Term 2 Midterm Material Flashcards
Describe the structure and functions of the three components of the cardiovascular system.
- Heart → a pump for moving blood
- Blood vessels → the system of tubes that conduct blood around the body
- Blood → a fluid connective tissue which distributes oxygen, carbon dioxide, nutrients, waste products, and hormones.
Describe the composition of blood. [3]
- Blood → contains specialized cell fragments (i.e., platelets) and proteins that give it the ability to form clots.
- Serum → the fluid that is left after blood clotting - it contains water, solutes, and blood proteins that are not related to clot formation
- Plasma → the aqueous component of undisturbed blood and contains protein clotting factors.
Explain the anatomy and physiology of a red blood cell, including the structure and function of haemoglobin.
- RBCs have flexible, biconcave shape, and lack a nucleus. They have high surface area to facilitate oxygen transfer.
- RBCs are full of haemoglobin, which contains iron and is responsible for oxygen binding. There are four heme molecules per haemoglobin molecule. The iron within each heme allows haemoglobin to carry oxygen.
Describe the main components of a complete blood count (CBC) and describe its usage.
A CBC determines the number and distribution of formed elements and measures RBC health. Both increases and decreases from normal values can indicate blood disorders.
- Haematocrit → the packed cell volume (% of formed elements in blood)
- MCH → measures of RBC maturity (Hb content)
- MCV → measure of RBC size
- Cell counts → measures which formed elements are present at normal levels.
Explain the events occurring during primary haemostasis.
-
Primary haemostasis
- Vascular phase → involves changes to the endothelial and smooth muscle cells of the blood vessel wall (contraction or ‘vascular spasm’ and increased endothelial stickiness)
- Platelet phase → platelets circulating in blood stick to the endothelial cells and basement membrane and become activated; once activated, they release chemicals which attract other platelets and help them stick to one another (= positive feedback loop)
Explain the role of bone marrow in the formation of formed elements and compare and contrast the formation of RBCs, WBCs and platelets.
- Yellow bone marrow → mostly adipocytes; found in medullary cavity; increased proportion as you age
- Red bone marrow → contains blood forming stem cells; found around spongy bone.
- Lymphoid → lymphocytes
- Myeloid → RBCs; platelets; progenitor cells (which give rice to monocytes, neutrophils, eosinophils, and basophils)
Explain the role of RBC antigens in blood type for both ABO and Rh groupings.
- An individual’s immune system will produce antibodies against RBC antigens only if their own RBCs lack that antigen.
- The antibodies will cause aggregation and destruction of any blood cells that do contain the antigen (a potential problem for blood donation).
- O- → universal donor
- AB+ → universal recipient
- The Rhesus factor is either present or absent.
- Exposure to Rh+ foetal RBCs (which occurs during labour and delivery) leads to antibody production in an Rh- mother.
- These antibodies can cross the placental barrier and destroy foetal Rh+ RBCs in the later stages of any subsequent pregnancies causing dangerous anemia.
- Rh+ mothers would not have to worry about this issue because they will not produce antibodies, meaning her children will not be affected.
- Exposure to Rh+ foetal RBCs (which occurs during labour and delivery) leads to antibody production in an Rh- mother.
Compare and contrast between plasma and interstitial fluid. [3]
- Plasma proteins → only present in plasma, including:
- Albumins → involved in transport and fluid balance
- Globulins → involved in immunity and transport
- Fibrinogen → clotting factor
- Plasma has a higher concentration of oxygen
- Both contain electrolytes, organic nutrients, wastes, enzymes, and hormones.
Explain how the different components of plasma and formed elements contribute to its functions.
- Oxygen transport → RBCs (more than 99% of formed elements in blood)
- Immune functions → monocytes, lymphocytes, eisinophil, neutrophil, basophil
- Clotting → platelets
A number of genetic variants that change the amino acid sequence of the haemoglobin molecule can lead to RBCs changing shape, causing sickle cell disease. These sickling variants are more common in some populations around the world than others.
- How would these RBC shape changes lead to disease?
- What trade-off has kept these variants in our populations?
