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Cardiovascular System Reviewer
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CARDIOVASCULAR SYSTEM: HEART
¾ Relatively small, roughly the same size (but not the same shape) as your closed fist; visualize the heart as a cone lying on its side. ¾ FEMALES: 250 g (8 oz) | MALES: 300 g (10 oz) ¾ Rests on the diaphragm, near the midline of the thoracic cavity; lies between two rigid structures: the vertebral column and the sternum
Mediastinum – an anatomical region that extends from the sternum to the vertebral column, from the first rib to the diaphragm, and between the lungs
Apex – tip of the left ventricle and rests on the diaphragm. It is directed anteriorly, inferiorly, and to the left. Base – its posterior surface. It is formed by the atria (upper chambers) of the heart, mostly the left atrium.
4 HEART SURFACES: R A I L 1. Anterior surface – deep to the sternum and ribs. 2. Inferior surface – between the apex and right border and rests mostly on the diaphragm 3. Right border – faces the right lung and extends from the inferior surface to the base. 4. Left border / pulmonary border – faces the left lung and extends from the base to the apex.
Pericardium – membrane that surrounds and protects the heart; It confines the heart to its position in the mediastinum, while allowing sufficient freedom of movement for vigorous and rapid contraction.
2 MAIN PARTS: Superficial to Deep Fibrous Pericardium – composed of tough, inelastic, dense irregular connective tissue. It resembles a bag that rests on and attaches to the diaphragm; its open end is fused to the connective tissues of the blood vessels entering and leaving the heart; prevents overstretching of the heart, provides protection, and anchors the heart in the mediastinum. The fibrous pericardium near the apex of the heart is partially fused to the central tendon of the diaphragm and therefore movement of the diaphragm, as in deep breathing, facilitates the movement of blood by the heart. 1. Serous Pericardium – is a thinner, more delicate membrane that forms a double layer around the heart Parietal Layer – is fused to the fibrous pericardium. Visceral Layer / Epicardium – is one of the layers of the heart wall and adheres tightly to the surface of the heart. Between the parietal and visceral layers of the serous pericardium is a thin film of lubricating serous fluid. Pericardial Fluid – (By Pericardial Cells) slippery secretion of the pericardial cells; reduces friction between the layers of the serous pericardium as the heart moves. Pericardial Cavity –space that contains the few milliliters of pericardial fluid
3 LAYERS OF HEART WALL: 1. Epicardium – is composed of two tissue layers. The outermost, as you just learned, is called the visceral layer of the serous pericardium. This thin, transparenouter layer of the heart wall is composed of mesothelium. The epicardium imparts a smooth, slippery texture to the outermost surface of the heart. The epicardium contains blood vessels, lymphatics, and vessels that supply the myocardium.
a) Mesothelium – variable layer of delicate fibro elastic tissue and adipose tissue. The adipose tissue predominates and becomes thickest over the ventricular surfaces, where it houses the major coronary and cardiac vessels of the heart. The amount of fat varies from person to person, corresponds to the general extent of body fat in an individual, and typically increases with age. 2. Myocardium – is responsible for the pumping action of the heart and is composed of cardiac muscle tissue. It makes up approximately 95% of the heart wall, many anastamoses and has their own blood vessels. The muscle fibers (cells), like those of striated skeletal muscle tissue, are wrapped and bundled with connective tissue sheaths composed of endomysium and perimysium. The cardiac muscle fibers are organized in bundles that swirl diagonally around the heart and generate the strong pumping actions of the heart (Figure 20). Although it is striated like skeletal muscle, recall that cardiac muscle is involuntary like smooth muscle. 3. Endocardium – a thin layer of endothelium overlying a thin layer of connective tissue. It provides a smooth lining for the chambers of the heart and covers the valves of the heart. The smooth endothelial lining minimizes the surface friction as blood passes through the heart. The endocardium is continuous with the endothelial lining of the large blood vessels attached to the heart.
