BIO-211 (Dr. Carter, Lecture) Midlands Tech: Exam 2 Study Guide UNFINISHED

Ch. 18 (44.) How will an increase in free intracellular calcium affect the myocardium? (Choose one of the following - it's a multiple choice study guide question.) a. Relaxation b. Contraction c. Repolarization d. Return to the resting membrane potential

b. Contraction

Ch. 18 (34.) What pressure must left ventricular pressure exceed to pump blood into the systemic circuit? Why?

• Afterload (the pressure that the ventricles must overcome to eject blood) is overcome in the left ventricle by exerting 80 mm Hg on the aortic semilunar valve. • The left ventricle does this to eject blood through the aorta.

Ch. 18 (35.) What pressure does the right ventricle have to overcome to pump blood into the pulmonary circuit? Why?

• Afterload (the pressure that the ventricles must overcome to eject blood) is overcome in the right ventricle by exerting 10 mm Hg on the pulmonary semilunar valve. • The right ventricle does this to eject blood through the pulmonary trunk.

Ch. 18 (25.) What kind of information does an EKG provide?

• An electrocardiograph monitors and amplifies the electrical signals of the heart and records it as an electrocardigram. * EKG and ECG are the same thing. Electrocardiograph translated into german is Elektrokardigraphie.

Ch. 18 (17.) Describe the properties of cardiac myocytes. Do cardiac myocytes use the sliding filament mechanism to contract? How does the absolute refractory period of cardiac myocytes compare to skeletal muscle fibers? What is the purpose? What are intercalated disks? What does the statement "the heart contracts as a unit or not at all" mean?

• Cardiac myocytes (muscle cells) are striated, short, branched, and contain only or two nuclei per cell. • Cardiac myocytes do use the sliding filament mechanism to contract. • In skeletal muscle, the absolute refractory period is much shorter than the contraction, allowing multiple contractions to summate (tetanic contractions). The absolute refractory period in the heart is nearly as long as the contraction itself. • If the heart were to contract tetanically, it would be unable to relax and fill, and would result in it being useless as a pump. Thus, the heart must contract in longer increments to prevent tetanic contraction. • Intercalated disks are dark staining junctions that contain anchoring desmosomes and gap junctions that allow the plasma membranes of adjacent cardiac cells to interlock like the ribs of two sheets of corrugated cardboard. • "The heart contracts as a unit or not at all," refers to the autorhythmicity of the cardiac muscle cells. These autorhythmic cells generate an action potential that spreads thoughout the myocardium (across gap junctions), causing the wave of depolarization to travel rom cell to cell across the heart, resulting in the heart contracting as a single unit.

Ch. 18 (37.) What is cardiac output?

• Cardiac output is defined as the amount of blood pumped out of a ventricle per minute, and is calculated as the product of stroke volume and heart rate.

Ch. 18 (32.) Which valves are open and which are closed during atrial systole and atrial diastole?

• During atrial systole the aortic and pulmonary valves are closed and atrioventricular valves are open. • During atrial diastole, the atrioventricular valves are closed the aortic and pulmonary valves are closed for the beginning but are open the vast remainder of the time.

Ch. 18 (42.) What happens inside the cardiac myocytes when preload is increased? Can preload be increased too much? What happens in that case? How will this affect stroke volume?

• During increased preload, the cell's sarcomere lengths increase as it stretches and begins to approach optimal overlap. This can produce dramatic increases in contractile force. * Increase in the strength of contraction, velocity of shortening, extent of shortening, and stroke volume. • Too great of an increase on preload will prevent overlap of the sarcomeres, and as such, the heart will not be able to contract at all. • If stroke volume is compromised, then as a result, cardiac output is as well. Issues with stroke volume can causes a decrease in cardiac output.

Ch. 18 (31.) Which valves are open and which are closed during ventricular systole and ventricular diastole?

• During ventricular filling (mid-to-late diastole) the aortic and pulmonary valves are closed and the atrioventricular valves are open. • During ventricular systole the atrioventricular valves are closed and the aortic and pulmonary valves are closed for the beginning, but are open the vast remainder of the time. • During early ventricular diastole the atrioventricular valves are closed and the aortic pulmonary valves are closed.