The sickle shape is inefficient at travelling through small blood vessels, so blood will not flow as well.
The shape also impacts the RBCs’ ability to carry oxygen.
However, the sickle shape makes it hard for Plasmodium to infect RBCs.
Plasmodium is the cause of malaria; thus, sickle cells protect against malaria.
Patient 1 (left); Patient 2 (right) → What measures are abnormal? What symptoms would you expect to see?
Patient 1 → low Hb = anemia; MCV is low = hypochromic; symptoms may include fatigue due to difficulty supplying oxygen to tissues to meet metabolic demands
Patient 2 → elevated platelets = thrombocytosis; symptoms could include increased risk of blood clot formation.
Explain the steps occurring in secondary haemostasis and the coagulation pathway.
-
Secondary haemostasis
- Coagulation phase → triggered by tissue damage or exposed connective tissue; takes at least 30 seconds to begin after vessel damage, and involves many enzymes which catalyze the formation of a fibrin mesh network around platelets, producing a clot. The ultimate effect of coagulation is to convert the soluble plasma protein fibrinogen into insoluble fibrin, which binds platelets into a clot.
-
Coagulation pathway → in the blood clotting cascade, activation of one clotting factor enzyme will catalyze the activation of another enzyme (and so on).
- Two distinct sets of enzymes converge on a common pathway where Factor IIa (Thrombin) catalyzes the formation of Factor Ia (Fibrin).
What happens after formation of a blood clot due to vessel damage?
Clot retraction, and fibrinolysis dissolves the clot after the vessel wall is repaired. This involves changes in the cytoskeleton of activated platelets and helps pull the edges of the cut vessel together.
As the clot forms, repair of the blood vessel wall begins. When the wall is repaired, the fibrin will be cleaved and the clot dissolved. Plasminogen (a plasma protein) is converted to plasmin, which breaks down fibrin.
It’s easy to get mixed between clots and scars.
- What is one similarity between a blood clot and scar tissue?
- What are (at least) two differences?
- Scar tissue is collagen protein.
- Blood clots involve the fibrin protein.
- Scar tissue is not dissolved after tissue repair.
- Blood clots are dissolved after tissue repair.
- Both are involved in tissue repair.
Describe platelet production and structure.
- Continually produced by megakaryocytes and survive for 9-12 days in the bloodstream.
- Megakaryocytes differentiate from myeloid stem cells and remain in bone marrow, shedding membrane packets containing structural proteins and enzymes (= platelets).
- Platelets lack organelles and are constantly removed by phagocytic cells (primarily by the spleen) and replaced.
Describe RBC production and briefly the lifespan of a RBC.
- RBCs come from myeloid stem cells stimulated by erythropoietin (EPO), which is secreted by the kidneys in response to hypoxia.
- During development, they lose their nucleus to pack in extra Hb.
- EPO stimulates RBC progenitors to divide and differentiate, enhancing RBC production.
- Most RBCs are recycled by phagocytic cells before they rupture and lose their contents.
- RBC maturation is completed after reticulocytes enter the bloodstream.
- The non-protein parts of Hb are converted to products that can be recycled by the digestive and urinary systems (i.e., the reticuloendothelial system).
Explain the functions of the two circuits of the cardiovascular system (pulmonary and systemic) and the direction of blood flow through these two circuits.
-
The pulmonary circuit moves blood from the heart to the lungs and back (picking up oxygen).
- Pulmonary veins carry oxygenated blood to the left atrium.
- Pulmonary arteries carry deoxygenated blood from the right ventricle.
-
The systemic circuit moves blood from the heart to all other organs in the body and back (delivering oxygen).
- Systemic veins carry deoxygenated blood to the right atrium.
- Systemic arteries carry oxygenated blood from the left ventricle.
Compare and contrast the structure of arteries, veins and capillaries and make connections to the functions of these vessel types.
- Arteries → intermediate diameter; three tissue layers (i.e., tunics); thick smooth muscle layer (i.e., tunica media); experience the highest pressure
- Capillaries → smallest diameter; single tissue layer (endothelium); gaps between endothelial cells (except in the brain) → allows certain components to diffuse into the ISF.
