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CardioResp > Week 2 > Flashcards

Week 2 Flashcards

1
Q

What occurs to the spacing between myosin and actin with short sarcomere length? Long sarcomere length?

A
  • Short sarcomere length corresponds with greater spacing between actin and myosin filaments
  • Long sarcomere length corresponds with less spacing between actin and myosin filaments
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2
Q

Explain the passive length – tension relationship of myocardium.

A
  • Passive force-length relation: as sarcomere length increase, tension rises slightly
  • Active force-length relation: as sarcomere length increase, tension rises
    • This is because there is an increase in cross-bridging between myosin and actin
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3
Q

Explain the active time varying elastance of myocardium.

A
  • Change in tension over length is elastance
    • Therefore, slight increase in tension will result in a corresponding increase in elastance
    • Elastance is the tendency of a material to recoil with removal of a compressing force (reciprocal of compliance)
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4
Q

Explain the active length – tension relationship of myocardium, and contrast it with skeletal muscle. ​

A
  • Cardiomyocytes live in the optimal length at all times due to titin
    • Titin is a protein that attaches the myosin filaments to the Z-line, ensuring that cardiac muscle fibers do not overstretch
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5
Q

Explain how myosin and actin bind using ATP (Full cycle)

A
  • ATP binds → myosin head detaches from actin → ATP hydrolyzes on myosin head into ADP + Pi → myosin head goes back to cocked position (“recovery stroke”) → myosin cross-bridges with actin → phosphate group is released → power stroke (“working stroke”) causes filaments to slide past each other → ADP released (rate-limiting step) → ATP binds
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6
Q

What are the three subunits of troponin and what do they each do?

A
  • Troponin: three subunits
    • TnT: binds tropomyosin
    • TnC: binds Ca++ to allow for contraction
      • The absence of Ca++ blocks binding site of myosin on actin molecule
    • TnI: inhibits myosin binding
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7
Q

Where is tropomyosin located, what does it attach to, and how many actin molecules does it span?

A
  • Tropomyosin: spans 7 subunits of actin to act as glue to troponin
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8
Q

What is the rate limiting step of the myosin-actin binding?

A
  • Contractile velocity – ADP release step is considered the “detachment limited model”
    • Myosin head cycling is limited by how fast myosin motors can detach
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9
Q

The generation of force in muscle contraction depends on what?

A
  • Force generation – the more myosin heads interacting with actin, the greater the force
    • This explains why greater resting length leads to greater force
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10
Q

Explain how/why rigor mortis occurs, based on the myosin-actin + ATP cycle?

A
  • Rigor mortis – muscle stiffness that occurs due to low [ATP], causing myosin to remain attached to actin
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11
Q

What are the steps of cardiac muscle contraction?

A
  • Steps of Contraction
    1. Action Potential Travels into T-tubules
    2. L-Type Ca++ Channels Open
    3. Direct Coupling Between L-Type Channel and RyR causes Ca++ release from SR
    4. Ca++ stimulates contraction – most of the Ca++ that actually stimulates contraction is from the SR (as opposed to the Ca++ coming in through the L-Type Ca++ channels)
    5. SERCA pump uses ATP hydrolysis on SR and NCX/NKX (sodium-calcium/sodium-potassium exchange) system on sarcolemma compete for Ca++ reuptake
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12
Q

Discuss the sympathetic stimulation of cardiac cells and indicate the steps that occur.

A
  • Sympathetic Stimulation
    • Beta-1 adrenergic receptors → activates cAMP-dependent PKA → Ca++ influx → increased force of contraction
    • Myosin Binding Protein C increases contractility by increasing cross-bridging between myosin heads and actin filaments after phosphorylation by PKA
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13
Q

Disccus the parasympathetic stimulation that occurs on cardiac cells.

A
  • Parasympathetic Stimulation
    • Decreases L-type Calcium Channel permeability, decreasing contractility (aka intracellular calcium concentration)
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14
Q

How is contraction terminated?

A
  • Phospholamban inhibits SERCA
    • Phospholamban is inactivated by phosphorylation by PKA
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15
Q

What is the general function of the Parasympathetic nervous system?

A

normal homeostasis – slows things down – rest and digest – can control specific things – body cavities and head

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16
Q

What is the general function of the sympathetic nervous system?

A

stress management – speeds things up and drives the autonomic system forward – fight or flight – system fire alarm – entire body

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17
Q

Where on the spinal cord do the sympathetic and parasympathetic nervous systems start?

A

Parsympathetic: Cranio-sacral region (brainstem and coccyx)

Sympathethic: Thoraco-lumbar area of the spine

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18
Q

Out of the preganglionic and postgangionic, which neuron is the short and which is the long for the parasympathetic nervous system and sympathetic nervous system?

  • What are the receptors (NT) at each point?
A

ALL FIRST ORDER NEURONS use Nicotinic Receptors (Ach).

