an opening between the right And left atria (patent Foramen Ovale) . or reduced size of SS or both.

Atrial Septal Defects (ASD) ‡ Occasionally. the opening is much larger and results in oxygenated blood from the left atrium passing over into the right atrium .

. This is the most Clinically significant ASD.Atrial Septal Defects (ASD) ‡ If the ASD is small. clinical Symptoms may be delayed as late as age 30. ‡ Premature closure of the Foramen Ovale (FO) is the closure of the FO during Prenatal life. This results in hypertrophy of the right side of the heart and underdevelopment of the left side.

.Congenital Anomalies Tetralogy of Fallot ‡ This congenital anomaly is responsible for about 9% of all congenital heart disease ‡ The anatomic abnormalities include large ventricular septal defect. which can occur at the infundibulum of the right ventricle or at the pulmonary valve. ‡ stenosis of the pulmonary trunk.

because of the high blood pressure in the right ventricle. ‡ Severe hypertrophy of the right ventricle.Tetralogy of Fallot ‡ exit of the aorta immediately above the ventricular septal defect (instead of from the left ventricular cavity only). .

‡ Squatting reduces the venous return by compressing the abdominal veins and increasing the systemic arterial resistance by kinking the femoral and popliteal arteries in the legs. .Tetralogy of Fallot ‡ Most children find that assuming the squatting position after physical activity relieves their breathlessness. both these mechanisms tend to decrease the right-to-left shunt through the ventricular septal defect and improve the pulmonary circulation.

causing enlargement of the right ventricle . ‡ They are found in the membranous part of the septum and can measure 1 to 2 cm in diameter. ‡ Blood under high pressure passes through the defect from left to right.Ventricular Septal Defects ‡ Ventricular septal defects (VSD)are less frequent than atrial septal defects.

Membranous Ventricular Septal Defect (VSD) ‡ This VSD is caused by the failure of the membranous IV septum to develop and it results in left to right shunting of blood through the IV foramen. ‡ Patients with left to-right shunting complain of excessive fatigue upon exertion This shunting of blood is non cyanotic ‡ Causes increased blood flow and pressure to the lungs (pulmonary hypertension). .

Coarctation of the Aorta ‡ Congenital narrowing of the aorta just proximal. or distal to the site of attachment of the ligamentum arteriosum ‡ Clinically. the cardinal sign of aortic coarctation is absent or diminished pulses in the femoral arteries of both lower limbs. opposite. .

‡ The dilated intercostal arteries erode the lower borders of the ribs. with dilatation of the internal thoracic. . which is seen on radiographic examination. subclavian. an enormous collateral circulation develops. producing characteristic notching.Coarctation of the Aorta ‡ To compensate. and posterior intercostal arteries.

Transposition of the great vessels ‡ Occurs when the (aorticopulmonary) AP septum fails to develop in a Spiral fashion and results in the aorta opening into the right ventricle and the pulmonary trunk opening into The left ventricle. ‡ This causes right-to-left shunting of blood with resultant cyanosis. ‡ Infants born alive with this defect must have other defects that allow mixing of oxygenated and deoxygenated blood. .

the ductus arteriosus closes within a few hours after birth via smooth ‡ Muscle contraction to form the ligamentum arteriosum. Normally.Patent ductus arteriosus (PDA) ‡ Occurs when the ductus arteriosus fails to close after birth. ‡ Prostaglandin E and intrauterine or neonatal asphyxia sustain patency of the ductus arteriosus .

Indomethacin.Patent ductus arteriosus ‡ Prostaglandin inhibitors (e. acetylcholine. histamine and catecholamines promote closure of the ductus arteriosus. ‡ PDA is common in premature Infants and cases of maternal rubella infection it causes a left-to-right shunting of blood .g.

‡ This results in a condition in which only one large vessel leaves the heart and it receives blood from both the right and left ventricles.Persistent truncus arteriosus ‡ Occurs when there is only partial development of the AP Septum. ‡ This causes right to. . This defect is always accompanied by membranous ventricular septal defect.left shunting of blood with resultant cyanosis.

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