- Veins → largest diameter; three tissue layers; thin smooth muscle layer; experience lower pressure than arteries; ‘stores’ blood
Describe the key features of the gross anatomy of the heart, and the tissues that make up the heart wall.
- The heart has four chambers, two associated with each circuit.
- Atria receive blood from veins and pass it to the ventricles which move blood to arteries.
- Blood flows through the right atrium, into to the right ventricle, then to the pulmonary circuit, then the blood returns to the heart via the left atrium, then into to the left ventricle and then is pumped through the systemic circuit.
- Atria receive blood from veins and pass it to the ventricles which move blood to arteries.
- The heart sits behind the thoracic cage, and in front of the trachea and is quite well protected by these bony and cartilaginous elements.
- The heart is surrounded by the pericardium, which creates the pericardial cavity.
- The double layer of the pericardial membranes contains a fluid filled space which helps to reduce friction as the heart contracts and relaxes.
- The three components of the heart wall: (1) pericardium, (2) myocardium, and (3) endocardium.
Discuss reasons why the heart is asymmetric between its left and right sides.
- The differences reflect the different sizes and volume of blood in the systemic circuit compared to the pulmonary circuit.
- The right ventricle is smaller than the left and has a thinner wall.
- The vessels of the systemic circuit are larger and thicker than the vessels of the pulmonary circuit.
- To reiterate, the left ventricle is bigger than the right, and blood vessels of the systemic circuit are thicker and larger than those of the pulmonary circuit.
Explain the roles of coronary blood vessels and make simple predictions about the consequences of damage to one of these structures.
The heart muscle has very high metabolic demands, which are met by coronary blood vessels that are a part of the systemic circuit. Damage to the coronary blood vessels could result in heart damage (i.e., a heart attack) due to inefficient oxygen supply.
Define the terms cardiac cycle, systole, and diastole.
-
Systole → contraction of a heart chamber
- Atrial systole is shorter in duration than ventricular systole
-
Diastole → relaxation of a heart chamber
- For around half the total cardiac cycle, both chambers are in diastole.
- Heart valves open when the proximal chamber’s pressure exceeds the distal chamber’s pressure, and close (with an audible sound) when the pressure gradient reverses.
Describe the flow of blood.
- Blood always flows from heart → arteries → capillaries → veins (true for both circuits)
- One exception to this flow pattern, found in two places in the body:
- Hypophyseal portal vein system in the pituitary
- Portal vein system in the liver
- Blood flows in these systems through capillaries → veins → capillaries
- These portal vein systems are used when there is reason to move something from one capillary bed to another without diluting the contents throughout the rest of the circulatory system. In the hypothalamus, for example, the releasing hormones are only meant to stimulate the anterior pituitary, hence the dedicated capillary to capillary system. In this manner, the releasing hormones are not diluted into the entire bloodstream.
- Blood flows in these systems through capillaries → veins → capillaries
Why do capillaries lack the outer layers (smooth muscle and connective tissue) present in arteries and veins?
To allow efficient diffusion and nutrient/waste exchange with body tissues.
Why do arteries have more smooth muscle than veins?
Arteries have more smooth muscle (and therefore more ability to constrict) than veins because arteries experience higher blood pressure than veins, so they need to be stronger, and they help produce pressure to push blood through the circuits.
Also note that arteries in the periphery are effective at controlling blood flow by constriction of their thick tunica media smooth muscle layer (i.e., which organs receiving more or less blood). Veins don’t have enough smooth muscle to control blood flow in this manner.
The right side of the heart receives blood from the systemic circuit and pushes it into the pulmonary circuit.
True or False?
True
The left side of the heart receives blood from the systemic circuit and pushes it into the pulmonary circuit.
True or False?
False.
The right side of the heart receives blood from the systemic circuit and pushes it into the pulmonary circuit.
The left side of the heart receives blood from the pulmonary circuit and pushes it into the systemic circuit.
The left side of the heart receives blood from the pulmonary circuit and pushes it into the systemic circuit.
True or False?
