Term 2 Midterm Material Flashcards

1
Q

Describe the structure and functions of the three components of the cardiovascular system.

A
  • 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.
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2
Q

Describe the composition of blood. [3]

A
  • 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.
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3
Q

Explain the anatomy and physiology of a red blood cell, including the structure and function of haemoglobin.

A
  • 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.
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4
Q

Describe the main components of a complete blood count (CBC) and describe its usage.

A

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.
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5
Q

Explain the events occurring during primary haemostasis.

A
  • 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)
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6
Q

Explain the role of bone marrow in the formation of formed elements and compare and contrast the formation of RBCs, WBCs and platelets.

A
  • 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)
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7
Q

Explain the role of RBC antigens in blood type for both ABO and Rh groupings.

A
  • 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.
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8
Q

Compare and contrast between plasma and interstitial fluid. [3]

A
  • 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.
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9
Q

Explain how the different components of plasma and formed elements contribute to its functions.

A
  • Oxygen transport → RBCs (more than 99% of formed elements in blood)
  • Immune functions → monocytes, lymphocytes, eisinophil, neutrophil, basophil
  • Clotting → platelets
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10
Q

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?
A

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.

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11
Q

Patient 1 (left); Patient 2 (right) → What measures are abnormal? What symptoms would you expect to see?

A

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.

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12
Q

Explain the steps occurring in secondary haemostasis and the coagulation pathway.

A
  • 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).
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13
Q

What happens after formation of a blood clot due to vessel damage?

A

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.

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14
Q

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?
A
  • 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.
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15
Q

Describe platelet production and structure.

A
  • 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.
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16
Q

Describe RBC production and briefly the lifespan of a RBC.

A
  • 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).
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17
Q

Explain the functions of the two circuits of the cardiovascular system (pulmonary and systemic) and the direction of blood flow through these two circuits.

A
  • 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.
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18
Q

Compare and contrast the structure of arteries, veins and capillaries and make connections to the functions of these vessel types.

A
  • 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
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19
Q

Describe the key features of the gross anatomy of the heart, and the tissues that make up the heart wall.

A
  • 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.
  • 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.
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20
Q

Discuss reasons why the heart is asymmetric between its left and right sides.

A
  • 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.
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21
Q

Explain the roles of coronary blood vessels and make simple predictions about the consequences of damage to one of these structures.

A

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.

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22
Q

Define the terms cardiac cycle, systole, and diastole.

A
  • 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.
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23
Q

Describe the flow of blood.

A
  • 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.
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24
Q

Why do capillaries lack the outer layers (smooth muscle and connective tissue) present in arteries and veins?

A

To allow efficient diffusion and nutrient/waste exchange with body tissues.

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25
Q

Why do arteries have more smooth muscle than veins?

A

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.

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26
Q

The right side of the heart receives blood from the systemic circuit and pushes it into the pulmonary circuit.

True or False?

A

True

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27
Q

The left side of the heart receives blood from the systemic circuit and pushes it into the pulmonary circuit.

True or False?

A

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.

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28
Q

The left side of the heart receives blood from the pulmonary circuit and pushes it into the systemic circuit.

True or False?

A

True

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29
Q

The right side of the heart receives blood from the pulmonary circuit and pushes it into the systemic circuit.

True or False?

A

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.

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30
Q

Describe differences between skeletal muscle and cardiac muscle.

A
  • 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.
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31
Q

Explain the roles of heart valves and make simple predictions about the consequences of damage to one of these structures.

A
  • 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.
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32
Q

Explain the roles of the conduction system and make simple predictions about the consequences of damage to one of these structures.

A
  • 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.
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33
Q

The endocardium lines the surface of ventricles and atria.

True or False?

A

True.

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34
Q

The coronary arteries and veins are part of the systemic circuit.

True or False?

A

True.

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35
Q

The aortic valve is part of the pulmonary circuit.

True or False?

A

False.

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36
Q

More pressure will be produced inside the left ventricle when it contracts than inside the right ventricle.

True or False?

A

True.

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37
Q

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?
A

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.

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38
Q

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?
A

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.

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39
Q

Explain the phases of the cardiac action potential in terms of which ion channels are active.

A
  • 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.
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40
Q

Explain why cardiac muscle cannot undergo tetanic summation when contracting.

A
  • 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).
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41
Q

Explain the role of the SA node, describe the phases of SA electrical activity in terms of ion channels.

A
  • 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.
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42
Q

Explain how the structural and functional features of the AV node, and ventricular conduction pathways relate to the pattern of ventricular contraction.

A
  • 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).
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43
Q

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.

A
  • 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.
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44
Q

What is the thickest layer of the heart wall?

A

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.

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45
Q

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.
A

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.

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46
Q

Describe the mechanisms of EC coupling in cardiac myocytes.

A
  • 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.
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47
Q

Compare the relationship between DHPRs and RYRs in cardiac vs skeletal muscle.

A
  • 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.
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48
Q

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.
A

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.

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49
Q

Explain how ANS activity can slow down or speed up SA activity (and thus heart rate).

A
  • 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.
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50
Q

Describe how ANS activity can speed up the heart rate.

A
  • 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.
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51
Q

Describe how ANS activity can slow the heart rate.

A
  • 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.
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52
Q

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?

A

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

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53
Q

Define Cardiac output.

A

Cardiac output = the volume of blood (mL) moved through the heart per time (minutes).

CO = mL/min = SV x HR

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54
Q

Define heart rate.

A

The number of times the heart goes through the entire cardiac cycle per minute.

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55
Q

Define stroke volume.

A

The volume of blood (mL) ejected into the aorta (or pulmonary trunk) during each ventricular systole.

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56
Q

Define end diastolic volume.

A
  • Atrial systole completes the filling of the ventricles, which reach their EDV = ventricles achieve their maximum volume.
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57
Q

Define end systolic volume.

A
  • A significant fraction of the EDV remains in the ventricle (= ESV)
  • SV = EDV - ESV
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58
Q

Define venous return.

A

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).

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59
Q

Define filling time.

A

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.

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60
Q

Define contractility.

A

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.

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61
Q

Define afterload.

A

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.

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62
Q

Define preload.

A

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.

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63
Q

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.

A
  • Atrial systole completes the filling of the ventricles (= EDV).
  • Ventricular systole involves a period of isovolumetric contraction and a period of ventricular ejection.
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64
Q

Explain why exercise is associated with increases in CO.

A
  • 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.
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65
Q

Identify the major factors that can alter heart rate and stroke volume during exercise, both during the exercise and because of prolonged training.

A
  • 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).
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66
Q

Compare and contrast the causes and consequences of eccentric and concentric hypertrophy of the ventricular myocardium.

A
  • 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.
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67
Q

Decreased end-diastolic volume increases stroke volume.

True or False?

A

False.

Decreased EDV = decreased stroke volume.

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68
Q

Increased end-diastolic volume increases stroke volume.

True or False?

A

True.

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69
Q

Decreased end-diastolic volume decreases stroke volume.

True or False?

A

True.

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70
Q

Increased end-diastolic volume decreases stroke volume.

True or False?

A

False.

Increased end-diastolic volume increases stroke volume.

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71
Q

Increased end-systolic volume increases stroke volume.

True or False?

A

False.

Increased EDV = decreased SV

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72
Q

Increased end-systolic volume decreases stroke volume.

True or False?

A

True.

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73
Q

Decreased end-systolic volume decreases stroke volume.

True or False?

A

False.

Increased ESV = decreased SV

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74
Q

Decreased end-systolic volume increases stroke volume.

True or False?

A

True

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75
Q

Vasodilation decreases afterload.

True or False?

A

True.

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76
Q

Vasodilation increases afterload.

True or False?

A

False.

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77
Q

Vasoconstriction increases afterload.

True or False?

A

True.

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78
Q

Vasoconstriction decreases afterload.

True or False?

A

False.

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79
Q

The greater the afterload, the lower the pumping efficiency of the heart, and the larger the ESV.

True or False?

A

True.

