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Block 4 > Week 1 > Flashcards

Week 1 Flashcards

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1
Q

What two things form the intercalated discs in cardiac muscle?

A
  1. fascia adherents
  2. desmosomes
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2
Q

What do the fascia adherents do? (transverse component)

A

anchors thin filaments to sarcolemma

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3
Q

How is sarcoplasmic reticulum in cardiac muscle different than in skeletal muscle?

A
  1. less developed than in skeletal muscle
  2. Has a dyad arrangement where SR end attached to T-tubule
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4
Q

What relays action potential to cardiomyocytes in heart?

A

purkinje fibers

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5
Q

CARDIAC EXCITATION-CONTRACTION

  1. (A blank) channels depolarize sarcolemma -> AP spreads
  2. AP travels down (B blank)
  3. DHPRs on (B blank) open to allow calcium to enter cell
  4. DHPRs are not physically linked to RyR in cardiac muscle…increasing Ca in cell opens RyRs to release Ca from sarcoplasmic reticulum.
  5. Released Ca binds troponin, tropomyosin moves, myosin binds actin and cross bridging begins
A

A blank - Sodium
B blank - T-tubules

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6
Q

CARDIAC EXCITATION-CONTRACTION

  1. Sodium channels depolarize sarcolemma -> AP spreads
  2. AP travels down T-tubules
  3. (blank A) on T-tubules open to allow (Blank B) to enter cell
  4. (Blank A) are not physically linked to RyR in cardiac muscle…increasing (Blank B) in cell opens RyRs to release (Blank B) from sarcoplasmic reticulum.
  5. Released (Blank B) binds troponin, tropomyosin moves, myosin binds actin and cross bridging begins
A
  1. Blank A- DHPRs
  2. Blank B - calcium
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7
Q

What is phospholamban?

A

protein on sarcoplasmic reticulum that modulates SERCA pump activity

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8
Q

What is digitalis?

A

Blocks the Na/K pump and causes an increases in Calcium inside cardiomyocyte because Na cannot leave the cell and continues to induce AP….leads to increased contraction

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9
Q

What is the function of pacemaker cells in SA node and purkinje fibers?

A

* These cells depolarize in a cyclic fashion
* Na channels leak ions and slowly raise potential until threshold is reached. Allows for continuous cycle of heart contraction

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10
Q

How does PKA play a part in heart contraction?

A

With increased PKA activity there is increased contractility

Elevated PKA activity enhances Ca2+ cycling and increases cardiac muscle contractility.

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11
Q

What activates PKA?

A

increased cAMP activates PKA which then increases contractility

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12
Q

What does PKA target to increase contractility? (3)

A
  1. DHPRs and RyRs - to increase calcium influx
  2. Phospholamban - to increased SERCA activity and thus amount of stored calcium
  3. Troponin- increases sensitivity to calcium
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13
Q

How does epinephrine and norepinephrine affect PKA activity?

A

Epinephrine/norepinephrine can increase cAMP and thus activate PKA

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14
Q

What are ways to reduce cardiac contraction? (4)

A
  1. parasympathetic activity - ACh hyperpolarizes cardiomyocyte (inhibit AP)
  2. Beta blockers- reduce cAMP/PKA activity
  3. Low pH exports K+ which makes cell more negative inside (hyperpolarizes) - harder to excite cell now
  4. Hypoxia - low oxygen levels lowers ATP available for cross bridge cycles
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15
Q

How does electricity/AP move through heart?

A
  1. SA node
  2. AV node
  3. bundle of His
  4. purkinje fibers
  5. purkinje fibers causes action potential in cardiomyocytes
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16
Q

How are purkinje fibers different from cardiomyocytes in terms of staining?

A

Stain lighter because more glucose uptake in purkinje fibers

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17
Q

what fuel source is preferred by cardiac tissue?

A
  1. Fatty acids
    also. …glucose/lactate (increased use with exercise) and ketones (least preferred but done in emergencies)
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18
Q

How does cardiac tissue receive oxygen and nutrients/

A
  1. cardiac tissue is filled with capillaries that bring oxygen and nutrients.
  2. cardiomycotes have high number of mitochondria -depend mostly oxidative phosphorylation
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19
Q

What nervous system (general) regulates smooth muscle?

A

autonomic nervous system

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20
Q

(sympathetic/parasympathetic) usually innervates blood vessels?

A

sympathetic nervous system

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21
Q

What is the enteric nervous system?

A

subdivision of autonomic nervous system that regulates GI tract. In control of gut peristalsis and digestive secretions

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22
Q

In smooth muscle, how are the axons different than in skeletal muscle?

A
  1. axons have several bead like swellings along length called varicosities
  2. Varicosities - release NT and NTs diffuse to surface of smooth muscle to initiate contraction
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23
Q

Differentiate multi-unit vs single unit in smooth muscle

A
  1. Multi unit - independent cells that contract separately
  2. Single unit - linked cells in sheets or bundles that are all connected by gap junctions
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24
Q

Multi-unit vs single unit

  1. nervous innervation or hormone+nerve regulation
  2. ECM separates+insulates cells in which unit?
  3. Where is each typically found?
A

Multi-unit

  1. Nervous innervation (single innervation)
  2. ECM separates + insulates cells
  3. Found in iris of eyes, arrector pili muscles of skin

Single Unit

  1. Regulated by hormones and nerves
  2. small ECM that doesn’t insulate
  3. Found in blood vessels, GI tract, uterus, and urinary tract
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25
Q

What is phasic contraction?

A

Contraction in a rhythmic or intermittent fashion. Common in single unit.

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26
Q

What is tonic contraction?

A

Smooth muscle has a constant or low level contraction. Common in multi-unit smooth muscle.

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27
Q

What are dense bodies in smooth muscle?

A

Analogous to Z lines in striated muscle. Serve as attachment sites for filaments and transmit contractile force to cell exterior and connect to other cells

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28
Q
  1. Why does myosin move through the cross bridge cycle at a much slower rate in smooth muscle vs skeletal muscle?
  2. Why is this beneficial for smooth muscle contraction?
A

*Myosin hydrolyzes ATP at a slower rate, and consequently stays bound to actin filaments for longer stretches of time.

*Smooth muscle requires much less ATP to maintain contractions so continued contraction can occur with less energy input.

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29
Q

Steps to smooth muscle excitation-contraction

  1. Calcium enters cell from extracellular environment + some calcium from SR (but minimal)
  2. (Blank A) is activated by calcium
  3. Activated (Blank A) activates (Blank B)
  4. Active (Blank B) phosphorylates inactive myosin. Myosin is now active and can bind to actin thin filaments –> contraction
A

Blank A- Calmodulin (CaM)
Blank B - MLCK

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30
Q

How do you stop smooth muscle contraction? (3)

A
  1. calcium pumps on sarcolemma and SR remove calcium - act much slower than in striated muscle
  2. Calmodulin becomes inactive
  3. Myosin phosphatase becomes active and removes phosphate from myosin - myosin folds up and stops contraction
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31
Q

What is the purpose myosin phosphatase?