True
The right side of the heart receives blood from the pulmonary circuit and pushes it into the systemic circuit.
True or False?
False.
The left side of the heart receives blood from the pulmonary circuit and pushes it into the systemic circuit.
The right side of the heart receives blood from the systemic circuit and pushes it into the pulmonary circuit.
Describe differences between skeletal muscle and cardiac muscle.
- Both are striated, unlike smooth muscle.
- Cardiac muscle is mononucleate (located near the centre of the cell); skeletal muscle is multinucleate (located on the periphery of the cell).
- Cardiac muscle lacks the neuromuscular junctions that can be found in skeletal muscle, so cardiac muscle fibres to not need a motor neuron to stimulate them to contract, but skeletal muscle fibres do.
- Cardiac myocytes are not innervated from somatic motor neurons.
- Cardiac myocytes have reduced T-tubules and sarcoplasmic reticulum compared to skeletal muscle.
- Cardiac myocytes form a functional syncytium, linked by intercalated discs (that physically link two cells at myofibril Z-lines), and gap junctions.
- Intercalated discs with gap junctions mean that myocytes are (1) physically and (2) electrochemically linked and can act as a single large unit.
Explain the roles of heart valves and make simple predictions about the consequences of damage to one of these structures.
- There are two sets - atrioventricular and semilunar valves.
- AV valves have associated structures (chordae tendineae and papillary muscles)
- SL valves have a structure that means that increased pressure on the receiving side just closes them more tightly.
- Heart valves open in response to pressure build-up, but only in one direction. They close when the pressure gradient reverses. This prevents backflow of blood.
- Damage to these valves could result in backflow of blood and disrupt the heart’s ability to pump blood throughout each circuit.
Explain the roles of the conduction system and make simple predictions about the consequences of damage to one of these structures.
- Cardiac muscle cells lack neuromuscular junctions.
- Instead, the heart coordinates the timing of atrial and ventricular contractions by a specialized internal conduction system formed from modified cardiac muscle tissue.
- This system transmits electrical depolarization (In the form of action potentials) from the right atrium to the rest of the heart, with a brief delay.
- Sometimes an irregular heartbeat, called an arrhythmia, is the first sign of a conduction disorder. If left untreated, severe conduction disorders can lead to sudden cardiac arrest, in which the heart suddenly stops beating.
The endocardium lines the surface of ventricles and atria.
True or False?
True.
The coronary arteries and veins are part of the systemic circuit.
True or False?
True.
The aortic valve is part of the pulmonary circuit.
True or False?
False.
More pressure will be produced inside the left ventricle when it contracts than inside the right ventricle.
True or False?
True.
Coronary disease occurs when plaques (mostly lipid deposits) accumulate within arterial walls, restricting blood flow through the coronary blood vessels.
- Why would this be a problem for heart function?
- What is it called if a coronary blood vessel becomes completely blocked, preventing blood flow to part of the heart wall?
Reducing blood flow through coronary vessels will reduce oxygen supply to the heart, reducing the heart’s ability to produce ATP to supply for its high metabolic demands.
The person may experience angina: pain related to reduced blood flow through the heart.
If a coronary blood vessel becomes completely blocked, preventing blood flow to part of the heart wall, a heart attack (i.e., myocardial ischemia) may result.
Valvular heart disease involves damage to at least one heart valve. One common cause for this is rheumatic heart disease (a bacterial infection related to strep throat).
- Why would this be a problem for heart function?
Damage to a heart valve would result in backflow through the valves. The heart will have to work a lot harder to accommodate this backflow.
Semilunar valves are easier to successfully replace because there are no accessory structures to worry about as is the case with AV valves.
Explain the phases of the cardiac action potential in terms of which ion channels are active.
- APs of cardiac muscle are slower and last ~200x longer than myofibre APs (which never have a plateau phase).
- The APs are prolonged because they involve the opening of L-Type voltage-gated calcium channels, which open slowly after depolarization, and remain open for long periods of time.
- The plateau phase represents the open VG-calcium channels, and because some VG-potassium channels are open as well.
Explain why cardiac muscle cannot undergo tetanic summation when contracting.