4 HEART CHAMBERS: CHAMBER CONTRACTION: pushes a volume of blood into a ventricle or out of the heart into an artery ATRIA: (entry halls or chambers) two superior receiving chambers Veins – The paired atria receive blood from blood vessels returning blood to the heart; carries blood towards the heart. Auricle – On the anterior surface of each atrium is a wrinkled pouchlike structure (resemblance to a dog’s ear) each auricle slightly increases the capacity of an atrium so that it can hold a greater volume of blood.
- Right Atrium – forms the right border of the heart; inside posterior (smooth) & anterior (rough) Receives blood from three veins: Superior vena cava
Inferior vena cava
Coronary sinus
pectinate muscles – muscular ridges that extend into the auricle giving smooth and rough texture 2. Left Atrium –same thickness as the right atrium and forms most of the base of the heart It receives blood from the lungs through four pulmonary veins. Like the right atrium, the inside of the left atrium has a smooth posterior wall. Because pectinate muscles are confined to the auricle of the left atrium, the anterior wall of the left atrium also is smooth.
Interatrial septum – thin partition in atria Fossa ovalis – oval depression; a prominent feature of the septum which is a remnant of foramen ovale, an opening in the interatrial septum of the fetal heart that normally closes soon after birth VENTRICLES: (little bellies) two inferior pumping chambers; Eject equal volumes of blood
SEMILUNAR VALVES – 3 crescent moon–shaped cusps attached to the arterial wall by its convex outer margin; prevents backflow into the ventricles; free borders of the cusps project into the lumen of the artery. OPEN: pressure in the ventricles exceeds the pressure in the arteries Ventricles Contract: pressure builds up within the chambers Ventricles Relaxed: back flowing blood fills the valve cusps, which causes the free edges of the semilunar valves to contact each other tightly and closes 3. Pulmonary valve / Pulmonary Semilunar valve – Blood passes from the right ventricle to... Pulmonary Trunk – large artery Right & Left Pulmonary Arteries – carries blood to the lungs. 4. Aortic Valve / Aortic Semilunar Valve – Blood passes from the left ventricle to... Ascending Aorta Coronary Arteries – carry blood to the heart wall. Arch of the aorta – carry blood throughout the body Descending aorta: thoracic aorta and abdominal aorta – carry blood throughout the body
FETAL LIFE: Ductus Arteriosus – temporary blood vessel that shunts blood from the pulmonary trunk into the aorta. Hence, only a small amount of blood enters the nonfunctioning fetal lung. Ligamentum Arteriosum – remnant after the ductus arteriosus closes shortly after birth; which connects the arch of the aorta and pulmonary trunk
Thickness depends on function:
VALVE: THICKNESS: FUNCTION: ATRIA thin deliver blood under less pressureinto the adjacent ventricles Right Atrium Left Atrium VENTRICLES thick pump blood under higherpressure over greater distances
Right Ventricle thick
smaller workload; short distance to the lungs at lower pressure, and the resistance to blood flow is small; perimeter of the lumen (space) is crescent-shaped
Left Ventricle thicker
Works harder; great distances to all other parts of the body at higher pressure, and the resistance to blood flow is larger; perimeter of the lumen (space) is roughly circular
FIBROUS SKLETON OF THE HEART
¾ 4 dense connective tissue rings that surround the valves of the heart, fuse with one another, and merge with the interventricular septum. ¾ Prevents overstretching, ¾ Point of insertion for bundles of cardiac muscle fibers ¾ Acts as electrical insulator between atria (from ventricles) and ventricles POSTNATAL (AFTERBIRTH) CIRCULATION: 2 closed circuits w/ each beats; arranged in series (output of one becomes the input of the other)
- Pulmonary Circulation – (right side) receives all the dark-red deoxygenated blood returning from the systemic circulation Right Atrium – TRICUSPID AV – Right Ventricle – PULMONARY SV – Pulmonary Trunk – Pulmonary Arteries – Lungs – Pulmonary Capillaries – Pulmonary Veins – Left Atrium
- Sytematic Circulation – (left side) receives bright red oxygenated (oxygen-rich) blood from the lungs Left Ventricle – AORTIC SV – Systemic Arteries – Arterioles – Systematic Capillaries – Systematic Venules – Systematic Veins – Right Atrium NOTE: No valves guarding the junctions between the venae cavae and the right atrium or the pulmonary veins and the left atrium. As the atria contract, a small amount of blood does flow backward from the atria into these vessels. (Backflow is minimized by a different mechanism; as the atrial muscle contracts, it compresses and nearly collapses the venous entry points) Nutrients are not able to diffuse quickly enough from blood in the chambers of the heart to supply all the layers of cells that make up the heart wall.