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80
Q

The greater the afterload, the higher the pumping efficiency of the heart, and the lower the ESV.

True or False?

A

False.

The greater the afterload, the lower the pumping efficiency of the heart, and the larger the ESV.

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81
Q

The greater the contractility, the smaller the end-systolic volume.

True or False?

A

True.

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82
Q

The greater the contractility, the larger the end-systolic volume.

True or False?

A

False.

The greater the contractility, the smaller the end-systolic volume.

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83
Q

In general, when venous return increases, stroke volume increases. When venous return decreases, stroke volume decreases.

True or False?

A

True.

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84
Q

In general, when venous return increases, stroke volume decreases. When venous return decreases, stroke volume increases.

True or False?

A

False.

In general, when venous return increases, stroke volume increases. When venous return decreases, stroke volume decreases.

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85
Q

Increase in filling time decreases the end diastolic volume.
True or false?

A

False.

Increase in filling time increases the end diastolic volume.

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86
Q

Increase in filling time increases the end diastolic volume.

True or False?

A

True.

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87
Q

Sympathetic stimulation increases heart rate and parasympathetic stimulation decreases heart rate.

True or False?

A

True.

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88
Q

Sympathetic stimulation decreases heart rate and parasympathetic stimulation increases heart rate.

True or False?

A

False.

Sympathetic stimulation increases heart rate and parasympathetic stimulation decreases heart rate.

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89
Q

Heart rate rises with increased body temperature and decreases with decreased body temperature.

True or False?

A

True.

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90
Q

Hormones (e.g., epinephrine and thyroxine) increase heart rate.

True or False?

A

True.

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91
Q

What is the atrial reflex?

A

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.

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92
Q

How does exercise affect venous return?

A

Muscular contractions compress veins and assist valves in directing venous blood toward the right atrium, increasing venous return.

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93
Q

How does blood volume affect venous return?

A

Large reductions in blood volume due to bleeding or dehydration reduce venous return.

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94
Q

How does blood flow affect venous return?

A

Changes in peripheral blood flow patterns can increase or decrease venous return.

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95
Q

Sympathetic stimulation increases heart rate and contractility.

True or False?

A

True.

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96
Q

Parasympathetic activation slows the heart rate and decreases contractility.
True or False?

A

False.

Parasympathetic activation slows the heart rate but has little influence on contractility.

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97
Q

Hormones decrease contractility.

True or False?

A

False.

Many hormones increase contractility.

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98
Q

If HR increases, CO decreases.

True or False?

A

False.

CO = SV x HR

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99
Q

If SV decreases, CO decreases.

True or False?

A

True.

CO = SV x HR

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100
Q

The CO from the left ventricle is typically larger than the CO from the right ventricle.

True or False?

A

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.

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101
Q

The CO from the right ventricle is typically larger than the CO from the left ventricle.

True or False?

A

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.

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102
Q

If a typical heart rate is 75bpm, and the typical stroke volume is 70mL, what is the CO?

A

CO = SV x HR = 5250mL/min

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103
Q

Define ejection fraction.

A

The % of EDV that is released during ejection phase.

SV/EDV x 100%

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104
Q

Which volumes (SV, EDV, ESV) would be affected if:

The AV valves shut early.

A

EDV decreases

ESV decreases

SV decreases

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105
Q

Which volumes (SV, EDV, ESV) would be affected if:

The SL valves open late but close at the normal time.

A

SV decreases

ESV increases

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106
Q

Which volumes (SV, EDV, ESV) would be affected if:

The ventricle contracts weakly compared to normal.

A

SV decreases

ESV increases

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107
Q

If there was a major blood loss (e.g., due to haemorrhage), preload would decrease.

True or False?

A

True.

108
Q

If there was a major blood loss (e.g., due to haemorrhage), preload would increase.

True or False?

A

False.

If there was a major blood loss (e.g., due to haemorrhage), preload would decrease.

109
Q

If there was major blood loss afterload would decrease.
True or False?

A

True.

110
Q

If there was major blood loss afterload would increase.

True or False?

A

False.

If there was major blood loss afterload would decrease.

111
Q

If the aortic valve stiffened, making it more difficult to open, preload would increase.

True or False?

A

False.

112
Q

If the aortic valve stiffened, making it more difficult to open, afterload would increase.

True or False?

A

True.

113
Q

Today’s lecture briefly noted the observation that exercise training tends to decrease HR (both max and resting) and increase SV.

  • On a functional level (or from an evolutionary perspective), why does it make more sense to increase CO through increases in SV rather than increases in HR?
A

Increasing stroke volume is more energy efficient than increasing heartbeat.

114
Q

What does the Frank-Starling Law describe?

A

The Frank-Starling law describes how increased filling of the ventricles produces increases in stroke volume, due to stretching the ventricular myocardium.

115
Q

Describe the state of the heart.

A

The atria are contracting (= atrial systole); the ventricles are still relaxed; the AV valves are open. Notice the rise and fall of pressure in the left atria and ventricle as pressure in the aorta continues to drop.

116
Q

Describe the state of the heart.

A

The atria relax; the ventricles contract; the AV valves shut; the SL valves will open. The AV valve shuts when the pressure is higher in the ventricle than the atria. Notice the aortic valve only opens when ventricular pressure exceeds that in the aorta. As such, there is a short period of time when the pressure is rising in the ventricle (i.e., both valves are shut), and there is no change in ventricular volume. Ventricular ejection is the top of the bell curve of ventricular pressure when blood is pumped into the aorta from the left ventricle.

117
Q

Describe the state of the heart.

A

Atria are still relaxed; the ventricles start to relax; the SL valves shut again.

118
Q

What determines EDV? [2]

A

Venous return and filling time.

119
Q

What determines ESV? [2]

A

Afterload and contractility

120
Q

CO increases greatly during exercise, due to increases in both heart rate and stroke volume.

Prolonged aerobic training tends to lead to increases in stroke volume and decreases in heart rate.

True or False?

A

True.

121
Q

CO increases greatly during exercise, due to increases in both heart rate and stroke volume.

Prolonged aerobic training tends to lead to decreases in stroke volume and increases in heart rate.

True or False?

A

False.

CO increases greatly during exercise, due to increases in both heart rate and stroke volume. Prolonged aerobic training tends to lead to increases in stroke volume and decreases in heart rate.

122
Q

Explain the relationship between blood pressure gradients, vascular resistance, and blood flow rate.

A
  • A pressure gradient will produce a force that moves fluid in the direction of lower pressure.
    • A larger pressure gradient creates more force.
  • The velocity (i.e., flow rate) is slowed by resistance (caused by friction between the walls of the tube and the fluid, as well as viscosity).
123
Q

Explain the four factors that can affect vascular resistance.

A
  • Length → the longer the vessel, the more surface that is in contact with the blood, thus the more friction blood will encounter (more length = more resistance)
  • Viscosity → a measure of resistance due to interactions among molecules in a moving fluid; blood is ~5x more viscous than water.
  • Diameter → in a small diameter vessel, proportionally more of the blood inside will be in contact or near the wall of the vessel, which is the source of most friction (smaller diameter = larger resistance)
  • Turbulence → occurs due to shifts or changes in the geometry of the vessel walls (i.e., branches, tight curves, irregular surfaces); turbulence increases resistance
124
Q

Describe how resistance, mean pressure, and blood flow change in a circuit as you move from arteries to veins.

A
  • The farther the vessels are from the ventricle (the source of the pressure gradient), the lower the average pressure within them.
  • Arterial pressure is highest during and just after ventricular systole, and lowest during diastole.
125
Q

Explain how the measurement of blood pressure occurs.

A
  • Cuff pressure blocks blood flow.
  • Pulse pressure = difference between systolic and diastolic pressure.
126
Q

What is the normal range for healthy blood pressure?

A

120-130 mm/Hg

70-80 mm/Hg

Systolic/diastolic

127
Q

Discuss how gravity can help or hinder blood flow and explain the roles of venous valves and muscle contractions in minimizing the effects of gravity on blood flow in the limbs.