A

Removes phosphate from myosin. Myosin folds up and cell relaxes (stops contraction)

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32
Q
  • What is slow wave potential in smooth muscle?
  • What is another name for this?
A
  1. Cells gradually depolarize to threshold and then initiate AP to make organ contract.
  2. Cyclic fashion/pacemaker waves
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33
Q

What is stretch response?

A

stretching triggers AP such as when someone is full and stretches intestines

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34
Q

What are the types of AP in single unit smooth muscle?

A
  1. Slow wave potential/pacemaker waves
  2. stretch response
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35
Q

How is contraction induced in a multi-unit smooth muscle?

A

NT binds to open channels and starts depolarization. depolarization can initiate contraction even if depolarization doesn’t end in AP

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36
Q

increasing extracellular calcium (Blank) strength of contraction

A

increases

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37
Q

NT/hormone signaling activates (Blank A). Signal cascade from (Blank A) makes IP3. This leads to calcium channels opening on SR to increase contraction

A

Blank A - PLC

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38
Q

What leads to reduced MLCK activity?
What does reducing MLCK activity cause?

A
  1. increased cAMP activates PKA
  2. activated PKA phosphorylates MLCK (myosin light chain kinase)
  3. Phosphorylated MLCK decreases contraction in smooth muscle
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39
Q
  1. What leads to increased myosin phosphatase activity?
  2. What does increased myosin phosphatase activity cause?
A
  1. increased cAMP levels
  2. decreases contraction of smooth muscle
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40
Q
  1. What leads to reduced myosin phosphatase activity?
  2. What does reducing myosin phosphatase activity cause?
A
  1. Activating RhoA/ROK signaling pathway which creates arachidonic acid and reduces myosin phosphatase activity
  2. increases contraction of smooth muscle
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41
Q

Norepinephrine does vasoconstriction or vasodilation?

A

vasoconstriction

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42
Q

Norepinephrine binds to what two receptors on vascular smooth muscle?

A

alpha 1 and alpha 2 receptor

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43
Q

What type of GPCR are alpha 1 and alpha 2 receptors?

A

Alpha 1 is Gq GPCR
Alpha 2 is Gi GPCR

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44
Q

What are the differing functions of alpha 1 and alpha 2 receptors?

A

Alpha 1 - more often found on vascular smooth muscle
Alpha 2 - weaker effect on blood vessels but much stronger effect in CNS and leads to vasodilation

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45
Q

What are the general cascade steps of Alpha 1 (two pathways) and Alpha 2 (one pathway) receptors?

A

photo

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46
Q
  1. Is angiotensin II a vasoconstrictor or vasodilator?
  2. What receptors does angiotestin II bind to?
  3. What type of GPCR is this receptor?
A
  1. Vasoconstrictor
  2. AT1
  3. Gq GPCR type
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47
Q

What are the general cascade steps of AT1 receptors (multiple pathways)

A

photo

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48
Q
  1. Is vasopressin a vasoconstrictor or vasodilator
  2. What receptor does it bind to
  3. What type of GPCR is it?
A
  1. vasoconstrictor
  2. V1
  3. Gq GPCR
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49
Q

General pathway of activated V1 receptor

A

photo

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50
Q
  1. is endothelin a vasoconstrictor or dilator?
  2. what receptor does it bind to?
  3. what type of GPCR is it?
A
  1. vasoconstrictor
  2. ETa
  3. Gq GPCR type
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51
Q

What is the general pathway of activated ETa receptor?

A

photo

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52
Q
  1. Where does bradykinin get produced?
  2. Why does it get produced?
  3. Steps for its production
A
  1. Kidneys
  2. When cells are damaged and inflammed
  3. This cell damage activates kallikrein which cleaves kininogen to make bradykinin
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53
Q
  1. What receptor does bradykinin activate?
  2. What occurs after receptor gets activated?
A
  1. B2 receptor on endothelial cells
  2. stimulates production of nitric oxide and prostacyclin on smooth muscle cells
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54
Q

Is bradykinin a vasoconstrictor or vasodilator?

A

Vasodilator- increases capillary permeability which is important for leukocyte movement but can cause edema

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55
Q

What is the general pathway of an activated H2 receptor? (activated by Histamine vasodilator)

A

photo

(activated MLCK typically allows for contraction)

(Histamine leads to vasodilation)

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56
Q

What is the difference in vasodilation between activated H1 vs H2 receptor?

A
  1. H1 causes fast acting, brief vasodilation
  2. H2 causes slow and sustained vasodilation
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57
Q

Prostaglandin I2/Prostacyclin

  1. What receptor does it activate and what type of GPCR is it?
  2. What is the general pathway of this activated receptor?
A
  1. IP - Gs GPCR
  2. photo
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58
Q
  1. What is the receptor for Nitric Oxide (vasodilator)?
  2. What is the general pathway of NO?
A
  1. there is no receptor….NO diffuses through sarcolemma
  2. photo + cGMP increases K channels which hyperpolarizes cell and thus makes it harder to initiate contraction
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59
Q

How is NO created in endothelial cells after reaction to shear stress, bradykinin, other stimulus?

A
  1. Increase in intracellular (in endothelial cell) calcium
  2. increased Ca levels activates calmodulin
  3. Calmodulin activates eNOS
  4. eNOS enzyme works on arginine + NADPH + O2 and makes NO
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60
Q

Myogenic definition

A

The heart is myogenic meaning the heartbeat is generated within the heart muscle without any extrinsic nerve stimulation

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61
Q
  1. What is the role of Ca2+ channels in AP at SA node?
  2. What type of Calcium channels?
A
  1. The upstroke of the action potential is caused by calcium channels - Calcium coming into cardiomyocyte
  2. L type Calcium channels
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62
Q
  1. What is the role of K+ channels in AP at SA node?
A
  1. The downstroke/repolarization stage is due to K+ channels. - K+ leaves cardiomyocyte
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63
Q

What is the funny current?

A
  1. Occurs after depolarization phase of AP in SA node
  2. It is a current that on its own slowly depolarizes until it reaches threshold to create AP
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64
Q
  1. What channel is in control of the funny current?
  2. What allows this channel to open?
  3. What ions move this channel to induce AP?
A
  1. IF channel - voltage gated channel
  2. Channel opens when HYPERPOLARIZATION occurs
  3. Na+ comes into cell and K+ comes out of cell –More Na+ comes into cell than K+ coming out (leads to depolarization effect)
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65
Q

What is phase 4 of the AP in SA node?