  • Parasympathetic nervous system: Long 1st order neuron, short 2nd order neuron near the organ
    • 2nd order: Muscarinic (Ach)
  • Sympathetic nervous system: Short 1st order neuron with synapse paravertebrally, long 2nd order neuron to the organ
    • 2nd order: Adrenergic (NE/Epi)
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19
Q

Explain the process of making neurotransmitters from tyrosine to epinepherine (recognize the enzymes involved).

A
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20
Q

List what organs the muscarinic receptors act on (M1-M5).

A

M1 – nerves

M2 – heart

M3 – glands, smooth muscle

M4 – CNS

M5 – CNS

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21
Q

How do the M odd receptors work?

A

M1, 3, & 5 (Modd): ­increased intracellular Ca2+ (Gq)

  • Activation results in stimulation of phospholipase C → PIP2 hydrolysis to IP3 (which acts on SR to increases [Ca2+]i) + DAG → DAG activates PKC to open Ca2+ channels on sarcolemma
  • ­increased intracellular Ca2+ increases muscle contraction via MLCK
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22
Q

How do the M even receptors work?

A

M2 & 4 (Meven): hyperpolarizes the cell (Gi)

activation results in inhibition of cAMP synthesis → causes K+ efflux which hyperpolarizes the cell

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23
Q

How can adrenergic transmission be terminated?

A

Termination of Adrenergic Transmission:

  • Reuptake: accounts for about 60%. NE, EPI transported back into nerve terminal. Inhibited by cocaine and drugs used for depression
  • Diffusion: accounts for about 20%. NE, EPI diffuse away from synaptic cleft
  • Metabolism: accounts for 20%. NE, EPI metabolized to inactive compounds (COMT & MAO)
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24
Q

How do alpha1 receptors work?

A

a1: increased ­intracellular Ca2+(Gq) by increased DAG and IP3

  • Vasoconstriction (BP increased­)
  • On smooth muscle of vessels, eye, and GI/urinary sphincters
  • Smooth muscle contraction by stimulating phospholipase C and Ca2+
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25
Q

What do alpha 2 receptors do?

A

a2: decreased cAMP (Gi), decreased Norepinephrine release (autoreceptor)

  • presynaptic nerve terminals and modulate nerve activity
  • inhibit cAMP synthesis; inhibits neuron activity by causing K+ efflux which hyperpolarizes the cell
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26
Q

What do beta 1 receptors do?

A

b1: increased ­cAMP (Gs), ­increased HR, ­increased Myocardial contractility

  • Found in heart; activation leads to increased ­contraction increased heart rate; causes renin secretion and lipolysis
  • coupled to Gproteins; increases ­adenylyl cyclase and cAMP
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27
Q

What do beta 2 receptors do?

A

b2: ­increased cAMP (Gs),

  • Vasodilation (non-innervated b2) lowering BP, bronchodialation
  • located on most tissues; activation leads to relaxation of smooth muscle (uterus, GI, bladder)
  • ­increased cAMP → activates PKA → phosphorylates MLCK, preventing it from phosphorylating myosin → decreases contraction
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28
Q

What do beta 3 receptors do?

A

b3: ­increased cAMP (Gs), ­increased lipolysis

  • least defined, but present on adipocytes; cause lipolysis coupled to Gproteins; ­increased adenylyl cyclase and cAMP
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29
Q

What are the side effects for muscarinic agonists?

A

Muscarinic Agonists:

  • Overall: “SLUD” (salivation, lacrimation, urination, defication) + hypotension / bronchoconstriction
  • Eyes: pupillary constriction (miosis)
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30
Q

What are the side effects for muscarinic antagonists?

A

Muscarinic Antagonists:

  • “Red as a beet, dry as a bone, blind as a bat, and mad as a hatter” (opposite of SLUD)
  • Eyes: mydriasis (relaxation causes wide pupils) and dry eyes
31
Q

List some muscarinic agonists and antagonists and what are they used for?

A

Agonist: muscarine, nicotine, varenicline

Antagonist: atropine (treat bradyarrhythmias), ipratropium/tiotropium (treat asthma/COPD)

32
Q

For Norepinephrine:

  • What is the receptor specificity?
  • What effect does it have/what is it used for?
A
  • alpha1 = alpha2 > beta1 > beta2
  • increases blood pressure
33
Q

For Epinephrine:

  • What is the receptor specificity?
  • What effect does it have/what is it used for?
A
  • beta1 = beta2 > alpha1 = alpha2
  • increases HR
34
Q

How does the reflex response occur for norepinephrine?

A

alpha1 and alpha2 stimulation causes BP to increase, causing baroreceptors to fire more, decreasing CNS response, leading to decrease in HR…beta1 stimulation causes increase in HR… overall neutral response

35
Q

List some of the alpha1 agonists (3).