Ch. 18 (3.) Which part of the heart is the base and which part is the apex?

• The base of the heart is directed toward the right shoulder. • The apex is points towards the left hip.

Ch. 18 (33.) What is the period of isovolumetric contraction? Why is there a period of isovolumetric contraction? What is the period of isovolumetric relaxation? What is that all about? Is there a time in the cardiac cycle when all valves are open?

• During ventricular systole (atrial diastole), isovolumetric contraction occurs during the split- second period when the ventricles are completely closed chambers, and the blood volume in these chambers remain constant as the ventricles contract. • The isovolumetric contraction period exists to allow necessary pressure changes that are essential for blood to flow into or out of the ventricles. * During this period, the ventricles contract, and the atrioventricular valves and semilunar valves are shut. • Isovolumetric relaxation allows the ventricles to fully relax, resulting in the ventricular filling needed to begin the cycle again. * During this period, the ventricles start to relax and the atrioventricular and semilunar valves close, except for at the very end when the ventricles fully relax and atrioventricular valves open. • There is no point in cardiac cycle when all valves are open at the same time.

Ch. 18 (38.) What is the definition of end systolic volume, end diastolic volume, and stroke volume?

• End systolic volume is the volume of blood remaining in a ventricle after it has contracted. • End diastolic volume is the amount of blood that collects in a ventricle during diastole. • Stroke volume is defined as the volume of blood pumped out by one ventricle with each beat.

Ch. 18 (28.) What causes heart sounds I and II? What causes heart murmurs? What is the difference between regurgitation and stenosis?

• Heart sound I, "lub" or "lup", corresponds to closure of the AV valves, and occurs during ventricular systole. • Heart sound II, "dub" or "dup", corresponds to the closure of the aortic and pulmonary valves, and occurs during ventricular diastole. • Regurgitation refers to the turbulent flow of blood backwards through a valve that does not close tightly. • Stenosis refers to the turbulent flow of blood forwards through valve that doesn't open completely.

Ch. 18 (43.) What 2 things will increase pre-load? How can you increase the time of ventricular filling? How can you increase the rate of ventricular filling? If you got the same answer I did doesn't that seem contradictory? So what's the point?

• Increase rate of filling by increasing heart rate (applies to exercise) • Increase of time of filling by decreasing heart rate. • Though contradictory, together, they balance the output between the ventricles

Ch. 18 (40.) What three things regulate stroke volume?

• Stroke volume is regulated by: 1. Preload * The degree to which cardiac muscle cells are stretched just before they contract. 2. Contractility * The contractile strength achieved at a given muscle length. 3. Afterload * The pressure that the ventricles must overcome to eject blood.

Ch. 18 (23.) How does sympathetic innervation affect the heart? How does parasympathetic innervation affect the heart? What is the dominant extrinsic influence on heart rate at rest?

• Sympathetic innervation affects the heart through sympathetic fibers that innervate both the SA and AV nodes of the myocardium, resulting in stimulation of pacemaker cells and increase in heart rate and contractility of the ventricles (especially the left ventricle). * It does this by enhancing Ca++ movements to the contractile cells. This enhanced contractility lowers end systolic volume, so systolic volume does not decline as it would if only heart rate increased. • Parasympathetic stimulation "puts the brakes on" the heart rate set by the SA node by inhibiting the cardiac pacemaker cells * This process is mediated by acetylcholine, which hyperpolarizes the membranes of its effector cells by opening K+ channels. • The dominant extrinsic influence on the heart rate at rest is inhibitory due to the parasympathetic stimulation through the vagus nerve.

Ch. 18 (27.) What are tachycardia, bradycardia, normal sinus rhythm, and heart block?