A

Pacemaker potential

  1. IF takes up first ⅔ of this phase
  2. Ca channel type T takes up last ⅓ of this phase
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66
Q

What is the first step of AP in SA node?

A
  1. K+ current (K+ leaving cardiomyocyte) occurs first
  2. Once the membrane potential hits a low enough voltage difference then IF channels open and rest of AP occurs
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67
Q
  1. How does sympathetic NS affect heart rate?
  2. Explain how its affects are related to pace maker AP
A
  1. increase heart rate
  2. Sympathetic NS increases cAMP which increases funny current in SA node - increasing slope in phase 4 and causing AP much faster
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68
Q

What determines what voltage range the IF channel opens at?

A

cAMP

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69
Q
  1. What does parasympathetic NS do to heart?
  2. Explain how its affects are related to pace maker AP
A
  1. Decrease heart rate
  2. Inhibits funny current while activating K+ current (K+ leaves cell) → leads to inside of cell being more negative. This decreases slow of phase 4 and makes it harder to reach threshold.
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70
Q
  1. What does hyperthyroidism do to heart rate? Explain?
  2. What about hypothyroidism?
A
  1. increases heart rate - T3 increases funny current by expressing HCN channels - leads to faster phase 4
  2. Decreases heart rate - due to opposite effect
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71
Q
  1. What does Hyperkalemia do to heart rate? Explain?
  2. What about Hypokalemia?
A
  1. Decreases heart rate - more extracellular K+ causes resting potential to be more positive. This change leads to less Na (funny channels) channels opening so less Na is coming into cell. Overall - it elongates AP length thus decreasing heart rate
  2. Increases heart rate - opposite effect as above
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72
Q

How does high body temperature affect heart rate?

A

Increases heart rate - temperature allows for faster movement of ions and leads to faster generation of AP

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73
Q

How does hypoxia affect heart rate?

A
  1. Decreases heart rate
  2. Less oxygen you get less ATP which is necessary to keep the Na/K pump going (Na out of cell and K into cell)
  3. End up with more Na inside cell which depolarizes cell and doesn’t allow for hyperpolarization necessary to open IF channels
  4. This is particularly important for bundle of His and ventricle AP
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74
Q

What is the pathway of AP through heart?

A
  1. SA node
  2. Atria
  3. AV node
  4. Bundle of His
  5. Purkinje fibers
  6. Ventricular muscle
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75
Q

Which parts of heart are pacemakers?

A
  1. SA node (Normal HR 60-100)
  2. AV node (Around 50 bpm)
  3. Purkinje fibers (lowest HR at 20 bpm)
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76
Q

Why is speed of conduction through AV node very slow?

A
  1. Allows for ventricles to fill with blood from atria contraction
  2. Acts as safety valve that prevents repetitive stimuli from hitting ventricles - this is done via AV node’s refractory period in which it cannot be excited for a brief period after sending signal out.
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77
Q

What is annulus fibrosis cordis?

A

part of heart along division of atria from ventricles…allows for signal to diminish after going through ventricles

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78
Q

How is the AP in non pacemaker tissue different from AP in pacemaker tissue?

A
  1. Phase 4 is a flat line due to inward rectifier
  2. Depolarization is due to Na+ only while in pacemaker there is a mix of Na+, K+, and Ca2+
  3. More differences seen in image
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79
Q

How do Beta blockers change velocity through heart?

A
  1. slows conduction velocity by blocking effects of norepinephrine
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80
Q
  1. What do catecholamines (epinephrine, norepinephrine) do conduction velocity through heart?
  2. Specifically what part of heart?
A
  1. Increase conduction velocity - particularly through AV node
  2. AV node
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81
Q
  1. What does Calcium channel blockers do to conduction velocity through heart?
  2. What part of the heart does it affect most?
A
  1. slows conduction velocity
  2. AV and SA node have AP that are calcium dependent (remember the pacemaker AP at these nodes)
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82
Q
  1. What do Na channel blockers do to conduction velocity through heart?
  2. What part of heart
A
  1. Slows conduction
  2. Bundle of His and ventricles
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83
Q

Explain

  1. P wave
  2. QRS complex
  3. T wave
A
  1. Atrial depolarization atrial contraction
  2. Electrical impulse as it spreads through the ventricles (Ventricle depolarization) - Ventricular contraction
  3. Ventricular repolarization
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84
Q

Explain

  1. PR interval
  2. QT interval
A
  1. When signal moves from SA node → atrium → AV node → bundle of HIS
  2. Full process of ventricular depolarization and repolarization
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85
Q

Explain

  1. PR segment
  2. ST segment
A
  1. electrical signal entering AV node
  2. beginning of ventricular repolarization
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86
Q

What causes positive or negative deflection on ECG?

A
  1. Positive deflection - wave of depolarization is moving toward positive electrode
  2. Negative deflection - wave of depolarization is moving away from positive electrode
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87
Q

Definition

  1. Diastole
  2. Systole
A
  1. Filling of the heart
  2. Contraction of heart
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88
Q

Describe phase 1 of cardiac cycle

  1. Name/Main Event
  2. Valves
  3. Aortic Pressure
  4. Atrial Pressure
  5. Ventricular pressure
  6. Ventricular volume
  7. Part of EKG
  8. Heart sounds
A
  1. Atrial Contraction
  2. AV valve (tricuspid or mitral) opens while aortic and pulmonic valves are closed
  3. slight decrease
  4. A wave- Atrial pressure rises and falls (hump) with contraction
  5. Ventricular pressure rises and falls (hump) at same time as atrial pressure change (#4)
  6. Increase until plateau met (last 10% of ventricular filling) - end in EDV (end diastolic volume)
  7. P wave to R part of QRS
  8. 4th heart sound
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89
Q

Describe phase 2 of cardiac cycle

  1. Name/Main Event
  2. Valves
  3. Aortic Pressure
  4. Atrial Pressure
  5. Ventricular pressure
  6. Ventricular volume
  7. Part of EKG
  8. Heart sounds
A
  1. Isovolumetric Contraction - heart is contracting but volume doesn’t change
  2. All valve closed
  3. Drops to minimal pressure
  4. C wave - slight increase and decrease in pressure possibly due to bulging on AV valve back onto atrium
  5. Ventricular pressure rapidly increases to match aortic pressure
  6. Plateau
  7. R-S part of QRS
  8. S1 heart sound
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90
Q