A
  • Gravity either opposes or enhances blood flow, according to the location of the vessels relative to the heart.
  • Veins contain valves to help prevent backflow → mostly not present in the head; less common in the torso, common in limbs.
  • Skeletal muscle contractions work with venous valves to provide a secondary pump that helps propel blood toward the trunk, countering the force of gravity.
128
Q

A change in diameter of a vessel wall will always produce a larger change in resistance than an equivalent change in length.

True or False?

A

True.

This is because the resistance associated with diameter is proportional to the radius4 (it relates to the volume inside the cylinder).

129
Q

A change in diameter of a vessel wall will always produce a lesser change in resistance than an equivalent change in length.

True or False?

A

False.

A change in diameter of a vessel wall will always produce a larger change in resistance than an equivalent change in length. This is because the resistance associated with diameter is proportional to the radius4 (it relates to the volume inside the cylinder).

130
Q

What factor relates to why blood flow is affected, and what is the direction of change in blood flow?

Arteriole smooth muscle relaxation

A

Vessel diameter increases → less resistance to flow → increased blood flow

131
Q

What factor relates to why blood flow is affected, and what is the direction of change in blood flow?

Atherosclerosis

A

Vessel diameter decreases and introduces turbulent flow due to the irregular surface → increases resistance to flow rate → decreases blood flow

132
Q

What factor relates to why blood flow is affected, and what is the direction of change in blood flow?

Increased ventricular contractility

A

Enhanced pressure gradient → increased blood flow

133
Q

What factor relates to why blood flow is affected, and what is the direction of change in blood flow?

Doping with EPO (to build up hematocrit and build up RBCs)

A

Increases viscosity → increases internal resistance to flow → decreases blood flow

134
Q

What factor relates to why blood flow is affected, and what is the direction of change in blood flow?

Being very tall

A

Increases vessel length → increases resistance to flow rate → decreases blood flow

135
Q

Why do changes in pressure increase chance of major disease? E.g., high diastolic pressure leads to progressive heart failure, isolated systolic hypertension elevates risk of heart attacks, and low blood pressure is associated with fainting

A
  • High diastolic pressure can lead to progressive heart failure because diastolic pressure is the main determinant of afterload, and increasing afterload means the heart muscle will have to work harder to reach the same level of cardiac output. In that case, there is extra demand on coronary arteries to supply the heart with a greater oxygen supply, but if they fail to meet the additional demand, then the heart muscle will become progressively weaker.
  • Isolated systolic hypertension is associated with elevated risk for ischemic incidents because increased pulse pressure exerts greater force on the blood vessels which increases the risk of plaque ruptures which may then lead to blood clots and heart attacks.
  • Low blood pressure is associated with risk of fainting because of the threat of low oxygen supply to the brain.
136
Q

If you hang upside down for a prolonged period, you start to feel thick-headed and uncomfortable. Sometimes we talk about this as ‘the blood rushing to your head’.

  • What’s a better explanation for what’s actually going on in this situation?
A

There’s no valves in the head veins because they are usually totally assisted by gravity. And there are also not a lot of postural muscles in the head and neck to provide an external pressure assistance. Blood isn’t necessarily rushing to the head as the arteries will be mostly unaffected. However, veins and sinuses will have a really hard time generating enough pressure to move the blood back up to the heart.

137
Q

What is a life-threatening consequence that can occur if blood pools in veins for long periods?

A

Deep vein thrombosis: when blood pools for too long in deep veins the clotting cycle may start even though there is no damage to the vessels → clot formation can lead to heart attacks.

138
Q

What can be done to improve venous return in people who aren’t able to get up or even move their legs, such as spinal cord injury patients?

A

Compression socks, low dose anticoagulants, elevation of lower limbs

139
Q

Higher pressure gradients and lower resistance lead to increased blood flow.

True or False?

A

True.

140
Q

Higher pressure gradients and lower resistance lead to decreased blood flow.

True or False?

A

False.

Higher pressure gradients and lower resistance lead to increased blood flow.

141
Q

What is the biggest contributor to overall resistance in a blood vessel circuit?

A

Luminal diameter → resistance increases as diameter decreases

Most resistance in the circuit comes from the many capillaries in it, which have the smallest lumen diameter.

142
Q

Mean blood pressure increases as blood moves through a circuit.

True or False?

A

False.

Mean blood pressure decreases as blood moves through a circuit.

143
Q

Mean blood pressure decreases as blood moves through a circuit.

True or False?

A

True.

144
Q

Why does flow rate increase in veins compared to capillaries?

A

Increased luminal diameter.

145
Q

What blood pressure do we measure?

A

Arterial pressure → fluctuates according to the cardiac cycle.

146
Q

Explain the components of a typical capillary wall and how they vary between different types of capillaries.

A

The capillary wall consists of a layer of endothelial cells and a basement layer.

Continuous → complete endothelial layer with no obvious gaps; some fluid can flow between endothelial cells, and transport can occur across the endothelial membrane

Fenestrated → pores allow for faster exchange of water and small solutes (including small peptides); found in many (neuro)endocrine organs (e.g., hypothalamus, pituitary, thyroid), and in areas involved in absorption (intestine) or filtration (kidneys); fenestrated capillaries can be found in the median eminence, for example, and in the parts of the hypothalamus that are responsible for sensing the osmolarity of blood plasma.

Sinusoidal → have a discontinuous basement membrane; even very large proteins (e.g., plasma proteins) can freely exchange into tissue fluid; found in some endocrine organs (e.g., adrenals) and in liver, bone marrow, and spleen, which produce or recycle large plasma proteins and blood cells.

147
Q

Describe how capillaries are organized in a capillary bed and explain two ways that blood flow through a capillary bed can be locally altered.

A
  • Capillaries form networks known as beds.
  • Precapillary sphincters produce pulses of contraction and dilation, causing blood flow to be pulsatile in each capillary
  • Arteriovenous anastomoses can dilate, diverting blood away from the higher resistance capillary bed.
  • Contraction of smooth muscle in arterioles can reduce blood supply to the entire capillary bed
148
Q

Define diffusion in the context of capillary exchange.

A

Diffusion refers to the passive movement of substances due to concentration differences.

It is always passive (does not require ATP) and it can be either free or facilitated (i.e., involving carrier proteins or channels).

149
Q

Define osmosis in the context of capillary exchange.

A

Osmosis is the diffusion of water molecules across a selectively permeable membrane.

Osmotic pressure → the force that is pushing water to flow by osmosis → can be measured by the force it takes to stop the flow

150
Q

Define filtration in the context of capillary exchange.

A

Filtration refers to the movement of fluid through small pores in response to pressure differences.

Hydrostatic pressure → refers to the force exerted on the vessel wall by the fluid inside it.

151
Q

Define CHP, BCOP, and NFP, and explain how these relate to filtration and reabsorption along the length of a capillary bed.

A

Capillary hydrostatic pressure, CHP → the pressure of the blood contents inside the capillary on the capillary walls.

Blood colloid osmotic pressure, BCOP → the pressure driving water from ISF due to the large, suspended molecules (especially proteins) in plasma that are unable to cross the capillary wall.

Net filtration pressure, NFP → the pressure gradient available to produce filtration.

NFP = CHP - BCOP

152
Q

Make predictions about how a given change in blood volume or blood composition will affect CHP, BCOP, and NFP.

A
  • BCOP is a constant value, and related to the concentration of colloidal particles in plasma.
  • CHP is initially (relatively) high in the proximal part of the capillary, as blood enters from the arteriole.
    • CHP > BCOP = +NFP
      • Meaning a pressure gradient that favours fluid movement into the ISF.
  • By the middle of the capillary bed, forces are balanced, and there will be no pressure gradient to drive filtration.
    • CHP = BCOP = 0NFP
      • No net movement in either direction
  • Near a venule, there is negative NFP, favouring reabsorption
    • CHP < BCOP = -NFP
      • Meaning a pressure gradient that favours fluid movement from interstitial fluid to plasma.
153
Q

Describe the sources of acid from metabolism, the methods by which these acids can be buffered.