• Tachycardia is an abnormally fast heart rate (more than 100 bpm). * It may result from elevated body temperature, stress, certain drugs, or her disease. • Bradycardia is a heart rate slower than 60 bpm. * It may results from low body temperature, certain drugs, or parasympathetic nervous activation. • Normal sinus rhythm, also known as a normal ECG trace, is driven by the SA node; indicates a healthy (normal) heart beat. • Heart block has three degrees: - 1st degree heart block refers to the prolongation of the P-Q interval due to refractoriness of the conductive cells in the AV node. - 2nd degree heart block refers to the fraction of atrial depolarizations that are conducted through the AV node, resulting more P waves than QRS complexes. The ratio is usually that of 2 small integers (2:1, 3:1, 3:2). * The block may be above or below the bundle, but if the block is below the bundle the ramifications are more severe. - 3rd degree heart block refers to a complete heart block, in which no atrial depolarization are conducted through the AV node. Atrial and ventricular contractions are completely independent, and the intrinsic depolarization of the ventricles (about 32 bpm) often results in syncope. * This condition is one of the most common requiring artificial pacemakers.

Ch. 18 (41.) According to the Frank-Starling law of the heart what is the critical factor controlling stroke volume?

• The Frank-Starling law of the heart states that the critical factor controlling stroke volume is the degree of stretch of cardiac muscle cells immediately before they contract.

Ch. 18 (12.) Which valves keep blood from flowing back into the venous circulation when the atria contract?

• The atrioventricular valves (AV valves), or the bicuspid (mitral) and tricuspid valves, keep the blood from flowing back into venous circulation when the atria contract.

Ch. 18 (16.) What causes the AV valves to open? What causes them to close? What causes the semilunar valves to open? What causes them to close?

• The atrioventricular valves are opened when the heart is relaxed, and are closed when the heart contracts. • The semilunar valves are closed when the heart is relaxed, and are opened when the heart contracts.

Ch. 18 (29.) What is the cardiac cycle? Define systole and diastole.

• The cardiac cycle is a sequence that includes all events associated with blood flow through the heart during one complete heartbeat (atrial systole and diastole followed by ventricular systole and diastole).

Ch. 18 (15.) What is the function of the chordae tendineae? What is the function of the papillary muscles?

• The chordae tendineae are tiny white collagen flaps attached to each atrioventricular valve flap. They anchor the cusps to the the papillary muscles. • The papillary muscles are muscular bundles that protrude from the ventricular walls. They play a role in valve function by contracting with the other ventricular musculature so they are able to take up the slack on the chordae tendineae as the full force of the ventricular contraction hurls the blood against the atrioventricular valve flaps.

Ch. 18 (26.) What does the P wave represent? What does the QRS complex represent? Why is it so complex? What does the T wave represent?

• The first and smallest wave, the P wave, represents the movement of the depolarization wave from the SA node to the atria, and lasts about 0.08 seconds. •The largest of the waves, known as the QRS complex, results from the ventricular depolarization and precedes ventricular contraction. • The QRS complex is so complex due to the complication in shape. This is because the paths of the depolarization waves through the ventricular walls change continuously, producing corresponding changes in current direction.

Ch. 18 (24.) If the pacemaker cells at the SA node depolarize at a rate of approximately 100 times per minute how can a normal resting heart rate be approximately 72 - 75 beats per minute?

• The heart rate is generally slower than it would be if the vagal nerves were not innervating it. This integral mechanism is known as vagal tone. * Cutting the vagal nerves results in an almost immediate increase in heart rate of about (25 bpm), which when added to the resting heat rate of 72-75 bpm, reflects the inherent rate (100 bpm) of the pacemaking SA node.

Ch. 18 (18.) How does the heart meet its energy demands? What fuels can cardiac myocytes use to power contraction?

• The heart relies exclusively on aerobic respiration for its energy demands. • Like skeletal myocytes, cardiac myoctyes use multiple fuel molecules, including glucose and fatty acids. However, the cardiac muscle tissue is much more adaptable than skeletal muscle tissue, and as such, it is able to readily switch metabolic pathways to use whatever nutrients are available, including lactic acid generated by skeletal muscle activity.

Ch. 18 (19.) What is the intrinsic conduction system of the heart? What are autorhythmic cells? What is a pacemaker potential? How does it make autorhythmic cells spontaneously depolarize?