A

Phenylephrine, midodrine, methoxamine

36
Q

For Phenylephrine, midodrine, methoxamine:

  • What action do they have?
  • What receptor do they act on?
A

Vasoconstriction leading to increased ­ BP

alpha1

37
Q

How does the phenylephrine reflex response with baroreceptors work?

A

alpha1 stimulation causes BP to increase, causing baroreceptors to fire more, decreasing CNS response, leading to decrease in HR… overall decreased HR

38
Q

What is the mechanism of action of psuedoepherine? What does it lead ot?

A

Vasoconstriction leading to ­increased BP

  • INDIRECT AGONIST: Stimulate release of pre-formed catecholamines, indirectly stimulating alpha1 receptor
39
Q

List two alpha2 agonist drugs.

A

Clonidine and Methyldopa

40
Q

How does clonidine work?

And what receptor does it act as an agonist for?

What happens if the drug is stopped abruptly?

A
  • Alpha 2
  • Blocks synthesis of catecholamines and hyperpolarizes cell to prevent depolarization
  • Chronic low [NE] release leads to upregulation of alpha 1 receptors (post-synaptic)
  • If drug is stopped abruptly, can lead to hypertension crisis because upregulated post-synaptic receptors will pick up the catecholamines that are being released
41
Q
  • How does methyldopa work?
  • What are some physiological effects related to this drug?
A
  • PRODRUG analog precursor that is metabolized by the same enzymes as dopamine
  • Displaces norepiphrine and dopamine synthesis because it uses same enzymes.
  • Has higher affinity for receptor than NE, giving rise to negative feedback preventing synthesis of NE
  • Parkinsonian symptoms (tremors)
42
Q

For Isoproterenol:

  • what is the receptor specificity?
  • What are the basic effects?
A
  • Beta1 = Beta2
  • Decreased BP and increased HR
43
Q

How does the basoreceptor reflex work for isoproterenol?

A

beta2 stimulation causes BP to drop, causing baroreceptors to fire less, allowing CNS to reflexively increase HR…beta1 stimulation causes increase in HR… overall HR is doubly increased

44
Q
  • What receptor does dobutamine work on?
  • What effect does dobutamine have?
  • What occurs with chronic use of beta agonists?
A
  • Beta1
  • Increases HR
  • Chronic use of beta-agonists will lead to downregulation of receptors
45
Q

How does the basoreceptor reflex work for dobutamine?

A

Beta1 stimulation causes no change to BP, causing no response by baroreceptors… overall HR increase

46
Q
  • What receptor does albuterol (short-acting)/salmeterol (large-acting) work on?
  • What effect does it have?
  • What are some physiological effects?
A
  • beta2
  • decreased BP; Vasodilation and bronchodialation
  • Increased blood flow due to smooth muscle relaxation causes hyperglycemia and tremors
47
Q

What is Laplace’s Law? It is an equation for force.

A

F = (Pr)/(2h)

48
Q

Based on the Laplace’s Law, what occurs to the force of contraction when pressure and radius increases?

A
  • As pressure increases and radius increases, force of contraction increases
49
Q

Based on Laplace’s Law, what happens to froce of contraction if the “h” (thickness of the cardiac wall) increases?

A
  • As the thickness of the cardiac wall, h, increases, force of contraction decreases
50
Q

Label A-D.

Also, what does the volume at A represent? C?

A
  • A = End Diastolic Volume; mitral valve closes
  • B = Aortic valve opens
  • C = End Systolic Volume; aortic valve closes
  • D = Aortic valve closes
51
Q

Define afterload. What is it in cardiac terms?

A
  • Afterload: force that resists ventricular contraction = aortic pressure
52
Q

What happens to the end systolic volume and stroke volume with decreased afterload?

A
  • Decreasing afterload → decreased ESV → increased SV
53
Q

What happens to the end systolic volume and stroke volume with increased afterload?

What are some diseases that cause increased afterload?

A
  • Increasing afterload → increased ESV → decreased SV
    • States of hypertension and aortic stenosis
54
Q

Define preload and what it means in cardiac terms.

A
  • Preload: end diastolic volume = blood that fills ventricle before systole
55
Q

What happens to the preload and stroke volume if ventricular compliance is decreased?

A
  • Ventricular Compliance: reduced (aka more stiff) → EDV decreases because ventricle cannot stretch with incoming blood → preload decreases → SV decreases
56
Q

What occurs to the stroke volume with increased contractility? What receptor causes increased contractility?

A
  • Increasing contractility increases SV
    • Beta-1 agonists
57
Q

What occurs to the stroke volume with decreased contractility? What diseases cause decreased contractility?