A
  • Metabolic acids are produced during breakdown or synthesis of nutrients (e.g., lactic acid, pyruvic acid, and ketone bodies)
  • Volatile acids (e.g., carbonic acid) are formed when certain gases like carbon dioxide dissolve in water.
  • Inside RBCs, protons can bind hemoglobin, buffering the pH and enhancing gas transport and exchange.
  • Plasma proteins are also able to buffer some protons in ECF because several R groups on amino acids can act as weak acids.
  • Blood and other body fluids contain a large reserve of bicarbonate which can bind and buffer protons generated from metabolism.
    • Carbonic acid is a volatile acid and can be broken down in RBCs by carbonic anhydrase to carbon dioxide and water, which can be easily eliminated by the lungs.
154
Q

A continuous capillary allows for most exchange of substances between blood and tissues.

True or False?

A

False.

Sinusoid capillaries allow for the most exchange; continuous allows the least.

155
Q

Fenestrated capillaries are found in the BBB.

True or False?

A

False.

Fenestrated capillaries are only found in parts of the brain lacking a blood brain barrier.

For example, the median eminence, and in the parts of the hypothalamus that are responsible for sensing the osmolarity of blood plasma.

156
Q

Thoroughfare channels and arteriovenous anastomoses both increase blood flow rate from arteriole to venule.

True or False?

A

True.

These tend to be lower resistance pathways than capillary beds due to fewer branching points and slightly wide diameters, which facilitates velocity of blood flow.

157
Q

Thoroughfare channels and arteriovenous anastomoses both allow exchange of substances between their lumen and surrounding tissues.

True or False?

A

False.

Arteriovenous anastomoses have a smooth muscle layer and is not a capillary, so does not allow exchange. Thoroughfare channels are capillaries and do allow exchange of substances.

158
Q

Will the described change affect CHP or BCOP, and in what direction? How does it alter NFP?

Decrease in blood volume

A

Decreases CHP → decreases NFP

159
Q

Will the described change affect CHP or BCOP, and in what direction? How does it alter NFP?

Increase plasma osmolarity (dehydration)

A

Increase BCOP → decreases NFP

160
Q

Will the described change affect CHP or BCOP, and in what direction? How does it alter NFP?

Decrease plasma proteins

A

Decreases BCOP → increases NFP

161
Q

Will the described change affect CHP or BCOP, and in what direction? How does it alter NFP?

Increase blood volume

A

Increase CHP → increases NFP

162
Q

Will the described change affect CHP or BCOP, and in what direction? How does it alter NFP?

Decrease venous return

A

Increases CHP → increases NFP

163
Q

What causes filtration > reabsorption (i.e., oedema) in capillaries? [3]

A

Decrease in plasma proteins

Increase in blood volume

Decrease in venous return

164
Q

What causes reabsorption > filtration (i.e., recall of fluids) in capillaries? [2]

A

Decrease in blood volume

Increase in plasma osmolarity (dehydration)

165
Q

Lactic acidosis (specifically, Type A lactic acidosis) is a potentially life-threatening condition involving decreases in blood pH due to build-up of metabolic acids. It can arise after periods of capillary hypoperfusion (reduced blood flow).

  • How would capillary hypoperfusion lead to acidosis (and specifically, acidosis from build-up of metabolic acids)?
A
  • Capillary hypoperfusion leads to acidosis (and specifically, acidosis from build-up of metabolic acids) because of anaerobic metabolism using ATP at a fast rate and generating wastes.
  • If there isn’t enough blood flow through the capillaries to allow enough oxygen per unit time to facilitate mitochondrial ATP production (i.e., aerobic metabolism), then the cells will switch to anaerobic metabolism, which generates significant lactic acid waste.
166
Q

Explain the role of vasoconstriction and vasodilation in controlling blood flow to different tissues and describe how these processes occur in terms of changes in vessel tissue layers.

A
  • Vasoconstriction and vasodilation refer to the amount of tension produced in the smooth muscle of the tunica media.
  • Smooth muscle shortens and produces tension in response to calcium elevation but has different contractile mechanisms than striated muscle.
  • Contraction reduces blood flow.
  • Dilation enhances blood flow.
167
Q

Compare and contrast the mechanisms of intrinsic (auto-) regulation of blood flow in terms of whether they are direct or indirect, metabolic or myogenic, and homeostatic or allostatic.

A
  • Intrinsic regulation → autoregulation of blood vessel diameter by factors occurring within the local environment of the blood vessel.
  • Direct stimuli known to cause vasodilation in peripheral tissues (i.e., increases blood flow and thereby oxygen delivery and waste removal):
    • Decreased oxygen concentration
    • Increased carbon dioxide concentration
    • Increased proton concentration
    • Increased potassium concentration
  • Indirect stimuli that can cause vasodilation
    • Paracrine factors → remain in their local environment (e.g., nitric oxide (NO) is a soluble gas that drives smooth muscle relaxation)
  • Metabolic → paracrine vasoconstriction factors which are constantly secreted at basal levels, helping to maintain baseline vessel tone.
  • Myogenic → stretching vascular smooth muscle triggers increased contraction, returning vessel diameter to original length.
168
Q

What are the intrinsic regulation methods and what are the extrinsic regulation methods?

A
  • Extrinsic regulation → mechanisms involving the organ system that integrate signals throughout the body (i.e., nervous and endocrine systems).
169
Q

Compare and contrast blood flow changes in striated muscles and skin during exercise (and thermal homeostasis).

A
  • Sympathetic activity is higher when the body is cold and lower when the body is warm.
  • Blood flow through blood vessels in skin is precisely regulated by the CNS to maintain homeostasis → constricts vessels when core temperature is low, dilates when high.
  • Although skin is not metabolically active during exercise, blood flow increases to skin driven by the CNS have a critical role to lose heat generated by skeletal muscle.
  • Extrinsic regulation > intrinsic regulation
170
Q

Analyze a pattern of blood flow changes in skeletal muscles during exercise in terms of whether they are driven by intrinsic or extrinsic regulation.

A
  • Intrinsic regulation > extrinsic regulation within skeletal muscles during exercise hyperaemia.
    • Although sympathetic activity increases during exercise, promoting vasoconstriction (alpha-1 receptors), this effect is much smaller than the vasodilation that occurs due to metabolic factors (e.g., decreased oxygen concentration, increased carbon dioxide and metabolic waste concentration).
  • Adenosine → a paracrine factor released when ATP is used → a key driver of vasodilation in coronary arterioles.
171
Q

During heavy exercise, cardiac output increases by ~3X, but blood flow to skeletal muscles increases ~10X.

  • Explain how alterations in arteriole and pre-capillary smooth muscle can make this pattern occur.
A

Dilation of arterioles in skeletal muscle and skin increases blood flow in those tissues; however, vasoconstriction in vessels of other areas like the GI tract will restrict blood flow there to direct more blood to the skin/skeletal muscle/heart.

Blood flows according to paths of least resistance. Since resistance is increased in vessels that are vasoconstricted, the blood will preferentially flow to areas of lesser resistance instead.

172
Q

Reactive hyperemia is an allostatic response.

True or False?

A

False.

It is a homeostatic response.

173
Q

Secretion of vasopressin (which can cause vasoconstriction) is an example of intrinsic regulation.

True or False?

A

False.

This is an example of extrinsic regulation.

174
Q

Increase in local carbon dioxide concentration will lead to constriction of arterioles & pre-capillary sphincters

True or False?

A

False.

This would lead to vasodilation.

175
Q

Metabolic autoregulation (e.g., through elevation of potassium cations) is an example of allostasis.

True or False?

A

False.

This is an example of homeostasis.

176
Q

Vasodilation in response to local release of immune signalling molecules is an example of allostasis.

True or False?

A

True.

177
Q

Compare alpha-1 receptors with beta-receptors.