Describe phase 3 of cardiac cycle

  1. Name/Main Event
  2. Valves
  3. Aortic Pressure
  4. Atrial Pressure
  5. Ventricular pressure
  6. Ventricular volume
  7. Part of EKG
  8. Heart sounds
A
  1. Rapid Ejection
  2. Aortic and pulmonic valves open when intraventricular pressure exceeds pressure within aorta+pulmonary artery and AV valves remain closed
  3. Increase in aortic pressure
  4. Rapid decrease in atrial pressure to expand atrial chamber followed by increase (starting to fill again from venous blood)
  5. Ventricular pressure rises (along side aortic pressure)
  6. ventricular volume decreases
  7. ST segment plus first half of T wave
  8. no heart sounds
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91
Q

Describe phase 4 of cardiac cycle

  1. Name/Main Event
  2. Valves
  3. Aortic Pressure
  4. Atrial Pressure
  5. Ventricular pressure
  6. Ventricular volume
  7. Part of EKG
  8. Heart sounds
A
  1. Reduced or Slow Ejection
  2. Aortic and pulmonic valves open and AV valves remain closed
  3. Slight decrease in aortic pressure
  4. Cont. Increase in atrial pressure
  5. Slight decrease in ventricular pressure
  6. Decrease in ventricular volume
  7. Last part of T wave
  8. No heart sounds
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92
Q

Describe phase 5 of cardiac cycle

  1. Name/Main Event
  2. Valves
  3. Aortic Pressure
  4. Atrial Pressure
  5. Ventricular pressure
  6. Ventricular volume
  7. Part of EKG
  8. Heart sounds
A
  1. Isovolumetric Relaxation
  2. All valves closed
  3. Dicrotic notch -indicates beginning of slight increase in aortic pressure before decrease (due to small backflow of blood into ventricles after valve closure)
  4. V wave- Max amount of atrial pressure due to venous blood coming in
  5. Decreases
  6. No change
  7. Between PQRST
  8. S2 heart sound
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93
Q

Describe phase 6 of cardiac cycle

  1. Name/Main Event
  2. Valves
  3. Aortic Pressure
  4. Atrial Pressure
  5. Ventricular pressure
  6. Ventricular volume
  7. Part of EKG
  8. Heart sounds
A
  1. Rapid Filling (rapid passive ventricular filling)
  2. AV valves open
  3. Decrease in aortic pressure
  4. Decrease in atrial pressure as blood flows out of atrium and into ventricles
  5. Ventricular pressure falls far below the atrial pressure to create negative pressure - w/passive ventricular filling the pressure then increases
  6. Increase with blood coming in
  7. Between PQRST
  8. Normally silent in adults but in children S3 sound
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94
Q

Describe phase 7 of cardiac cycle

  1. Name/Main Event
  2. Valves
  3. Aortic Pressure
  4. Atrial Pressure
  5. Ventricular pressure
  6. Ventricular volume
  7. Part of EKG
  8. Heart sounds
A
  1. Reduced/Slow Filling (slow passive ventricular filling-diastasis)
  2. AV valves still open
  3. Cont. to fall
  4. No change
  5. No change
  6. continue to increase ventricular volume
  7. between PQRST
  8. No heart sound
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95
Q
  1. What does A wave represent?
  2. C wave
  3. X descent (after C wave)
  4. V wave
  5. Y descent
A
  1. Atrial systole
  2. bulging of AV valve into the atria
  3. Atrial relaxation
  4. Passive filling of the atria
  5. sudden dumping of blood from atria to ventricles when AV valves open
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96
Q

Identify what parts of PV loop represents this…

  1. Filling phase
  2. Ejection phase
  3. Isovolumetric contraction
  4. Isovolumetric relaxation
A
  1. Bottom
  2. Top
  3. Right
  4. Left
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97
Q

Identify what parts of PV loop represents this…

  1. EDV (end diastolic volume)
  2. ESV (end systolic volume)
A
  1. Bottom right
  2. Top left
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98
Q

Identify what parts of PV loop (left ventricle) represents this…

  1. Mitral valve closing
  2. Aortic valve opening
  3. Aortic valve closing
  4. Mitral valve opening
A
  1. Bottom right
  2. Top right
  3. Top left
  4. Bottom left
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99
Q
  1. What is valve stenosis?
  2. What is valve incompetence
A
  1. Valve fails to open fully
  2. Valve fails to seal properly
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100
Q
  1. What is aortic valve stenosis?
  2. What causes murmur? What kind of murmur?
  3. How does this look in cardiac cycle?
A
  1. When the aortic valve (opening between left ventricular and aorta) fails to open fully. —– This obstructs blood flow from going from left ventricle to aorta during systole
  2. turbulent flow through the valve sets up a vibration hears as Crescendo-decrescendo murmur
  3. Between phase 3 and 4 Aortic pressure is higher than ventricular pressure
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101
Q
  1. What is Tricuspid or mitral valve incompetence?
  2. What causes murmur? What kind of murmur?
A
  1. Failure of tricuspid or mitral valve to seal properly when closed
  2. When ventricle contracts, blood goes back through either mitral or tricuspid valve and causes regurgitation. -pancystolic murmur
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102
Q
  1. What is Aortic valve incompetence?
  2. What causes murmur? What kind of murmur?
  3. Changes to aortic pressure
A
  1. Aortic valve fails to seal properly when closed
  2. Blood leaks back into ventricle from aorta - early diastolic decrescendo murmur
  3. Aortic pressure falls down very quickly
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103
Q
  1. What part of the circulatory system does pulse dampening
  2. What part of the circulatory system has largest amount of blood flow resistance
  3. What part of the circulatory system has capacitance
A
  1. Aorta
  2. Arterioles
  3. Venous system (venules, veins, inferior+superior vena cava)
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104
Q

What is capacitance (AKA compliance) in circulatory system?

A
  1. Ability to increase the volume of blood in blood vessels without a large increase in blood pressure
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105
Q

Why are resistance vessels necessary for circulatory system?

A

Necessary to have ability to locally control blood flow to certain organs. The aorta dampens the pulse via elastic recoil which makes blood flow continuous.

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106
Q

What equation determines mean arterial pressure?

A

MAP = DP + ⅓ PP

DP = diastolic pressure (mm Hg)

PP = Systolic Pressure-Diastolic Pressure

107
Q

What is the equation to determine relationship between pressure, flow, and resistance? (Ohm’s Law)

A

Q = ▵ P/ R

  • pressure difference between two ends of the vessel
  • R is resistance of vessel
108
Q
  1. How does diameter of vessel change flow (turbulent/laminar)
A
  1. With decrease in diameter causes turbulent flow
109
Q
  1. What does Reynolds number mean?
  2. Equation for this
A
  1. Measures the tendency for turbulence to occur
  2. Reynolds number = (velocity X diameter X density)/ viscosity
110
Q
  1. Resistance is (Blank) proportional to RadiusX
  2. What does this mean?
A
  1. Blank - inversely
  2. X = 4
  3. larger the radius the smaller the resistance
111
Q

Equation for serial resistance in vascular system?