• The intrinsic conduction system of the heart is made up of specialized cardiac cells that initiate and distribute impulses, ensuring that the heart depolarizes in an orderly fashion. • Autorhyhtmic cells, or self-excitable cells, are cells that generate action potentials that spread in waves to all the cardiac contractile cells, causing a coordinated heart contraction. • Autorhythmic cells have an unstable or drifting resting potential, called a pacemaker potential, which results in slow depolarization. * When the resting potential "drifts up" to threshold the cells rapidly generate an action potential. * Depolarization is followed by repolarization, although the inward flu of Ca++ extends the absolute refractory period and inhibits rapid sequential depolarizations.

Ch. 18 (8.) Which side of the heart pumps blood to the systemic circuit? Which side receives blood from the systemic circuit?

• The left side of the heart pumps blood to the systemic circuit. • The right side of the heart receives blood from the systemic circuit.

Ch. 18 (2.) What is the myocardium? What is the endocardium? What kind of cells make up each?

• The myocardium is the middle layer of the heart wall that forms the bulk of the heart, and is composed mainly of cardiac muscle cells. • The endocardium is the third layer of the heart wall that lines the chambers of the heart, and is made up a glistening white sheet of endothelium (squamous epithelium) resting on a thin connective tissue layer.

Ch. 18 (9.) How does the myocardium receive oxygen and nutrients? Where does the coronary circulation begin? Where does blood from the coronary circulation return to the heart? Is the coronary circulation really necessary? What happens if it is blocked?

• The myocardium receives oxygen and nutrients through coronary circulation. • Coronary circulation begins with the left and right coronary arteries that arise from the baes of the aorta and encircle the heart in the coronary sulcus. • Blood fro coronary circulation returns to the heart through the coronary sinus, which empties blood into the right atrium. • Coronary circulation is necessary because due to the myocardium's thickness, it cannot practically receive oxygen and nutrients through diffusion. • If coronary circulation is blocked it can cause angina pectoris (a thoracic pain cause by a fleeting deficiency in blood delivery to the myocardium). Prolonged coronary blockage can lead to myocardial infarction (more commonly known as a heart attack).

Ch. 18 (4.) Know the path of blood through the heart: be able to trace the flow of blood from somewhere out in the systemic circuit through the heart and back to the starting place.

• The pathway of blood through the heart: - Superior vena cava (O2 poor) - Inferior vena cava (O2 poor) - Right atrium (O2 poor) - Tricuspid valve (O2 poor) - Right ventricle (O2 poor) - Pulmonary semilunar valve (O2 poor) - Pulmonary trunk (O2 poor) - Pulmonary arteries (O2 poor) (To the lungs to pick up oxygen) - Pulmonary veins (O2 rich) - Left atrium (O2 rich) - Bicuspid (mitral) valve (O2 rich) - Left ventricle (O2 rich) - Aortic semilunar valve (O2 rich) - Ascending aorta (O2 rich) - Aortic arch (O2 rich) - Descending aorta (O2 rich) - Thoracic aorta (O2 rich) - Abdominal aorta (O2 rich) (To the rest of the body)

Ch. 18 (1.) What is the pericardium? What is the difference between the fibrous pericardium and the serous pericardium?

• The pericardium is a double-walled sac that encloses the heart. • The differences between the fibrous pericardium and serous pericardium: - The fibrous pericardium is made up of a tough, connective tissue layer that protects the heart, anchors it to surround structures, and prevents overruling of the heart with blood. - The serous pericardium is a thin, slippery, two layer serous membrane that forms a closed sac around the heart.

Ch. 18 (30.) What portion of the electrocardiogram represents the quiescent phase of the cardiac cycle? Be able to correlate the phase of the cardiac cycle with each part of the EKG (atrial systole/diastole, ventricular systole/diastole, etc.).

• The quiescent phase refers to isovolumetric relaxation in early ventricular diastole until atrial contraction (the end of the T wave to the beginning of the next P wave). • The phases of the cardiac cycle: - Ventricular filling: mid-to-late diastole (includes atrial systole, P-Q interval). - Ventricular systole: isovolumetric contraction and ejection phase (Q-T interval). - Isovolumetric relaxation: early ventricular diastole (brief phase following the T wave).