- Cardiac / Coronary Circulation – blood vessels of myocardium Coronary Arteries: from ascending aorta and encircle the heart. HEART CONTRACT: little blood flows in the coronary arteries because they are squeezed shut. HEART RELAXES: high pressure of blood in the aorta propels blood through the coronary arteries – capillaries – coronary veins 2 CORONARY ARTERIES:
- Right Coronary Artery – supplies small / atrial branches to the right atrium. It continues inferior to the right auricle and ultimately divides into the posterior interventricular and marginal branches. Posterior Interventricular Branch –supplies the walls of the two ventricles with oxygenated blood Marginal Branch – beyond the coronary sulcus runs along the right margin of the heart; oxygenated blood to the right ventricle.
- Left Coronary Artery – passes inferior to the left auricle and divides into the anterior interventricular and circumflex branches. Anterior Interventricular Branch / Left Anterior Descending (LAD) Artery – oxygenated blood to the walls of both ventricles.
potential. Rather, they repeatedly depolarize to threshold spontaneously (every 0 second or 100 times per minute). The spontaneous depolarization is a pacemaker potential. When the pacemaker potential reaches threshold, it triggers an action potential. The contraction rhythm or rate that is faster than that of any other autorhythmic fibers 2. Along atrial muscle fibers, the action potential reaches the Atrioventricular (AV) Node, located in the interatrial septum, just anterior to the opening of the coronary sinus; action potential slows considerably as a result of various differences in cell structure (smaller diameters and fewer gap junctions.) Delay provides time for the atria to empty their blood into the ventricles. 3. Enters the Atrioventricular (AV) Bundle / Bundle of His, only site where action potentials can conduct from the atria to the ventricles. 4. Enters both the Right and Left Bundle Branches. The bundle branches extend through the interventricular septum toward the apex of the heart. 5. Finally, the large-diameter Purkinje Fibers rapidly conduct the action potential beginning at the apex of the heart upward to the remainder of the ventricular myocardium. (Ventricular Contraction)
MODIFIES TIMING AND STRENGTH OF HEARTBEAT: do not establish the fundamental rhythm ANS Nerve impulses Acetylcholine (Parasympathetic Division) – slows SA node (0 second or 75 action potentials per minute) Blood-borne hormones: epinephrine modify the timing and strength of each heartbeat
Contractile Fibers – working atrial and ventricular muscle fibers ACTION POTENTIAL IN CONTRACTILE FIBER: 1. Depolarization: activated via threshold by an action potential from neighboring fibers; by inflow of Na down the electrochemical gradient Voltage-gated fast Na channels open rapidly. (Na inflow: cytosol of contractile fibers is electrically more negative than interstitial fluid and Na concentration is higher in interstitial fluid.) Within a few milliseconds, the fast Na channels automatically inactivate and Na inflow decreases. 2. Plateau (0 secs): only found in contractile fiber; a period of maintained depolarization = Ca inflow just balances K outflow. Just before the plateau phase begins, Sarcolemma’s K channels open, allowing potassium ions to leave the contractile fiber. Opening of voltage-gated slow Ca channels in the sarcolemma. When these channels open, calcium ions move from the interstitial fluid (which has a higher Ca concentration) into the cytosol. SR Ca channels opens Increased Ca concentration in the cytosol ultimately triggers contraction. 3. Repolarization: recovery of the resting membrane potential
After a prolonged delay; additional voltage-gated K channels open. (Outflow = Restore Negative Resting Membrane Potential – 90mV) Ca channels in the sarcolemma and SR are closing
The mechanism of contraction is similar in cardiac and skeletal muscle: The electrical activity (action potential) leads to the mechanical response (contraction) after a short delay. As Ca2 concentration rises inside a contractile fiber, Ca2 binds to the regulatory protein troponin, which allows the actin and myosin filaments to begin sliding past one another, and tension starts to develop. Substances that alter the movement of Ca2 through slow Ca2 channels influence the strength of heart contractions.