- Because of the duration of the AP, cardiac myocytes cannot produce tetanus.
- A single AP generates a single contraction.
- The very long AP outlasts the twitch (i.e. the single contraction), which prevents temporal summation (i.e., tetanus).
Explain the role of the SA node, describe the phases of SA electrical activity in terms of ion channels.
- The SA node membrane potential is never at rest - it constantly depolarizes, triggering an AP, then repolarizes, etc…
- SA node is connected to the medulla oblongata via the vagus nerve which can adjust heart rate as necessary.
- Gradual repolarization always occurs after depolarization in an SA node cell (= pacemaker cells).
- Electrical activity can be broken into two parts:
- (1) Action potentials → depolarization generated by T-type VG-calcium channels, instead of VG-sodium channels.
- (2) Pacemaker potential → slow depolarization that automatically occurs.
- VG-K channels are still involved in the repolarization phase of the SA node AP.
- The ‘funny channel’ is opened by hyperpolarization. During the pacemaker potential, the ‘funny current’ flows across the cardiac myocyte plasma membrane, due to opening of the ‘funny channel’.
- The ‘funny channel’ (HCN-channel) is a VG-cation channel that ONLY opens when the membrane is hyperpolarized. This channel allows sodium to enter the cell, leading to depolarization, brining the membrane back toward action potential threshold.
Explain how the structural and functional features of the AV node, and ventricular conduction pathways relate to the pattern of ventricular contraction.
- SA node cells are electrically coupled to both the neighbouring cardiac myocytes and the next components in the conduction pathway.
- The internodal pathways allow the depolarization to rapidly spread across both atria.
- The second node in the pathway = AV node, slows the spread of SA depolarization through the system.
- Due to reduced gap junctions between AV node cells (AV node can also act as a pacemaker, but its intrinsic rhythm is much slower than the SA node, so SA node determines heart rate.
- Atrial contraction occurs during the 100ms delay at the AV node.
- The geometry of the ventricular conduction pathways ensures that contraction first occurs far from the arteries, ensuring that blood is efficiently pushed into arteries and not trapped in the ventricle. (i.e., the parts of the ventricle closest to the atrium are the last to be depolarized since the impulse is directed down through the Purkinje fibres and then back up (= apex of the heart contracts first).
Describe how events in the heart rate relate to the three waves of a typical EgG and make simple predictions about heart disorders based on changes in ECG.
- The P wave relates to atrial wall depolarization
- Note, you will never see an electrical signal of the atria repolarizing because it occurs while the much larger ventricles are depolarizing.
- P-R interval → conduction through AV node and AV bundle.
- QRS complex → ventricular walls depolarize
- T wave → repolarization of the ventricle myocytes at the end of their APs.
What is the thickest layer of the heart wall?
The myocardium.
It is principally composed of cardiac muscle cells (myocytes).
Cardiomyocytes have a characteristic branched structure which join to others to form an interconnected branched network which provides structural strength to the beating heart.
Which of these is cardiac muscle, and which is skeletal?
- Name one feature that is shared.
- Name one feature that is a difference in degree.
- Name one feature that is a difference in kind.
Cardiac = A; Skeletal = B
Both types have sarcomeres, myosin and actin fibres, and striations.
Cardiac nuclei are in the centre of the cell and skeletal muscle nuclei are on the periphery of the cell. Cardiac muscle only has one nuclei and skeletal myofibers are multinucleate
Skeletal muscle has more T-tubules and a more extensive sarcoplasmic reticulum than cardiac.
Cardiac muscle has gap junctions and intercalated discs, and skeletal muscle does not.
Cardiac muscle lacks neuromuscular junctions.
Describe the mechanisms of EC coupling in cardiac myocytes.
- Involves calcium-induced calcium release.
- L-type VG-channels allow calcium ions to enter the cell (following their electrochemical gradient).
- Increased intracellular calcium concentration causes the release of much, much, much more calcium from stores in the sarcoplasmic reticulum.
- Depolarization of the sarcolemma opens VG-CC, allowing calcium to enter the cell.