A
  • Impaired contractility decreases SV
    • Coronary artery disease (MIs)
    • Chronic volume overload (regurgitation of mitral and aortic valves)
    • Dilated cardiomyopathy
58
Q

Provide the equations for mean arterial pressure, cardiac output, and stroke volume. Use the following variables:

  • CO
  • R
  • HR
  • EDV
  • ESV
A
  • MAP = CO*R
  • CO = SV*HR
  • SV = EDV - ESV
59
Q

What are the 4 components of the arterial baroreceptor reflex (think afferrent nerve, processor, efferrent nerve, effector)?

A
  • Arterial Baroreceptor Reflex
    • Components
      • Afferent nerve: Vagus nerve
      • Processor: Medullary vasomotor center
      • Efferent nerves: Vagus nerve and Sympathetic nerve
      • Effector: blood vessels and heart
60
Q

What is the sequence of events for the arterial baroreceptor reflex

  • after an increase in BP
  • after a decrease in BP
A
  • Sequence of events
    • Increase in BP: baroreceptors fire more → stimulate nuclei in the medullary vasomotor center → activates parasympathetic nerves and inhibits sympathetic nerves → decrease in HR
    • Decrease in BP: baroreceptors fire less → sympathetic nerves are not inhibited → sympathetic nerves fire to beta-1 and alpha-1 receptors to increase BP
61
Q

Provide the equation for BP in terms of cardiac output.

What ranges of BP are the baroreceptor reflexes most sensitive for firing?

A
  • BP = CO x TPR
  • Sensitive in BP ranges 80-120
62
Q

Contrast arterial baroreceptors and cardiopulmonary baroreceptors. Where are they usually located and what kind of pressure (high or low) do they work with?

A
  • Arterial baroreceptors are high pressure receptors usually located near or in the aorta (arterial blood) while cardiopulmonary baroreceptors are low pressure receptors usually located in superior vena cava (venous blood).
63
Q

Describe the sequence of events in cardiopulmonary receptors after an increase in venous pressure to lead to a decrease in BP.

A
  • Sequence of events: increase in venous pressure → increase in receptor firing → stimulate nuclei in the medullary cardiovascular centers → decrease sympathetic activity and vasopressin release → increase renal flow and urine volume → decrease blood volume → decreased venous return → decreased BP
64
Q

What are the 4 components of the arterial chemoreceptor reflex (think afferrent nerve, processor, efferrent nerve, effector)?

A
  • Arterial Chemoreceptor Reflex
    • Components
      • Afferent nerve: Vagus nerve
      • Processor: Medullary vasomotor/respiratory center
      • Efferent nerves: Vagus nerve and Sympathetic nerve
      • Effector: blood vessels/heart/lungs
65
Q

For chemoreceptors, baroreceptors, CNS ischemic respons, and renal body fluid, how quick is the response after a change in pressure?

A
66
Q

What is the location of the arterial chemoreceptors?

A
  • Location: arch of the aorta and common carotids
67
Q

When are chemoreceptors most sensitive to what arterial PO2?

A
  • Chemoreceptors are sensitive to arterial PO2 <100
68
Q

What occurs if PO2 or pH goes down or PCO2 goes up?

A
  • If PO2 or pH goes down or PCO2 goes up, chemoreceptors fire →
    • Activates medullary respiratory centers → increases ventilation → increases HR
    • Activates medullary vasomotor center → activates parasympathetic nerves to decrease HR and activates sympathetic nerves to vasoconstrict
69
Q

What is the neural mechanism for blood pressure and blood volume regulation?

A
  • Neural mechanism:
    • Sympathetic nervous system → activates adrenal medulla → release of NE/EPI → systemic adrenergic effects (vasoconstriction/vasodilation)
70
Q

What is the renal mechanism for blood pressure and blood volume regulation?

A
  • Renal mechanism:
    • Low BP → activates sympathetic B1 receptors on kidney → increased renin release →
      • Aldosterone release → Increased water and sodium reabsorption → increased blood volume
      • Activates angiotensinogen to angiotensin I → angiotensin II → vasoconstriction
71
Q

Explain how the cardiovascular reflexes play arole in the upright posture (orthostasis).

A
  • Upright posture (orthostasis):
    • Laying down, blood pools at the thoracic cavity
    • Standing up, blood pools in the legs → cardiac output decreases → BP falls →
      • Oxygenated blood delivery to brain falls → fainting
      • Decreased in arterial/cardiopulmonary baroreceptor activity → Medullary center activation → sympathetic nerve activity increases → causes vasoconstriction and increase in BP
72
Q

Explain how the cardiovascular reflexes play a role in hemorrhage (blood loss).

A
  • Hemorrhage
    • Blood volume decreases → cardiac output drops → BP drops
    • Reflex: medullary center activation → sympathetic nerve activity increases →
      • Increases cardiac output
      • Increases vascular vasoconstriction
      • Increases reabsorption of Na+ and H2O
73
Q
A

CardioResp (14 decks)

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