Ch. 18 (5.) Which chambers are the receiving chambers of the heart? Which chamber receives deoxygenated blood? Which chamber receives oxygenated blood?

• The right and left atria are the receiving chambers of the heart. • The right atrium receives deoxygenated blood. • The left atrium receives oxygenated blood.

Ch. 18 (7.) Which side of the heart pumps blood to the pulmonary circuit? Which side receives blood from the pulmonary circuit?

• The right side of the heart pumps blood to the pulmonary circuit. • The left side of the heart receives blood from the pulmonary circuit.

Ch. 18 (36.) Why is the right ventricular wall thinner than the left?

• The right ventricular wall is thinner than the left because the left ventricle needs to pump blood to most of the body, while the right ventricle only needs to pump blood to the lungs.

Ch. 18 (21.) What is the route of conductance of electrical activity through the heart?

• The route of conductance of electrical activity through the heart is as follows: 1. The SA node generates a depolarization wave (impulse) that will set the pace for heart. 2. The impulse pauses (0.1 seconds) at the AV node, allowing the atria to respond and complete their contraction before the ventricles contract. 3. The AV bundle connects the atria to the ventricles, as the two are not adjacent to one another and are not connected by gap junctions, the AV bundle is the only electrical connection between them. 4. The right and left bundle branches conducts the impulse through the interventricular septum and toward the heart apex. 5. The subendocardial conduction network (also called the Purkinje fibers) completes the pathway through the interventricular septum, penetrates into the heart apex, and turns superiorly into the ventricular walls, depolarizing the contractile cells of both ventricles.

Ch 18. (20.) What is the pacemaker of the heart? If it "blows out" what can take over?

• The sinoatrial (SA) node is known as the pacemaker of the heart because it sets the pace for the heart due to its superior rate of depolarization. • If the SA node "blows out," or becomes defective, then an ectopic focus can take over the pacing of the heart rate (or, in this situation, the AV node can also become the pacemaker).

Ch. 18 (22.) What contributes to extrinsic regulation of heart rate?

• The sympathetic nervous system (the "accelerator") increases both the rate and force of the heartbeat via the nerves of T1-T5 level of the thoracic spinal cord. The parasympathetic nervous system (the "brakes") slows the heart rate via the vagus nerve.

Ch. 18 (10.) What is the valve between the left atrium and the left ventricle? What is the valve between the right atrium and right ventricle? What do they do?

• The valve between the left atrium and left ventricle is the bicuspid (mitral) valve. • The valve between the right atrium and the right ventricle is the tricuspid valve. • The bicuspid (mitral) and tricuspid valves prevent backflow into the atria when the ventricles contract.

Ch. 18 (11.) What is the valve between the right ventricle and pulmonary artery? What is the valve between the left ventricle and aorta? What do they do?

• The valve between the right ventricle and pulmonary artery is the pulmonary semilunar valve. • The valve between the left ventricle and the aorta is the aortic semilunar valve. • The pulmonary and aortic semilunar valves precent backflow of blood into the ventricles.

Ch. 18 (6.) Which chambers pump blood out of the heart? Which chamber pumps blood into the pulmonary trunk? Which pumps blood into the aorta?

• The ventricles pump blood out of the heart. • The right ventricle pumps blood into the pulmonary trunk. • The left ventricle pumps blood into the (ascending) aorta.

Ch. 18 (39.) How do ESV, EDV, heart rate, and stroke volume affect cardiac output?

• To calculate the cardiac output, you must first have stroke volume, and to calculate stroke volume, you must have end diastolic volume and end systolic volume. * Cardiac output = heart rate x stroke volume * Stroke volume = end diastolic volume - end systolic volume

Ch. 18 (13.) When atria contract which valves are open? Which are closed?

• When the atria contract, the atrioventricular valves open and the semilunar valves are closed.

Ch. 18 (14.) When ventricles contract which valves are open? Which are closed? Which valves are open and which valves are closed when the ventricles are relaxed?

• When the ventricles contract, the semilunar valves open and the atrioventricular valves close. • When the ventricles are relaxed, the semilunar valves close and atrioventricular valves are pushed open as blood flows into the ventricles.