- Elevated calcium concentration triggers the opening of RyR, allowing calcium to escape the sarcoplasmic reticulum.
- Elevated cytoplasmic calcium concentration triggers actin-myosin ATPase.
Compare the relationship between DHPRs and RYRs in cardiac vs skeletal muscle.
- In skeletal muscle → no ion flow through DHPR; mechanical coupling of DHPR and RyR
- In cardiac muscle → calcium flows through DHPR into cytosol; biochemical coupling of DHPR and RyR.
- Once calcium is present, the contraction cycle in a cardiac myocyte closely resembles what occurs in a skeletal muscle fibre.
Calcium is involved in the contraction of both skeletal and muscle fibres and cardiac myocytes.
- Describe one similarity and one difference in the role(s) calcium plays in excitation and contraction in these two muscle types.
One similarity = calcium binds troponin in the contraction cycle to expose the binding site for myosin.
One difference = the DHPR/RyR interaction is mechanical coupling in skeletal muscle where calcium does not flow through DHPR; the DHPR/RyR interaction is biochemical coupling in cardiac muscle where calcium does flow through the DRPR into the cytosol.
Explain how ANS activity can slow down or speed up SA activity (and thus heart rate).
- The main target of the ANS synapses in the heart are the two nodes in the conduction system, especially the SA node.
- Parasympathetic slows the heart rate, sympathetic speeds.
- An ANS synapse may cause ligand binding to the funny channel to increase permeability to sodium and allow more ion flow. The increased activation of funny channels results in more APs and a faster heart rate.
- Norepinephrine (NE) released by sympathetic post ganglionic axons enhances the activation of funny channels, leading to more depolarization and a more rapid return to threshold. NE works through metabotropic receptors that lead to the production of cyclic-AMP (the cyclic nucleotide that enhances the function of the funny channels). The cAMP allows the channels to stay open for longer and contribute more to the more rapid depolarization.
- Increasing the number of open VG-K channels will hyperpolarize the membrane and can create an IPSP to slow down the heart rate.
- Acetylcholine leads to the opening of additional voltage-gated potassium channels, hyperpolarizing the cell and prolonging the pacemaker potential phase. During the repolarization phase, during parasympathetic stimulation, hyperpolarization will occur. This slows the heart rate because there will be slower depolarization via the funny channels and more time will be spend in the pacemaker phase.
Describe how ANS activity can speed up the heart rate.
- Sympathetic activation
- An ANS synapse may cause ligand binding to the funny channel to increase permeability to sodium and allow more ion flow. The increased activation of funny channels results in more APs and a faster heart rate.
- Norepinephrine (NE) released by sympathetic post ganglionic axons enhances the activation of funny channels, leading to more depolarization and a more rapid return to threshold. NE works through metabotropic receptors that lead to the production of cyclic-AMP (the cyclic nucleotide that enhances the function of the funny channels). The cAMP allows the channels to stay open for longer and contribute more to the more rapid depolarization.
Describe how ANS activity can slow the heart rate.
- Parasympathetic division
- Increasing the number of open VG-K channels will hyperpolarize the membrane and can create an IPSP to slow down the heart rate.
- Acetylcholine leads to the opening of additional voltage-gated potassium channels, hyperpolarizing the cell and prolonging the pacemaker potential phase. During the repolarization phase, during parasympathetic stimulation, hyperpolarization will occur. This slows the heart rate because there will be slower depolarization via the funny channels and more time will be spend in the pacemaker phase.
Which (A or B) is more likely in a patient with a damaged SA node? What about a heart attack that has damaged the ventricular wall?
Damaged SA node: A → abnormal P wave
Damaged ventricular wall: B → abnormal, longer than usual T wave → current is not spreading normally through the ventricular wall
Define Cardiac output.
Cardiac output = the volume of blood (mL) moved through the heart per time (minutes).
CO = mL/min = SV x HR
Define heart rate.
The number of times the heart goes through the entire cardiac cycle per minute.
Define stroke volume.
The volume of blood (mL) ejected into the aorta (or pulmonary trunk) during each ventricular systole.