A
  1. RT = R1+R2+R3+…Rn
112
Q

Equation for parallel resistance in vascular system?

A
  • 1/RT = 1/R1 +1/R2 + 1/R3 +…1/Rn
  • Human body has more parallel resistance
113
Q

Equation for

  1. Cardiac output
  2. Venous return
A
  1. Heart rate X stroke volume
  2. Heart rate X loading volume
114
Q

Explain how these aspects can increase central venous pressure ….

  1. Venous compliance
A
  1. DECREASED venous compliance can increase central venous pressure
115
Q

Explain how these aspects can increase ventricular preload ….

  1. Blood volume
  2. Muscle pump
  3. Gravity
  4. Inspiration
  5. Ventricular compliance
  6. Atrial inotropy
  7. Heart rate
  8. Ventricular inotropy
A
  1. Increased blood volume increases ventricular preload
  2. Increased muscle pump increases blood flow back to heart
  3. Head down leads to more blood flow to heart
  4. Causes negative pressure in thoracic cavity - pressure leads to more blood coming back to heart
  5. Increased ventricular compliance- accept more blood
  6. Increased atrial inotropy - increased atrial contraction which leads to increased preload
  7. Slow heart rate gives more time to fill ventricles
  8. decreased ventricular inotropy leaves some blood behind making next preload larger
116
Q

What is inotropy?

A

Heart contraction

117
Q
  1. Increased atrial inotropy
  2. Decreased ventricular inotropy

How does these affect EDV (End Diastolic Volume)

A
  1. Increased
  2. Increased
118
Q

Increase in preload …how does this affect

  1. EDV (end diastolic volume)
  2. Stroke volume
  3. ESV (end systolic volume)
A
  1. Increase
  2. Increase
  3. Same
119
Q

Increase in afterload …how does this affect

  1. EDV (end diastolic volume)
  2. Stroke volume
  3. ESV (end systolic volume)
A
  1. Same
  2. Decreased
  3. Increased
120
Q

What is afterload?

A

Afterload is the force or load against which the heart has to contract to eject the blood.

121
Q

What is the Frank-Starling Relationship

  1. Length-tension relationship
  2. Limitations
A
  1. The greater the stretch on the myocardium before systole (preload), the stronger the ventricular contraction.
  2. Should not operate on a heart to the right of the max active tension point
122
Q

Describe the following so it leads to increased afterload (5)

  1. aortic pressure
  2. systemic vascular resistance
  3. Valvular abnormalities
  4. Ventricle dilation/constriction
  5. Ventricular wall abnormalities
A
  1. increased aortic pressure
  2. increased systemic vascular resistance
  3. aortic stenosis (more turbulence)
  4. Ventricular dilation
  5. Thinning of ventricular wall (increases pressure diff between ventricle and aorta/pulmonary artery)
123
Q

Sympathetic NS → cardiac function

  1. What nerve innervates SA node and AV node
  2. What NT is used
  3. Receptors used
  4. Effects
A
  1. Right vagus nerve →SA node ;;;; Left vagus nerve →AV node
  2. Norepinephrine
  3. Beta adrenoreceptors
  4. increased heart rate, increased inotropy, increased conduction velocity
124
Q

Sympathetic NS → vascular function

  1. method of NT release on vascular system
  2. What NT is used
  3. Receptors used
  4. Effects
A
  1. varicosities of axons
  2. Norepinephrine
  3. alpha-adrenoreceptors
  4. Causes contraction of vascular smooth muscle
125
Q

Parasympathetic NS → Cardiac function

  1. What NT is used
  2. Receptors used
  3. Effects
A
  1. ACh
  2. Muscarinic receptors
  3. Decreases heart rate
126
Q

Parasympathetic NS → Vascular function

  1. What NT is used
  2. Receptors used
  3. Effects (2)
A
  1. ACh
  2. Muscarinic receptors
  3. Vasodilatory action;; stimulate bradykinin production + increased capillary permeability
127
Q

Arterial Baroreceptors

  1. locations
  2. associated cranial nerves
A
  1. Carotid sinus (at bifurcation of external and internal carotids) + aortic arch
  2. Glossopharyngeal nerve (IX cranial nerve) → innervates carotid sinus baroreceptors
  3. Vagus nerve (Cranial nerve X) → innervates aortic arch
128
Q

What is the purpose of baroreceptors?

A
  1. Sense arterial pressure and respond to stretching of arterial wall
  2. If arterial pressure suddenly rises → walls of these vessels expand/stretch and cause increase in AP firing in baroreceptors
  3. If arterial pressure suddenly falls, decreased stretch leads to decrease receptor firing
129
Q
  1. Where does AP firing on baroreceptors get transported to in the brain?
  2. What does this part of the brain regulate? –overall goal of baroreceptors
A
  1. Cranial nerves → Nucleus tract solitarius (NTS) in medulla of brainstem
  2. Regulates sympathetic and parasympathetic neurons to regulate autonomic control of heart and blood vessels to regulate BP
130
Q

Cardiopulmonary baroreceptors

  1. Location
  2. Respond to changes in what part of heart
A
  1. atria, ventricles, pulmonary vessels
  2. Respond to atrial filling (venous return)
131
Q

Decrease firing from cardiopulmonary baroreceptors leads to ….

  1. Heart rate changes
  2. ADH levels
A
  1. Increases heart rate when heart rate is low
  2. Increased firing decreases ADH release - less water released (keep more water in body) via nephron
132
Q
  1. What is the function of chemoreceptors?
  2. Peripheral vs central chemoreceptors locations
A
  1. (a) Regulate respiratory activity. (b) Sense chemical composition of blood. ( c) directly/indirectly affects cardiovascular function
  2. Peripheral: carotid and aortic bodies ——central: medulla
133
Q

Chemoreceptors

  1. If PO2 is too low or PCO2 is too high then what happens to respiration?
  2. How does this affect arterial blood pressure?
A
  1. Increase
  2. Increased sympathetic outflow to increase blood pressure BUT ONLY IF respiratory activity increases at the same time
134
Q
  1. Where is epinephrine released from?
  2. What about norepinephrine?
A
  1. adrenal medulla (mostly releases epinephrine - 80%)
  2. adrenal medulla - but primary source is spillover from sympathetic nerves innervating blood vessels
135
Q

Epinephrine effects

  1. via beta 1 adrenoreceptors
  2. via alpha 1 and 2 adrenoreceptors
  3. Blood pressure (via low epinephrine concn. and high concn.s)
  4. Changes in vascular system (dilation/constriction) - in muscle+liver w/low compared to high concns
A
  1. Increase heart rate and inotropy
  2. vasoconstriction in systemic arteries and veins
  3. Low concns- increased pulse pressure but no change in MAP;;; high concns - increased MAP
  4. Low concns- vasodilation in muscle+liver vasculatures ;;;; High concns-vasoconstriction
136
Q

Norepinephrine effects

  1. via beta 1 adrenoreceptors
  2. via alpha 1 and 2 adrenoreceptors
A
  1. increased heart rate but only transient + inotropy
  2. Vasoconstriction in most systemic arteries and veins
137
Q

What is the function of RAAS (renin–angiotensin–aldosterone system)?