Epinephrine, for example, increases contraction force by enhancing Ca2 flow into the cytosol.
In muscle, the refractory period (re-FRAK-to-re ̄) is the time interval during which a second contraction cannot be triggered. The refractory period of a cardiac muscle fiber lasts longer than the contraction itself (Figure 20). As a result, another contraction cannot begin until relaxation is well under way. For this reason, tetanus (maintained contraction) cannot occur in cardiac muscle as it can in skeletal muscle. The advantage is apparent if you consider how the ventricles work. Their pumping function depends on alternating contraction (when they eject blood) and relaxation (when they refill). If heart muscle could undergo tetanus, blood flow would cease.
ATP Production in Cardiac Muscle ¾ Produces little of the ATP by anaerobic cellular respiration; it relies almost exclusively on aerobic cellular respiration in its numerous mitochondria. ¾ The needed oxygen diffuses from blood in the coronary circulation and is released from myoglobin inside cardiac muscle fibers. Cardiac muscle fibers use several fuels to power mitochondrial ATP production. ¾ Resting: oxidation of fatty acids (60%) and glucose (35%), with smaller contributions from lactic acid, amino acids, and ketone bodies. ¾ Working: lactic acid, creatine phosphate.
Electrocardiogram (ECG / EKG) – recording of electrical signals; composite record of action potentials produced by all the heart muscle fibers during each heartbeat via Electrocardiograph; Electrodes are positioned on the arms and legs (6 limb leads) and 6 chest leads; amplifies the heart’s electrical signals and produces 12 different tracings from different combinations of limb and chest leads. Each limb and chest electrode records slightly different electrical activity because of the difference in its position relative to the heart. By comparing these records with one another and with normal records, it is possible to determine: If the conducting pathway is abnormal, If the heart is enlarged
Note: During the next 0 sec, contractile fibers in both the atria and ventricles are relaxed. At 0 sec, the P wave appears again in the ECG, the atria begin to contract, and the cycle repeats.
THE CARDIAC CYCLE (1 Heartbeat): Systole and Diastole of atria and ventricles CONTRACTION: Chamber has higher pressure – Fluid pushed from higher to lower concentration shows the relation between the heart’s electrical signals (ECG) and changes in atrial pressure, ventricular pressure, aortic pressure, and ventricular volume during the cardiac cycle; pressures on the right side are considerably lower. Each ventricle, however, expels the same volume of blood per beat, and the same pattern exists for both pumping chambers. Heart Rate:75 beats/min Cardiac Cycle:0 sec. Atrial Systole (0 sec): 1. Depolarization of the SA node causes atrial depolarization, marked by the P wave in the ECG. 2. Atrial depolarization causes atrial systole. As the atria contract, they exert pressure on the blood within, which forces blood through the open AV valves into the ventricles. 3. Atrial systole contributes a final 25 mL of blood to the volume already in each ventricle (about 105 mL). The end of atrial systole is also the end of ventricular diastole (relaxation). Thus, each ventricle contains about 130 mL at the end of its relaxation period (diastole). This blood volume is called the end-diastolic volume (EDV). 4. The QRS complex in the ECG marks the onset of ventricular depolarization. Ventricular Systole (0 sec): 1. Ventricular depolarization causes ventricular systole. As ventricular systole begins, pressure rises inside the ventricles and pushes blood up against the atrioventricular (AV) valves, forcing them shut. For about 0 seconds, both the SL (semilunar) and AV valves are closed. This is the period of isovolumetric contraction (ı ̄-so ̄-VOL-u-met-rik; iso- same). During this interval, cardiac muscle fibers are contracting and exerting force but are not yet shortening. Thus, the muscle contraction is isometric (same length). Moreover, because all four valves are closed, ventricular volume remains the same (isovolumic). 2. Continued contraction of the ventricles causes pressure inside the chambers to rise sharply. When left ventricular pressure surpasses aortic pressure at about 80 millimeters of mercury (mmHg) and right ventricular pressure rises above the pressure in the pulmonary trunk (about 20 mmHg), both SL valves 3. open. At this point, ejection of blood from the heart begins. The period when the SL valves are open is ventricular ejection and lasts for about 0 sec. The pressure in the left ventricle continues to rise to about 120 mmHg, whereas the pressure in the right ventricle climbs to about 25–30 mmHg. 4. The left ventricle ejects about 70 mL of blood into the aorta and the right ventricle ejects the same volume of blood into the pulmonary trunk. The volume remaining in each ventricle at the end of systole, about 60 mL, is the end-systolic volume (ESV). Stroke volume, the volume ejected per beat from each ventricle, equals end-diastolic volume minus end-systolic volume: SV EDV ESV. At rest, the stroke volume is about 130 mL 60 mL 70 mL (a little more than 2 oz).