Define end diastolic volume.
- Atrial systole completes the filling of the ventricles, which reach their EDV = ventricles achieve their maximum volume.
Define end systolic volume.
- A significant fraction of the EDV remains in the ventricle (= ESV)
- SV = EDV - ESV
Define venous return.
The volume of blood that is delivered to the right atrium during the cardiac cycle.
VR is affected by CO and by constriction of vessels or compression of veins.
Note CO may not always = VR due to the stretchy and compressible nature of veins (i.e., veins can store deoxygenated blood).
Define filling time.
The duration of ventricular diastole, which determines the time the AV valves are open. Filling time is a function of heart rate. Increased HR = decreased filling time. Thus, HR also decreases EDV due to decreased filling time.
Define contractility.
The amount of force produced during a contraction for a given preload.
When contractility is enhanced (e.g., by sympathetic activity or by epinephrine), a higher SV is produced for the same EDV.
Define afterload.
The amount of force the ventricle must generate to open its semilunar valve. Increased aortic pressure or pulmonary artery pressure = increased afterload.
Afterload is directly affected by resistance (pressure) in blood vessels.
Define preload.
The amount of stretching of the heart wall due to blood within the ventricle. Increased EDV = increased stretch = increased tension (force) produced upon contraction = increased pressure generated due to optimized sarcomere length.
Describe the relationship between ventricular systole/diastole and stroke volume during the cardiac cycle using a standard graph of pressures in the left side of the heart and aorta.
- Atrial systole completes the filling of the ventricles (= EDV).
- Ventricular systole involves a period of isovolumetric contraction and a period of ventricular ejection.
Explain why exercise is associated with increases in CO.
- Skeletal muscles use more oxygen and nutrients, and generate more waste products and heat. Thermal homeostasis must be maintained by radiating heat away at the dermis.
- These changes all require more blood flow.
- During exercise, sympathetic activity increases, including increased epinephrine secretion from the adrenal medulla leading to increased heart rate, and increased CO.
- As HR increases, length of diastole decreases, filling time decreases, EDV decreases, and ejection fraction and stroke volume will also decrease.
- HOWEVER, during exercise sympathetic activity increases as does skeletal muscle contraction, which increases venous return and increases contractility, thereby increasing SV.
Identify the major factors that can alter heart rate and stroke volume during exercise, both during the exercise and because of prolonged training.
- During activity, sympathetic activity increases, as does skeletal muscle contraction, which leads to increased venous return, increased contractility, and increased SV (= increased CO).
- Increased HR decreases filling time, decreasing EDV, ejection fraction, and SV (= decreased CO).
- Prolonged training requiring increased oxygen use increases production of RBCs, and thus increases blood volume, therefore increases venous return and increases myocyte stretching, which triggers addition of sarcomeres (= eccentric hypertrophy).
Compare and contrast the causes and consequences of eccentric and concentric hypertrophy of the ventricular myocardium.
- Concentric → seen in CVD and causes increased afterload and increased ventricular wall thickness (pressure overload)
- Eccentric → associated with athletic training and pregnancy, and is related to increased venous return and increases in ventricular volume (volume overload)
- Myocytes in the heart wall get their oxygen from coronary arteries. Concentric hypertrophy increases the oxygen requirement in the heart, but there are no coronary arteries to supply the new myocytes. So concentric hypertrophy is associated with insufficient oxygen supply to the heart. Eccentric hypertrophy does not have this problem with oxygen supply.
Decreased end-diastolic volume increases stroke volume.
True or False?
False.
Decreased EDV = decreased stroke volume.
Increased end-diastolic volume increases stroke volume.
True or False?
True.
Decreased end-diastolic volume decreases stroke volume.
True or False?
True.
Increased end-diastolic volume decreases stroke volume.
True or False?
False.
Increased end-diastolic volume increases stroke volume.
Increased end-systolic volume increases stroke volume.
True or False?
False.
Increased EDV = decreased SV
Increased end-systolic volume decreases stroke volume.
True or False?
True.
Decreased end-systolic volume decreases stroke volume.
True or False?
False.