A
  1. Regulates blood volume and systemic vascular resistance → together influence cardiac output and arterial pressure
  2. Typically seen to increase/regulate blood pressure
138
Q

what are the three components of RAAS?

  • Where is each component released from?
  • Function of each component
A
  1. renin - released by kidney - stimulates formation of angiotensin in blood and tissue
  2. Angiotensin II - released by blood and tissue - stimulates release of aldosterone
  3. Aldosterone - released by adrenal cortex - Increased Na reabsorption in distal nephron + K secretion into urine
139
Q

What stimulates the release of renin in RAAS?

A
  1. sympathetic nerve activation (beta 1 adrenoreceptors)
  2. Renal artery hypotension
  3. Decreased Na delivery to distal tubules of the kidney
140
Q

What are the effects of angiotensin II? (in RAAS system)

A
  1. stimulates release of aldosterone from adrenal cortex
  2. vasoconstriction
  3. increased Na reabsorption from renal tubules
  4. stimulates thirst
  5. stimulates ADH release
  6. enhances norepinephrine release (increase HR)
141
Q

What is the function of ANP (atrial natriuretic peptide)?

A
  1. When ANP is secreted it indicates increase in blood volume - noticed by stretched atria
  2. Interacts with kidneys to increase filtration/GFR
  3. vasodilation
  4. Natriuresis (excretion of Na in urine) within kidneys to lose volume
142
Q

ANP (atrial natriuretic peptide)

  1. what is the stimulus for ANP
  2. Site of release
A
  1. Atrial distension/stretch
  2. cardiac atria (atrial myocytes)
143
Q

What stimulates release of ADH?

  1. blood volume
  2. blood pressure
  3. plasma osmolality
  4. (blank) receptors activated in hypothalamus
A
  1. Hypovolemia
  2. Hypotension
  3. Increased plasma osmolality
  4. Ang II receptors activated in hypothalamus leads to ADH release
144
Q

Where is ADH released from?

A
  1. Released from Posterior pituitary
  2. but made in hypothalamus
145
Q

Function of ADH

  1. Main function
  2. Heart function
A
  1. Regulate renal handling of water; more ADH means more water retention/less urine production
  2. ADH above normal levels can induce vasoconstriction
146
Q

What nerves innervate on anterior wall of chest cavity? (include what nerve roots are included)

A
  1. Supraclavicular nerves _ C3 and C4
  2. Anterior (ventral) rami of thoracic spinal nerves (intercostal nerves)
147
Q

What nerves innervate on posterior wall of chest cavity?

A
  1. posterior (dorsal) rami of throacic spinal nerves
148
Q
  1. What nerve has a common origin with supraclavicular nerve?
  2. What issues does this cause?
A
  1. Frenic nerve (C3, C4, C5)
  2. Leads to confusion on brain on origination of pain
149
Q

What are true ribs and how many are there?

A
  1. ribs that has costal cartilage that articulate directly with sternum
  2. 1-7 (7 ribs)
150
Q
  1. How many false ribs are there?
  2. What are the two types of false ribs?
A
  1. 5 ribs
  2. ribs #8-10 - costal cartilage of rib articulates with costal cartilage of the rib just superior —ribs #11-12 are floating ribs
151
Q

What are the parts of the sternum?

A
  1. Manubrium
  2. Sternal body
  3. Xiphoid process
152
Q

What are the boundaries of the thoracic inlet?

A
  1. Manubrium of sternum
  2. Medial margin of rib 1
  3. First thoracic vertebra
153
Q

What is the suprapleural membrane?

A
  • It is anchored by ribs-a dense fascial layer that is attached to the inner border of the first rib and costal cartilage anteriorly
  • Creates fluid to allow lungs to move
154
Q

What are the boundaries of the thoracic outlet?

A
  1. Xiphoid process
  2. Costal margin
  3. Distal end of rib 11
  4. Rib 12
  5. Body of T12
155
Q

Manubriosternal Joint

  1. What does it connect?
  2. What type of joint is it?
A
  1. Manubrium and sternal body
  2. Fibrocartilaginous joint
156
Q

Xiphisternal Joint

  1. What does it connect?
  2. What type of joint is it?
A
  1. Connects sternal body to xiphoid process
  2. Fibrocartilaginous joint
157
Q

Sternocostal Joint

  1. What does it connect?
  2. What type of joint is it?
A
  1. between the medial end of the costal cartilages of ribs one to seven
  2. 1st joint is fibrocartilaginous joint —2nd to 7th joint is synovial
158
Q

Joints between the ribs and vertebra

  1. What are points of articulation on one side of one vertebra
A
  1. 2 vertebral bodies and one transverse process
159
Q

What are the joints between ribs and spine? (2) (overall term costovertebral joints)

A

Costovertebral joints

  1. Costocorporeal joint (rib and vertebral body)
  2. Costotransverse joint (rib and tranverse process)
160
Q
  1. what is the Suprasternal notch?
  2. With what vertebral level does this align with?
A
  1. picture
  2. T2/T3
161
Q
  1. What is the sternal angle?
  2. With what vertebral level does this align with?
A
  1. picture
  2. T4/T5
162
Q
  1. What is the Xiphisternal angle?
  2. With what vertebral level does this align with?
A
  1. picture
  2. T9/T10
163
Q

Sternal angle

  1. Marks the vertebral level T4/T5
  2. (Blank A) costal cartilage articulates with sternum
  3. Separates (Blank B) from (Blank C) mediastina
  4. Marks superior limit of (Blank D)
  5. Marks where (Blank E) ends and (Blank F) begins
  6. Marks where (Blank G) begins and ends
  7. Level at which the (Blank H) bifurcates
A
  • Blank A= second
  • Blank B= superior
  • Blank C= inferior
  • Blank D=pericardium
  • Blank E=Ascending aorta
  • Blank F= descending aorta
  • Blank G= aortic arch
  • Blank H= trachea
164
Q

What innervates the intercostal muscles?