- The T wave in the ECG marks the onset of ventricular repolarization. Relaxation Period(0 sec): both relaxed. As the heart beats gets faster relaxation period becomes shorter whereas the durations of atrial and ventricular systole shorten only slightly.
- Ventricular repolarization causes ventricular diastole. As the ventricles relax, pressure within the chambers falls, and blood in the aorta and pulmonary trunk begins to flow backward toward the regions of lower pressure in the ventricles. Backflowing blood catches in the valve cusps and closes the SL valves. The aortic valve closes at a pressure of about 100 mmHg. Rebound of blood off the closed cusps of the aortic valve produces the dicrotic wave on the aortic pressure curve. After the SL valves close, there is a brief interval when ventricular blood volume does not change because all four valves are closed. This is the period of isovolumetric relaxation.
- As the ventricles continue to relax, the pressure falls quickly. When ventricular pressure drops below atrial pressure, the AV valves open, and ventricular filling begins. The major part of ventricular filling occurs just after the AV valves open. Blood that has been flowing into and building up in the atria during ventricular systole then rushes rapidly into the ventricles. At the end of the relaxation period, the ventricles are about three-quarters full. The P wave appears in the ECG, signaling the start of another cardiac cycle.
Auscultation – the act of listening to sounds within the body, is usually done with a stethoscope. The sound of the heartbeat comes primarily from blood turbulence caused by the closing of the heart valves. Smoothly flowing blood is silent. Compare the sounds made by white-water rapids or a waterfall with the silence of a smoothly flowing river.
4 HEART SOUNDS: (1 cardiac cycle) Lubb (S1) – louder and a bit longer than the second sound; blood turbulence associated with closure of the AV valves soon after ventricular systole begins. Dupp (S2) – shorter and not as loud as the first; blood turbulence associated with closure of the SL valves at the beginning of ventricular diastole. Note: Although S1 and S2 are due to blood turbulence associated with the closure of valves, they are best heard at the surface of the chest in locations that are slightly different from the locations of the valves. This is because the sound is carried by the blood flow away from the valves. S3 is due to blood turbulence during rapid ventricular filling S4 is due to blood turbulence during atrial systole.
CLINICAL CONNECTIONS:
Pericarditis – Inflammation of the pericardium Acute Pericarditis – Most common; Begins suddenly and sometimes linked to a viral infection; chest pain that may extend to the left shoulder and down the left arm (often mistaken for a heart attack) and pericardial friction rub (a scratchy or creaking sound heard through a stethoscope as the visceral layer of the serous pericardium rubs against the parietal layer of the serous pericardium). Lasts for about 1 week and is treated with drugs that reduce inflammation and pain, such as ibuprofen or aspirin. Chronic Pericarditis – begins gradually and is long-lasting; buildup of pericardial fluid. Cardiac Tamponade –great deal of fluid accumulates and compresses the heart; life- threatening condition; ventricular filling is decreased, cardiac output is reduced, venous return to the heart is diminished, blood pressure falls, and breathing is difficult; sometimes caused by conditions such as cancer and tuberculosis. Treatment consists of draining the excess fluid through a needle passed into the pericardial cavity. Myocarditis – inflammation of the myocardium; complication of a viral infection, rheumatic fever, or exposure to radiation or certain chemicals or medications; often has no symptoms. However, if they do occur, they may include fever, fatigue, vague chest pain, irregular or rapid heartbeat, joint pain, and breathlessness. Severe cases can lead to cardiac failure and death Usually mild and recovery occurs within 2 weeks. Treatment consists of avoiding vigorous exercise, a low-salt diet, electrocardiographic monitoring, and treatment of the cardiac failure. Endocarditis –inflammation of the endocardium and typically involves the heart valves; caused by bacterial endocarditis. Signs and symptoms of endocarditis include fever, heart murmur, irregular or rapid heartbeat, fatigue, loss of appetite, night sweats, and chills. Treatment is with intravenous antibiotics. Stenosis – narrowing of a heart valve opening that restricts blood flow Insufficiency / Incompetence – failure of a valve to close completely Mitral Stenosis – scar formation or a congenital defect causes narrowing of the mitral valve. Aortic Stenosis – aortic valve is narrowed, and in aortic insufficiency there is backflow of blood from the aorta into the left ventricle.