Increased ESV = decreased SV
Decreased end-systolic volume increases stroke volume.
True or False?
True
Vasodilation decreases afterload.
True or False?
True.
Vasodilation increases afterload.
True or False?
False.
Vasoconstriction increases afterload.
True or False?
True.
Vasoconstriction decreases afterload.
True or False?
False.
The greater the afterload, the lower the pumping efficiency of the heart, and the larger the ESV.
True or False?
True.
The greater the afterload, the higher the pumping efficiency of the heart, and the lower the ESV.
True or False?
False.
The greater the afterload, the lower the pumping efficiency of the heart, and the larger the ESV.
The greater the contractility, the smaller the end-systolic volume.
True or False?
True.
The greater the contractility, the larger the end-systolic volume.
True or False?
False.
The greater the contractility, the smaller the end-systolic volume.
In general, when venous return increases, stroke volume increases. When venous return decreases, stroke volume decreases.
True or False?
True.
In general, when venous return increases, stroke volume decreases. When venous return decreases, stroke volume increases.
True or False?
False.
In general, when venous return increases, stroke volume increases. When venous return decreases, stroke volume decreases.
Increase in filling time decreases the end diastolic volume.
True or false?
False.
Increase in filling time increases the end diastolic volume.
Increase in filling time increases the end diastolic volume.
True or False?
True.
Sympathetic stimulation increases heart rate and parasympathetic stimulation decreases heart rate.
True or False?
True.
Sympathetic stimulation decreases heart rate and parasympathetic stimulation increases heart rate.
True or False?
False.
Sympathetic stimulation increases heart rate and parasympathetic stimulation decreases heart rate.
Heart rate rises with increased body temperature and decreases with decreased body temperature.
True or False?
True.
Hormones (e.g., epinephrine and thyroxine) increase heart rate.
True or False?
True.
What is the atrial reflex?
It involves adjustments to heart rate in response to an increase in venous return. When the walls of the right atrium are stretched, stretch receptors there stimulate sympathetic activity to increase heart rate.
How does exercise affect venous return?
Muscular contractions compress veins and assist valves in directing venous blood toward the right atrium, increasing venous return.
How does blood volume affect venous return?
Large reductions in blood volume due to bleeding or dehydration reduce venous return.
How does blood flow affect venous return?
Changes in peripheral blood flow patterns can increase or decrease venous return.
Sympathetic stimulation increases heart rate and contractility.
True or False?
True.
Parasympathetic activation slows the heart rate and decreases contractility.
True or False?
False.
Parasympathetic activation slows the heart rate but has little influence on contractility.
Hormones decrease contractility.
True or False?
False.
Many hormones increase contractility.
If HR increases, CO decreases.
True or False?
False.
CO = SV x HR
If SV decreases, CO decreases.
True or False?
True.
CO = SV x HR
The CO from the left ventricle is typically larger than the CO from the right ventricle.
True or False?
False.
SV and HR are the same for each ventricle despite their structural differences. The left ventricle is more powerful than the right because it does more work to propel the blood throughout the systemic circuit. The pulmonary circuit does not necessitate such force, so the smaller right ventricle is adequate.
The CO from the right ventricle is typically larger than the CO from the left ventricle.
True or False?
False.
SV and HR are the same for each ventricle despite their structural differences. The left ventricle is more powerful than the right because it does more work to propel the blood throughout the systemic circuit. The pulmonary circuit does not necessitate such force, so the smaller right ventricle is adequate.
If a typical heart rate is 75bpm, and the typical stroke volume is 70mL, what is the CO?
CO = SV x HR = 5250mL/min
Define ejection fraction.
The % of EDV that is released during ejection phase.
SV/EDV x 100%
Which volumes (SV, EDV, ESV) would be affected if:
The AV valves shut early.
EDV decreases
ESV decreases
SV decreases
Which volumes (SV, EDV, ESV) would be affected if:
The SL valves open late but close at the normal time.
SV decreases
ESV increases
Which volumes (SV, EDV, ESV) would be affected if:
The ventricle contracts weakly compared to normal.
SV decreases
ESV increases