A

intercostal nerves

165
Q

What makes up the intercostal muscles (5)

A
  1. external intercostal
  2. internal intercostal
  3. innermost intercostal
  4. Subcostales
  5. Transversus thoracis
166
Q

Explain the orientation of external, internal, and innermost muscles?

A
  1. picture
167
Q

Where are the subcostales and transversus thoracis muscles located?

A
  1. Subcostales are located in posterior thoracic wall
  2. Transversus thoracis are located in anterior thoracic wall
168
Q

How are the intercostal artery, nerve, and vein positioned in the neurovascular bundle within intercostal spaces?

A

VAN

  1. intercostal vein (superior)
  2. intercostal artery
  3. intercostal nerve (inferior)
169
Q

What is the function of the external intercostal muscle?

A
  1. elevate ribs during inspiration (increase lateral and anterior movement)
  2. Work in coordination with diaphragm muscle to increase volume of thoracic cavity
170
Q

What is the function of the internal and innermost intercostal muscle?

A
  1. depress ribs during expiration (diaphragm relaxes)
171
Q
  1. (Blank A) ribs are most commonly affected (result in rib fracture)
  2. (Blank B) rib fractures can injure diaphragm, liver, or spleen
  3. (Blank C) rib fractures can damage the pleura and cause pneumothorax
A

Blank A - middle

Blank B - lower

Blank C - upper

172
Q
  1. What is flail chest?
  2. What does it prevent?
  3. Odd movements?
A
  1. MULTIPLE rib fractures that allow for free movement of the thoracic wall.
  2. prevents full expansion of the lung and impairs ventilation
  3. flail segment moves inward during inspiration (when it should go outward) and outward during expiration (when it should go inward) - paradoxical movement
173
Q
  1. Where is the needed located in thoracentesis?
  2. What to avoid
A
  1. At lower border of intercostal space (or above rib)
  2. Avoid inferior edge of rib to preserve intercostal neurovascular bundle
174
Q
  1. What is another name for internal thoracic artery?
  2. What is it a branch of?
A
  1. Internal mammary artery
  2. Subclavian artery
175
Q
  1. What does the internal thoracic artery pass through?
  2. What is its path?
A
  1. superior thoracic aperture/thoracic inlet
  2. Descends posterior to the costal cartilages lateral to the sternum (on both sides of sternum)
176
Q

What is anterior intercostal arteries a branch of?

A

Internal thoracic artery

177
Q

What does the internal thoracic vein drain into?

A

The brachiocephalic vein

178
Q

What (arterial) anastomosis occurs in the intercostal space?

A

Anterior and posterior intercostal arteries anastomose for collateral circulation

179
Q

What (venous) anastomosis occurs in the intercostal space?

A

Anterior and posterior intercostal veins anastomose for collateral venous drainage

180
Q

What sections of the spine take part in the intercostal nerves?

A

anterior rami of T1 to T11

181
Q

What are the boundaries of the mediastinum?

  1. Anterior?
  2. Posterior?
  3. Superior?
  4. Inferior?
  5. Lateral?
A
  1. Anterior: sternum
  2. Posterior: thoracic vertebrae
  3. Superior: Thoracic inlet
  4. Inferior: diaphragm
  5. Lateral: pleural sacs
182
Q

What are the divisions of mediastinum? (and any further divisions)

A
  1. superior and inferior
  2. Inferior has
    1. Anterior mediastinum
      1. Middle mediastinum
        1. Posterior mediastinum
183
Q

What part of the mediastinum holds the

  • pericardium and heart
  • phrenic nerves, cardiac plexus
  • pulmonary trunk
  • ascending aorta
  • sup and inferior vena cava
  • tracheal bifurcation
  • right and left bronchi
  • right and left pulmonary arteries and veins
A

Middle mediastinum

184
Q

What is the pericardium?

A

Fibroserous sac that encloses the heart and the roots of the great vessels

185
Q

What is the

  • white outline
  • black outline
  • red outline
A
  1. White - fibrous pericardium
  2. Black - pericardial cavity in between the parietal and visceral layer
  3. OUTER red layer is the parietal layer and INNER red layer is the visceral layer (both make up the serous pericardium)
186
Q

How are parietal layer and visceral layer related?

A
  1. Both are a part of the serous pericardium
  2. The parietal layer becomes the visceral layer when it folds inwards
187
Q

What is the function of the fibrous and serous pericardium?

A
  1. Provides support and protection for the heart
  2. Secretes serous fluid
188
Q

What are the pericardial sinuses? (2)

A
  1. Transverse pericardial sinus
  2. Oblique pericardial sinus
189
Q

What is the purpose of transverse pericardial sinus?

A
  • Separates the arteries from veins
  • When finger is placed in this sinus the aorta is in front of the finger and superior vena cava is behind finger
190
Q

What is the purpose of oblique pericardial sinus?

A
  1. It is posterior to the heart. It is a small space of serous pericardium behind the base of the heart and separates base from descending aorta and esophagus
191
Q

What is the nerve supply to the pericardium?

  1. sensory function
  2. autonomic nervous system function (2)
A
  1. Phrenic nerve (C3-C5; pain)
  2. sympathetic trunk and vagus nerve
192
Q

Blood supply (arterial and venous) for pericardium? (3 for each -atleast know first one)

A
  1. Arterial supply is internal thoracic artery, superior phrenic artery, thoracic aorta
  2. Venous drainage is internal thoracic vein, superior phrenic vein, and azygous system of veins
193
Q

What is the coronary sulcus?

A

external groove between atria and ventricles

194
Q

What is the interventricular sulcus?

A

External groove between the ventricles

195
Q
  1. What is the central venous pressure? (AKA right atrial pressure)
  2. What does it determine?
A
  1. Blood pressure in the thoracic vena cava near right atrium
  2. Determines preload of right and left ventricle, and therefore stroke volume
196
Q

What factors can increase central venous pressure?

  1. blood volume
  2. muscle action
  3. respiration
  4. hint: body maneuver (3)
  5. systemic vascular resistance
  6. cardiac output
A
  1. increase in blood volume
  2. muscle pump moves more blood into venous drainage
  3. a. valsalva maneuver/bearing down, reclining, and squatting
  4. Decreased venous compliance moves blood out of peripheral veins to central veins
  5. Decreased systemic vascular resistance/arterial dilation - more blood flow from arteries to veins which eventually increases CVP
  6. Decreased cardiac output - blood backs up on the right side which increases CVP
197
Q

What is venous return?

A

IT IS A FLOW (L/min)

  • volume of systemic blood returning to the right atrium per minute
198
Q

What is venous return equal to?