Mitral Valve Prolapse (MVP) – most common valvular disorders. It is more prevalent in women than in men; backflow of blood from the left ventricle into the left atrium; one or both cusps of the mitral valve protrude into the left atrium during ventricular contraction. Rheumatic fever – an acute systemic inflammatory disease that usually occurs after a streptococcal infection of the throat. The bacteria trigger an immune response in which antibodies produced to destroy the bacteria instead attack and inflame the connective tissues in joints, heart valves, and other organs; weaken the entire heart wall but most often it damages the mitral and aortic valves. Myocardial Ischemia – by Partial obstruction of blood flow in the coronary arteries; a condition of reduced blood flow to the myocardium; causes hypoxia which may weaken cells without killing them. Silent Myocardial Ischemia – without pain; dangerous because the person has no forewarning of an impending heart attack. Angina Pectoris – (strangled chest) severe pain that usually accompanies myocardial ischemia; tightness or squeezing sensation, as though the chest were in a vise; pain to the neck, chin, or down the left arm to the elbow. Myocardial Infarction / Heart Attack – A complete obstruction to blood flow in a coronary artery. Because the heart tissue distal to the obstruction dies and is replaced by noncontractile scar tissue, Myocardial Ischemia and Infarction the heart muscle loses some of its strength. Presence of creatine kinase (CK) in blood – catalyzes transfer of a phosphate group from creatine phosphate to ADP to make ATP. Normally, CK and other enzymes are confined within cells. Injured or dying cardiac or skeletal muscle fibers release CK into the blood. Treatment for a myocardial infarction may involve injection of a thrombolytic (clot- dissolving) agent such as streptokinase or t-PA, plus heparin (an anticoagulant), or performing coronary angioplasty or coronary artery bypass grafting; replaced with noncontractile fibrous scar tissue over time. Fortunately, heart muscle can remain alive in a resting person if it receives as little as 10–15% of its normal blood supply. Infarction – death of an area of tissue because of interrupted blood supply; Depending on the size and location; may disrupt the conduction system of the heart and cause sudden death by triggering ventricular fibrillation.
If the AV valves or chordae tendineae are damaged, blood may regurgitate (flow back) into the atria
when the ventricles contract.
fail before the other. If the left ventricle fails first, it can’t pump out all the blood it receives. As a result, blood backs up in the lungs and causes pulmonary edema, fluid accumulation in the lungs that can cause suffocation if left untreated. If the right ventricle fails first, blood backs up in the systemic veins and, over time, the kidneys cause an increase in blood volume. In this case, the resulting peripheral edema usually is most noticeable in the feet and ankles.
Larger P Waves – enlargement of an atrium Enlarged Q Wave – myocardial infarction Enlarged R Wave – enlarged ventricles Flatter T Wave – heart muscle is receiving insufficient oxygen—as, for example, in coronary artery disease. Elevated T Wave – Hyperkalemia (high blood K level) Elevated S–T Segment – acute myocardial infarction
Depressed S –T Segment – heart muscle receives insufficient oxygen
Cardiovascular System Reviewer
Course: BS Nursing (BSN)
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