A
  • Alpha-1 receptors → elevate intracellular calcium, enhancing smooth muscle contraction (i.e., vasoconstriction)
    • Most sensitive to NE.
  • Beta receptors → elevate intracellular cAMP, reducing smooth muscle contraction (i.e., vasodilation)
    • Most sensitive to E
    • Note: β receptor activation has the opposite effect on contraction in cardiac muscle because of the different contraction pathways in smooth and striated muscle. β receptor activation in cardiac muscle enhances contraction, and in smooth muscle β receptor activation inhibits contraction.
178
Q

β receptor activation in cardiac muscle enhances contraction, and in smooth muscle β receptor activation inhibits contraction.

True or False?

A

True.

179
Q

β receptor activation in cardiac muscle inhibits contraction, and in smooth muscle β receptor activation enhances contraction.

True or False?

A

False.

β receptor activation in cardiac muscle enhances contraction, and in smooth muscle β receptor activation inhibits contraction.

180
Q

Beta receptors are most sensitive to norepinephrine.

True or False?

A

False.

Beta-receptors are most sensitive to epinephrine (E)

181
Q

Alpha-1 receptors are most sensitive to norepinephrine (NE).

True or False?

A

True.

182
Q

Alpha-1 receptors are most sensitive to epinephrine.

True or False?

A

False.

Alpha-1 receptors are most sensitive to norepinephrine.

183
Q

How does the ANS influence vasoconstriction/dilation?

A
  • Sympathetic postganglionic axons of the ANS make synapses on vascular smooth muscle → vasomotor fibres
  • Action potentials in vasomotor fibres lead to enhanced contraction in smooth muscle (= increased ‘vasomotor tone’)
  • The parasympathetic division does not synapse on blood vessels.
184
Q

Analyze a pattern of blood flow changes in erectile tissue in terms of whether they are driven by intrinsic or extrinsic regulation.

A
  • Erectile tissue in the reproductive system is one exception where there is parasympathetic innervation of vascular tissue.
  • Parasympathetic postganglionic neurons that innervate erectile tissue release NO (instead of or in addition to ACh)
  • NO leads to vasodilation.
  • Viagra enhances the NO-mediated signalling pathway to maintain vasodilation.
185
Q

Describe one component of the cardiovascular response to exercise where autoregulation (intrinsic factors) drive hyperemia.

A

Adenosine causes vasodilation in coronary arterioles which increases blood flow to the heart.

186
Q

Describe one component of the cardiovascular response to exercise where extrinsic factors drive hyperemia.

A

Sympathetic nervous system vasodilates superficial vessels of skin in extremities when temperature is high to radiate heat for thermal homeostasis.

187
Q

Sildenafil (and related PDE5-inhibitin drugs) shouldn’t be taken:

  • (1) if you are on drugs that treat some forms of hypertension (nitrates – these drugs act by increasing NO production)
  • (2) if you have hypotension (very low blood pressure).
    • Explain why ED drugs can lead to serious side effects if taken in either situation.
A

ED drugs cause blood vessels to dilate. Taking multiple drugs that cause vasodilation and lower blood pressure could lead to dangerously low blood pressure. If already hypotensive, taking ED to vasodilate blood vessels could lead to dangerous hypotension as well. If you have low blood pressure, the heart will have a hard time pumping blood all the way up to the brain.

188
Q

Why should someone seeking ED medications get their CV health checked?

A

Sex is a form of exercise for most people that causes increases in cardiac output.

This increases strain on the cardiovascular system. There is a very strong link between erectile dysfunction and heart disease, so increasing strain on the cardiovascular system could be dangerous.

189
Q

Describe the benefits and limitations of changes to total blood volume and vasoconstriction to mitigate changes in blood pressure.

A
  • Altering vasomotor tone requires constant neural (and cardiac) activity - energy intensive
  • Adjustments to blood volume are slow, but they can maintain blood pressure through the circulatory system without constant energy input.
190
Q

Describe the basic components of baroreceptive and chemoreceptive reflexes.

A
  • Sensors → neurons in large elastic arteries
  • Integrators → neurons in the hindbrain
  • Effectors → organs of the CV system
  • Regulated variables → mean arterial blood pressure (baro); blood pH, PO2, and PCO2 (chemo)
191
Q

Predict the direction of changes in CO and vasomotor tone you would see in response to an elevation of arterial baroreceptor activity or chemoreceptor activity.

A

Chemoreceptor (increasing CO2, decreasing pH) → The cardioaccelerator and vasomotor centres will be stimulated, cardioinhibitory centre will be inhibited → increased cardiac output and vasoconstriction (i.e., blood pressure). Vasoconstriction helps with venous return to get more blood to the heart to help increase cardiac output, and to increase capillary hydrostatic pressure to increase the amount of filtration that’s happening in every capillary bed.

Baroreceptor (increasing mean arterial pressure) → When blood pressure is high the cardioinhibitory centre will be stimulated, cardioacceleratory centre and vasomotor centres will be inhibited → decreased CO and vasodilation. Vasodilation helps increase blood flow and reduce blood pressure. When blood pressure is low, just the opposite occurs.

192
Q

Explain the roles of EPO, renin, angiotensin II, aldosterone, and ADH in the long-term response to hypotension.

A

Low blood pressure (or blood volume) leads to lower levels of perfusion through kidney tissue, stimulating the release of EPO and renin.

EPO → drives RBC production, increases blood volume

Renin → part of the hormonal axis known as the RAAS - it catalyzes the first step in the production of angiotensin II and leads to increased plasma volume.

Angiotensin II → has short-term effects on blood pressure → produces vasoconstriction in most blood vessels → it also acts as a regulatory hormone, enhancing the release of aldosterone, and anti-diuretic hormone (ADH).

Aldosterone → a mineralcorticoid (synthesized in the adrenal cortex) hormone that primarily acts on the kidney to retain sodium cations which contributes to water retention.

ADH → secreted from the posterior lobe of the pituitary gland → stimulates water retention by the kidney and acts inside the brain to produce thirst

193
Q

Compare and contrast the endocrine and neural responses to blood pressure or blood volume changes in terms of speed and effector hormones.

A

Long-term hormonal responses are more energy efficient but slower.

Short-term neuronal responses are energy intensive but are much faster.

  • Short term responses to blood loss involve neural reflexes and the physiological stress response.
  • Medium term → reductions in blood pressure leads to reductions in CHP, which lead to ‘recall of fluid’ from the ISF.
  • Long term → increases in ADH and aldosterone leads to increased fluid intake and fluid retention, while EPO restores RBCs.
194
Q

Define the term hypovolemic shock and explain the transition to irreversible shock.

A
  • Occurs after major blood loss (>20% volume lost)
  • Rapid, weak pulse, cold, pale, thirsty, sweating
  • The transition to irreversible shock is triggered by baroreceptor and chemoreceptor reflexes that attempt to maintain blood flow to the brain at the expense of all the other organs → leads to a fatal positive feedback loop.
195
Q

Baroreceptors fire more action potentials per second when blood pressure is high than when it is low.

True or False?

A

True.

196
Q

Inhibiting baroreceptors will lead to a reduction in heart rate.

True or False?

A

False.

Inhibiting baroreceptors leads to increased CO and increased HR.

197
Q

If baroreceptors are stimulated, parasympathetic nervous system activity will increase.

True or False?

A

True.

198
Q

Describe how blood pressure is subject to both homeostatic and allostatic regulation.

A
  • When blood pressure is disturbed, blood pressure is restored to the set point (i.e., homeostasis).
  • When blood chemistry is disturbed, blood pressure is moved to a new set point (i.e., allostasis).
199
Q

As we’ve just seen, the long-term response to low blood pressure (hypotension) involves a multi-organ endocrine system.

  • Would you characterize this as a direct feedback loop? Why or why not?
  • Why does this loop start at the kidneys? What makes a kidney an organ that can act well as a sensor for blood pressure reduction?
A

All blood must be filtered by the kidneys. This is an indirect feedback loop. In a direct feedback loop everything is detected in a single step, but in this loop multiple stages and multiple effectors are involved.

200
Q

Explain the roles of natriuretic peptides in the long-term response to hypertension.

A

High blood pressure (or blood volume) leads to increasing stretching in heart chamber walls, which leads to the release of natriuretic peptides (ANP, and BNP).

  • ANP → released by the atria
  • BNP → released by the ventricles
  • These peptides are regulatory hormones that inhibit the release of renin (and therefore aldosterone), ADH, and epinephrine.
  • These peptides also stimulate the kidneys to increase excretion of sodium cations, which also leads to water loss.
  • They also produce vasodilation in most blood vessels.
201
Q

The long-term response to high blood pressure (hypertension) also involves an endocrine-mediated negative feedback loop.

  • Why does this loop start at the heart? What makes the heart an organ that can act well as a sensor for blood pressure elevation?
  • What’s the trade-off? Why do you think the long-term regulation mechanisms involve hormones while short term mechanisms involve neural reflexes?
A

The heart is a good sensor because the atria sense high blood volume with stretching. The heart uses pressures to move blood and can detect it. Long-term hormonal responses are more energy efficient but slower. Short-term neuronal responses are energy intensive but are much faster.

202
Q

A patient in circulatory shock will show a distinct set of symptoms:

  • Rapid, weak pulse
  • Cold
  • Pale
  • Thirsty
  • Sweating
    • Explain at least two of these symptoms (what part of the physiological response is causing that symptom?)
    • Emergency training courses tell you: never give alcohol to ‘warm up’ someone who is experiencing shock. Why not?
A
  • Skin is pale because venous return is diverted to deep veins.
  • The patient is cold because there is reduced blood flow to the integument.
  • Sweating is because of sympathetic nervous system activation.
  • Thirst is because of more ADH being produced.
  • The pulse is weak because of low blood volume.
  • The pulse is rapid because the heart is pumping rapidly to attempt to ensure the body still has a blood supply.
  • Alcohol is a vasodilator and can rapidly decrease blood pressure.
203
Q

Explain the primary function of the respiratory system (external respiration), and at least one secondary function.

A

External respiration = exchange of oxygen and carbon dioxide between blood, lung tissue, and the external environment = primary function of the respiratory system.

Secondary functions:

  • Sensory → neurons in the nasal cavity detect smells
  • Barrier → keeps foreign substances in air from entering the body
  • Communication → airflow may be manipulated for speech/song.
204
Q

Describe how the respiratory system can be divided into conducting vs respiratory structures and compare the tissue specializations and functional anatomy in these different regions.

A
  • Upper parts → responsible for conditioning inhaled air, and reabsorbing heat and water from exhaled air.
  • Lower parts → conduct air to gas exchange surfaces (and perform gas exchange.
  • Conducting portions are a series of flexible, branching tubes:
    • Larynx
    • Trachea
    • Bronchi (3 types)
    • Bronchioles (2 types)
      • 1 tracheaa → 2 primary bronchia → 5 lobar bronchia → 10s of 1000s of terminal bronchioles → ~150,000,000 alveoli per lung
  • Respiratory portions are the pulmonary lobules → respiratory bronchioles and alveolar sacs which contain capillary-wrapped alveoli (gas-exchange structures).
205
Q

Explain how skeletal muscle movements produce pulmonary ventilation by generating pressure gradients.

A
  • During quiet breathing, the diaphragm and external intercostals contract and expand the thoracic cavity, then relax.
  • Movements of inspiratory muscles during inhalation expand the lungs, creating a negative pressure gradient that pulls air through the airways to the lungs. When the muscles stop contracting, they resume the original position, and the pressure gradient reverses.
206
Q

Describe the basic roles of the brainstem and spinal motor neurons in generating the movements of ventilation.

A
  • Somatic motor neurons located in the cervical and thoracic spinal cord innervate inspiratory skeletal muscles to produce breathing movements that are rhythmic.
  • Phrenic motor neurons send their axons in the phrenic nerve and innervate the myofibres of the diaphragm → no phrenic motor neuron activity = no breathing!
  • Respiratory centres in the pons integrate information from the forebrain and sensory neurons and can adjust the ongoing rhythm generated by the respiratory centres in the medulla (which synapse onto motor neurons that drive breathing muscles) → no medullary respiratory centre activity = no breathing!
207
Q

Define tidal volume.

A

A single quiet breath moves ~500mL into and then back out of the lungs (the resting tidal volume).

208
Q

Define vital capacity.

A

Vital capacity → Expiratory reserve volume + tidal volume + inspiratory reserve volume

209
Q

Define residual volume.

A

Some air remains in the lungs even after maximal exhalation = residual volume.

210
Q

A functioning respiratory system is necessary for both external and internal respiration.

True or False?

A

True.

211
Q

Parts of both the upper and lower respiratory tract are shared with the digestive tract.

True or False?

A

False.

Only the upper respiratory tract shares parts with the digestive system.

212
Q

Most of the surface area in lung tissue is found with pulmonary lobules, not conducting regions.

True or False?

A

True.

213
Q

If all skeletal muscles were paralyzed, external respiration could continue.

True or False?

A

False.

External respiration will fail (i.e., the diaphragm is a skeletal muscle)

214
Q

The larynx belongs to the lower respiratory system.

True or False?

A

True.

215
Q

Explain why an infection in the lower respiratory tract is generally much more serious than an infection in the upper respiratory tract.

A

Mucous protection in the upper respiratory tract is more effective than macrophages in the lower respiratory tract. The lower respiratory tract is where the lungs and alveoli are – infections there will directly affect gas exchange.

216
Q

Now that you’ve seen the anatomy of pulmonary capillaries and alveoli, can you think of another reason why pressures need to be lower in the pulmonary circuit (than the systemic circuit)?

A

Pressure needs to be lower in the pulmonary circuit to prevent damage to the single epithelial layer between air/blood. The capillaries should neither rupture, nor force fluid out to make gas exchange and external respiration as efficient as possible.

217
Q

One of the biggest health problems experienced by very pre-term infants (born before 32 weeks) is a lack of surfactant production. Explain why this leads to reduced respiratory function.

A

The force of surface tension after exhalation will cause alveoli to collapse, leading to decreased surface area for gas exchange. This leads to difficulty breathing.

218
Q

Both the respiratory cycle and the cardiac cycle involve constantly repeated sets of movements. If either one stops, the body’s systems will all fail.

  • What are two similarities between the movements during pulmonary ventilation and the movements during a heartbeat or where they are generated?
  • What are two differences?
A

Similarities: They’re both pumps that create a pressure gradient.

Differences: The heart doesn’t require CNS intervention but breathing does.

Pericardium (heart cavity) vs. pleura (lung cavity).

Cardiac muscle (cardiac) vs. skeletal muscle (respiratory).

219
Q

Swimming legend Michael Phelps has been estimated to have a total lung capacity of 12L (i.e., about double that of a typical morphological male.

  • Would you expect that this (crazy) lung capacity helped him to achieve his remarkable record of success? Explain how.
  • He also famously enjoys a bong now and again. Do you think TLC will interact with his ability to get high this way? How?
A

His high lung capacity increases the alveolar surface area which makes gas exchange more efficient for him. He can extract more oxygen per breath than the average male. In the same way, his total lung capacity increases the amount of THC (from weed) that he can exchange in one breath, so he may get high faster than the average male.

220
Q

Explain the factors that are used to calculate both VE and VA and explain the anatomical reason for why these measurements differ.

A
  • Respiratory minute volume (VE) measures the amount of air moved into the respiratory system per minute.
    • VE = respiratory rate (f) x tidal volume (VT)
  • Alveolar ventilation (VA) is a measure of the amount of air that reaches the alveoli per minute.
    • VA = breaths per minute (f) x (Tidal volume - anatomical dead space)
    • These measurements differ due to the anatomical dead space → some inhaled air never reaches the alveoli.
221
Q

Identify three different types of stimuli that can trigger respiratory reflexes, and briefly explain how they change respiratory rate and/or pattern.

A
  • (1) Protective reflexes → cause forceful exhalation against partial constriction of the airways, which create high pressures to clear the airway.
    • Sneeze → triggered by presence of irritants in nasal cavity
    • Cough → triggered by irritants in the lower respiratory tract
  • (2) Inflation (and deflation) reflexes are activated by baroreceptors in the lungs.
    • Regulate breathing rhythm to avoid over or under inflation.
  • (3) Chemoreceptor reflexes are activated from sensors in elastic arteries and the medulla oblongata.
    • Sensitive to changes in PCO2 → elevations in metabolic activity increase respiratory rate
222
Q

Define the terms resistance and compliance of pulmonary function.

A
  • Resistance → a measure of how much force is needed to make air flow rapidly through conducting pathways.
  • Compliance → a measure of how much work it takes to expand the lungs at a given pressure
    • More force required for expansion = LOWER compliance
    • Less force required for expansion = HIGHER compliance
      • Relates to (1) properties of lung tissue or (2) properties of skeletomuscular elements.
223
Q

Identify at least one example of a restrictive lung disease, and one example of an obstructive lung disease, and describe how spirometry measures differ between these.

A
  • Restrictive → lower capacity for air across most measures of lung function
    • Respiratory distress syndrome → reduced/absent surfactant
    • Arthritis in rib articulations
  • Obstructive → increased residual capacities
    • Asthma → inflammation and bronchoconstriction
    • Chronic bronchitis → inflammation leading to overproduction of mucous that clogs airways
224
Q

Explain emphysema in terms of changes in pulmonary anatomy, pulmonary compliance, and respiratory rate and effort.

A
  • Caused by destruction of respiratory tissue → loss of alveolar structure and gas exchange surfaces → result of prolonged exposure to toxic particulates
    • Alveoli walls deteriorate, leading to merging of adjacent alveoli → walls may even tear
  • Associated with increased compliance → less tissue in alveolar wall → lungs are easier to inflate
    • Lack of elastic recoil in lung tissue means exhalation is comparatively harder → accessory muscles are used even in quiet breathing.
  • Respiratory rate increases due to reduction in gas exchange surfaces (equivalent to increased anatomical dead space)
    • Carbon dioxide cannot be adequately removed
    • Chemoreceptor and baroreceptor reflexes increase respiration rate to attempt to maintain blood oxygenation and try to correct the high PCO2.
225
Q

Describe inflation and deflation reflexes

A
  • Deflation
    • Stretch receptors in smooth muscle around bronchioles → stimulated by lung expansion
    • Respiratory muscles are inhibited by the respiratory rhythmicity centres → inhalation stops
    • Expiratory centres stimulated → forced exhalation
  • Inflation
    • Stretch receptors in the alveolar walls are stimulated as elastic fibres recoil and the alveolar volume is reduced
    • Expiratory centres are inhibited → exhalation stops
    • Forced inhalation begins by stimulation of inspiratory centres in the pons
  • These baroreceptors send information to respiratory centres in the pons, which regulates breathing rhythm to prevent over or under inflation.
226
Q

Describe chemoreceptor reflexes. [3]

A
  • Chemoreceptors in the respiratory centres in the medulla oblongata respond to concentration of hydrogen ions (pH) and carbon dioxide in cerebrospinal fluid
    • Trigger reflexive adjustments in the depth and rate of respiration
  • Chemoreceptors of carotid bodies are sensitive to changes in pH, PCO2 and PO2 in arterial blood
    • By cranial nerve IX
      • Trigger reflexive adjustments in respiratory and cardiovascular activity
  • Chemoreceptors of aortic bodies are sensitive to changes in pH, PCO2, and PO2 in arterial blood
    • By cranial nerve X
      • Trigger reflexive adjustments in respiratory and cardiovascular activity
  • These chemoreceptors are more sensitive to changes in PCO2 than changes in PO2.
227
Q

Sneezing is a local reflex within the upper respiratory tract but coughing requires changes in CNS activity.

True or False?

A

False.

They both require changes in CNS activity.

228
Q

Baroreceptors are in multiple parts of the respiratory tract (as well as in the aorta and carotid arteries).

True or False?

A

True.

Baroreceptors are also found in the digestive system.

229
Q

Increased stretching of bronchiole walls promotes exhalation and inhibits further inhalation.

True or False?

A

True.

230
Q

Increased stretching of bronchiole walls inhibits exhalation and promotes further inhalation.

True or False?

A

False.

Increased stretching of bronchiole walls promotes exhalation and inhibits further inhalation.

231
Q

Elevations in metabolic activity leading to acidemia will trigger a decrease in breathing frequency.

True or False?

A

False.

Elevations in metabolic activity leads to an increase in breathing frequency.

232
Q

Using examples, and explain how compliance and resistance are altered in restrictive and obstructive lung disease.

A
  • Restrictive lung disease → reduced compliance → patient unable to fully fill their lungs → characterized by lower capacity for air across most measures of lung function → easier to detect and diagnose through forced vital capacity because resting tidal volume is small
    • A patient does more work to get the same total volume of air, examples:
      • Respiratory distress syndrome → absence of surfactant
      • Arthritis in rib articulations
  • Obstructive lung disease → increased resistance → lung volume is normal, but conducting pathways are obstructed → characterized by increased residual capacities → reduction is seen during the first second of a forced expiration → typically measured from the ratio of FEV1/FVC.
    • Getting air into the lungs will take more time because resistance affects flow rate, or it will require a much stronger initial pressure gradient to compensate, examples:
      • Asthma → caused by inflammation and bronchoconstriction in airways.
      • Chronic bronchitis → caused by inflammation leading to overproduction of mucous that clogs airways
233
Q

Restrictive lung disease is associated with reduced compliance.

True or False?

A

True.

234
Q

Obstructive lung disease is associated with reduced compliance.

True or False?

A

False.

Obstructive lung disease is associated with increased resistance.

235
Q

Obstructive lung disease is associated with increased resistance.

True or False?

A

True.

236
Q

Restrictive lung disease is associated with increased resistance.

True or False?

A

False.

Restrictive lung disease is associated with reduced compliance.

237
Q

Restrictive lung disease is characterized by a lower capacity of air across most measures of lung function.

True or False?

A

True.

238
Q

Obstructive lung disease is characterized by a lower capacity of air across most measures of lung function.

True or False?

A

False.

Obstructive lung disease is characterized by increased residual capacities.

239
Q

Obstructive lung disease is characterized by increased residual capacities.

True or False?

A

True.

240
Q

Restrictive lung disease is characterized by increased residual capacities.

True or False?

A

False.

Restrictive lung disease is characterized by lower capacity for air across most measures of lung function.

241
Q

The simplest, most sensitive measure for detecting whether a breathing problem is due to obstructive lung disease is to calculate the ratio of FEV1/FVC.

  • Explain why this ratio is so good at diagnosing obstructive lung disease but not restrictive lung disease.
A
  • FEV1 is a great measure of resistance.
  • FVC is variable from person to person.
  • In obstructive lung disease, FEV1 is reduced due to an obstruction of air escaping from the lungs, so the ratio will be reduced.
  • In restrictive lung disease, FEV1 and FVC are equally reduced, so the ratio will be approximately normal.
242
Q

Would you expect her spirometry results (as an emphysema patient) to look more like those of someone with restrictive or obstructive lung disease?

A

Emphysema is not associated with reduced compliance like restrictive lung disease is, it is associated with increased compliance.

Thus, it is more likely to look like obstructive lung disease (which has increased resistance).

243
Q

Emphysema isn’t associated with pain, so why is morphine prescribed to these patients?

A

Morphine helps with anxiety by relieving shortness-of- breath. Opioids makes you breathe more slowly and less deeply, helping the patient to feel calmer.

244
Q

Define partial pressure and explain the main differences in gas composition of inhaled air, alveolar air, and exhaled air in terms of respiratory anatomy and physiology.

A
  • Partial pressure → pressure exerted by a single gas within a mixture of gases (Dalton’s law = pressure contributions for each individual gas can be considered independently according to their proportion in the mixture)
  • Oxygen content is lower in alveolar air compared to inhaled air
245
Q

Describe the direction of O2 and CO2 diffusion at the alveolar-blood barrier and in typical systemic capillaries.

A
  • Blood arriving at pulmonary capillaries is deoxygenated (low PO2) and relatively high in PCO2.
    • The thin wall created by alveolar type I cells and pulmonary capillary endothelial cells allows for oxygen to diffuse into blood, and CO2 to diffuse into the alveolar cavity.
  • Blood arriving at systemic capillaries is oxygenated (high PO2) and relatively low in PCO2.
    • Oxygen can diffuse down its concentration gradient into tissue, while the pressure gradient favours the uptake of CO2 into blood.
246
Q

Explain and/or predict how changes to the surface area, barrier thickness, and pressure gradient will affect gas distribution rates.

A
  • Fick’s Law → Diffusion of a particular gas at a given temperature is enhanced by (1) a large surface area and (2) a steep partial pressure gradient, and reduced by a thick barrier.
247
Q

Explain how O2 is carried in blood.

A
  • The vast majority of O2 in blood is transported bound to Hb in RBCs.
  • Hb binds O2 cooperatively.
    • If one of its four subunits is bound to oxygen, the others become more likely to bind as well → keeps oxygen saturation high at rest, even in systemic venous blood.
248
Q

Describe and compare the three routes by which CO2 is transported in blood – including their relative capacity, reversibility, and interactions with O2 transport.

A
  • (1) Dissolved in solution, (2) bound to Hb, or (3) converted to carbonic acid and bicarbonate/H+
  • CO2 can reversibly bind Hb (especially when PO2 is low)
  • Most will be converted to carbonic acid by carbonic anhydrase
    • H+ generated by carbonic acid dissociation can also bind Hb → buffering against changes in pH → favours O2 offload (and thus CO2 uptake) by Hb.
249
Q

Discuss or analyze how high altitude creates major physiological challenges for the body due to changes to external respiration. What are the short-term consequences and long term compensations?

A
  • At higher altitudes, the air is ‘thinner’ (lower total atmospheric pressure). Although the proportions of the gas molecules are the same, the partial pressures of each gas are lower.
    • The changes in PCO2 are negligible, but because PO2 is lower, alveolar oxygen levels are also lower, and the rate of diffusion of O2 across the blood-air barrier will be slower (due to a reduced PO2 gradient).
  • Altitude sickness leads to hyperventilation and alkalosis in the short term.
    • Hypoxia stimulates respiratory reflexes → increases minute ventilation (VE) → loss of CO2 from blood → alkalosis → O2 offload is less efficient → HR (therefore CO) increases to maintain O2 delivery → leads to higher demands
  • Long-term compensation is driven by endocrine signalling
    • Hypoxia triggers EPO release → increases RBC levels in blood → improves oxygen transport even at lower alveolar PO2.
250
Q
  • Why is the oxygen content lower in alveolar air compared to inhaled air?
  • Why does the water vapour content go up?
  • How would these measurements change if you were stuck in a completely sealed room?
  • If you were way up high in the Rocky Mountains, how would the measurements change?
A
  • The oxygen content lower in alveolar air compared to inhaled air because of air that is stuck in the anatomical dead space that mixes with the inhaled air.
  • The water vapour goes up because air is humidified by the structures of the upper respiratory system upon inhalation.
  • If you were stuck in a completely sealed room CO2 would increase, O2 would decrease, and water vapour in the room would increase.
  • If you were way up high in the mountains everything would be proportionally lower because the total pressure at high altitude is decreased.
251
Q

Several respiratory diseases, including lower respiratory tract infections (such as severe COVID-19) cause inflammation, leading to fluid accumulation in the interstitial space between alveoli and capillaries.

  • How will this fluid accumulation affect external respiration?
  • What downstream effects will this have on internal respiration?
A
  • This fluid accumulation will affect external respiration because the inflammation increases the distance between the alveoli and capillaries (i.e., the thickness of the barrier increases), so there will be a lower rate of diffusion and less efficiency in gas exchange.
  • This decrease in gas exchange will result in less O2 delivery to tissues.
  • Since the blood in the pulmonary circuit is not fully oxygenated, there will be a decreased PO2 in the blood going out to the tissues, so there will be less of an oxygen gradient in other tissues, which will slow down the rate of diffusion in those tissues as well.
252
Q

Use O2-Hb dissociation curves to explain three ways that metabolically active tissues can enhance oxygen delivery without increasing blood flow.

A
  • During exercise, skeletal muscle metabolic rate increases, and oxygen is used for aerobic ATP production → decrease in PO2 promotes offloading of oxygen by Hb, meaning substantial oxygen can be delivered even without an increase in blood flow.
  • Bohr effect → During exercise, skeletal muscles create more CO2 and may create metabolic acids if metabolism becomes anaerobic → both factors lead to increased H+ and therefore decreased pH → decreased pH leads to ‘right-shift’ in the Hb saturation curve, favouring oxygen offload to tissues even at a higher PO2
  • When tissues increase in temperature (heat is a by-product of ATP production), Hb saturation curves shift, favouring oxygen offload → higher temperatures favour offload → again enhancing oxygen delivery to active tissues.
253
Q

When Hb saturation is high, more O2 molecules are bound to Fe-Haem complexes (than when it is low).

True or False?

A

True.

254
Q

If PO2 decreases, more O2 molecules will bind to Hb.

True or False?

A

False.

255
Q

If PO2 decreases, fewer O2 molecules will bind to Hb.

True or False?

A

True.

256
Q

Increases in H+ are the same thing as increases in pH: both lead to increased O2 binding to Hb.

True or False?

A

False.

Increasing pH = more basic

Increasing H+ → decreasing pH = more acidic

257
Q

A right shift in a Hb saturation curve indicates less oxygen will be bound to Hb for a given partial pressure (compared to ‘normal’).

True or False?

A

True.

258
Q

A right shift in a Hb saturation curve indicates more oxygen will be bound to Hb for a given partial pressure (compared to ‘normal’).

True or False?

A

False.

A right shift in a Hb saturation curve indicates less oxygen will be bound to Hb for a given partial pressure (compared to ‘normal’).

259
Q

Venous blood oxygen saturation decreases during aerobic exercise.

True or False?

A

True.

260
Q

Venous blood oxygen saturation increases during aerobic exercise.

True or False?

A

False.

Venous blood oxygen saturation decreases during aerobic exercise.

261
Q

Only a small fraction of the total carbon dioxide produced by the blood is converted to carbonic acid inside RBCs.

True or False?

A

False.

262
Q

Increased carbon dioxide production will favour extra oxygen offload by Hb in systemic capillaries.

True or False?

A

True.

263
Q

Increased carbon dioxide production will favour extra oxygen pick-up by Hb in pulmonary capillaries.

True or False?

A

False.

More CO2 leads to more carbonic acid production → decreased pH → right-shift of Hb saturation curve → favours oxygen offload

264
Q

Increased production of carbon dioxide will lead to stimulation of acid-sensing chemoreceptors that can drive respiratory reflexes.

True or False?

A

True.

265
Q

Which heart valves are easier to successfully replace surgically should they become damaged, and why?

A

Semilunar valves are easier to successfully replace because there are no accessory structures to worry about as is the case with AV valves.

266
Q

Compare and contrast mechanisms of extrinsic regulation of blood flow and explain the different roles of alpha1 and beta adrenergic receptors in changes to vessel diameter.

A
  • The most important hormone to consider for local control of blood flow is epinephrine because smooth muscle in different tissues expresses different adrenergic receptor subtypes which can produce opposite effects since they couple to different G-proteins that lead to different biochemical changes when activated.
  • α1 receptors → elevate intracellular calcium, enhancing smooth muscle contraction (i.e., vasoconstriction)
    • Most sensitive to norepinephrine (NE)
  • β receptors → elevate intracellular cAMP, reducing smooth muscle contraction (i.e., vasodilation)
    • Most sensitive to epinephrine (E)
    • β receptor activation has the opposite effect on contraction in cardiac muscle because of the different contraction pathways in smooth and striated muscle.
      • β receptor activation in cardiac muscle enhances contraction, and in smooth muscle β receptor activation inhibits contraction.