A

Cardiac output

199
Q

What factors increase venous return? (3)

A
  • Increase in mean arterial pressure
  • Decrease in right atrial pressure
  • Decrease in systemic vascular resistance

Think of flow equation

Venous return = (MAP-RAP)/SVR

200
Q

What factors decrease venous return? (3)

A
  • Decrease in mean arterial pressure
  • Increase in right atrial pressure
  • Increase in systemic vascular resistance

Think of flow equation

Venous return = (MAP-RAP)/SVR

201
Q

Does central venous pressure equal venous return?

A

No it does not.

  • increased venous return can increase CVP
  • BUT increased CVP by itself can decrease venous return because when increasing pressure on venous side you are decreasing pressure on arterial side –which decreases venous return
202
Q

What does the vascular function curve look like and what does it compare?

A
  1. image
  2. Venous return (or cardiac output because its the same) vs right arterial pressure
203
Q

Describe what happens on vascular function curve with

  1. Increased right atrial pressure
  2. Decreased cardiac output
A
  1. Increased right atrial pressure decreases venous return
  2. Decreased cardiac output increases right atrial pressure
204
Q

What does the x intercept on x axis mean on vascular return curve?

A

MCP- mean circulatory pressure - When CO is 0 (if heart were to stop) and pressure evens out throughout the system, MCP is the pressure

205
Q

What happens to the venous function curve if…

  1. Increase in blood volume
A
  1. slope stays the same
  2. whole line moves upward
  3. MCP increases
206
Q

What happens to the venous function curve if…

  1. Decrease in systemic vascular resistance
  2. Increase in systemic vascular resistance
A
  1. image
207
Q

What does the cardiac function curve look like and what does it compare?

A
  1. image
  2. Comparing cardiac output and right atrial pressure
208
Q

When combining vascular function curve and cardiac function curve…. What does the equilibrium point mean?

A
  1. where heart typically operates so CO = venous return
209
Q

How does inotropic state affect cardiac function curve?

A

With increased inotropic state (more contraction) - this makes cardiac function curve shift to the left

  • increased CO
  • Decreased RAP
210
Q

How does increased volume expansion on vascular function curve affect position of cardiac curve?

  1. changes of cardiac function curve
  2. changes of vascular function curve
  3. Slope change?
  4. Result
A
  • Vascular function curve moves up -point of equilibrium moves upward on cardiac function curve
  • Then with increased volume you get increased BP which decreases sympathetic activation→ decreased contraction of heart→decreased systemic vascular resistance→increased CVP/RAP
  • slope of vascular curve increases
  • Result::: increased cardiac output at elevated right atrial pressure and MCP
211
Q

What does sympathetic stimulation do to vascular function+cardiac function curve?

  1. shift of cardiac function curve
  2. shift of vascular function curve
  3. Slope change?
  4. Result
A
  1. increased contractility shifts cardiac function curve to the left
  2. Decreased venous compliance shifts the vascular function curve right (increased MCP)
  3. Increased systemic vascular resistance decreases slope of the vascular function curve

Result: Increased cardiac output at slightly decreased right atrial pressure and increased MCP

212
Q

What type of Autonomic innervation does the heart have?

A
  1. parasympathetic (long preganglionic fibers and short postganglionic fibers)
  2. sympathetic (shorted preganglionic fibers than postganglionic)
213
Q

Where on the heart does the parasympathetic innervation occur? (3)

A
  1. SA node
  2. AV node
  3. Atrial muscle
214
Q

Where on the heart does the sympathetic innervation occur? (5)

A
  1. SA node
  2. AV node
  3. Atrial muscle
  4. Ventricle muscle
  5. Conduction system
215
Q
  1. What receptors on heart receive sympathetic innervation?
  2. What NT activates them?
A
  1. Beta 1 and Beta 2 receptors
  2. Norepinephrine → increases cAMP → increases HR
216
Q
  1. What receptors on heart receive parasympathetic innervation?
  2. What NT activates them?
A
  1. M2 receptors
  2. ACh binds → decreases cAMP → decrease HR
217
Q
  1. What are some agonists of Beta 1 and beta 2 receptors (sympathethic) on heart? (2)
  2. What is its purpose?
A
  1. Dobutamine (beta 1)
    1. Albuterol (beta 2)
  2. Increase HR - both are not typically used in clinic to increase HR*
218
Q
  1. What are some antagonists of Beta 1 and beta 2 receptors (sympathethic) on heart? (3)
  2. What is its purpose?
A
  1. Propranolol (beta blocker)
    1. Atenolol (beta blocker)
      1. Metoprolol (beta blocker)
  2. Decrease HR-used clinically to decrease HR
219
Q
  1. What are some agonists of M2 receptors (parasympathethic) on heart? (2)
  2. What is its purpose?
A
  1. Acetylcholine (M agonist)
    1. Bethanechol (M agonist)

2. Decrease HR - both are typically not used in clinic to decrease HR just found in body

220
Q
  1. What are some antagonists of M2 receptors (parasympathethic) on heart?
  2. What is its purpose?
A
  1. atropine (M blocker)
  2. Increase HR
221
Q

What autonomic innervation do blood vessels have?

A
  1. only sympathetic innervation
222
Q
  1. What receptors in blood vessels direct vasodilation?
  2. Method of inducing vasodilation
A
  1. M3 and M5 receptors
  2. IP3/DAG pathway begins and synthesizes NO which leads to vasodilation
223
Q
  1. What receptors on blood vessels receive sympathetic innervation?
  2. What NT activates them?
A
  1. A1
    1. A2
      1. B2
  2. Norepinephrine
224
Q

Where are A1, A2, B2 receptors of blood vessels found?

A
  1. A1 - skin, GI sphincters, kidney, brain
  2. A2- Skin
  3. B2- skeletal muscle, coronary arteries, hepatic arteries
225
Q
  1. What does activation of A1 receptors found in blood vessels do?
  2. What about A2 receptors
  3. What about B2 receptors
A
  1. induced IP3/DAG pathway which causes vasoconstriction
  2. Decrease cAMP which causes vasoconstriction
  3. Increases cAMP which leads to vasodilation
226
Q
  1. What are agonists that act on A1 receptors of blood vessels?
  2. What would this cause?
A
  1. NE, Epi, phenylephrine
  2. Constrict arteries (because activation of A1 causes vasoconstriction)
227
Q
  1. What are antagonists that act on A1 receptors of blood vessels?
  2. What would this cause?
A
  1. A1 blocker - Prazosin (dilates arteries)
228
Q

What occurs at low doses of epinephrine vs high doses of epinephrine?

A
  1. Vasodilation and increased HR - beta receptors (heart + blood vessels) effects dominate
  2. Vasoconstriction of majority of arteries and vasodilation of certain arteries - net effect is vasoconstriction (combination of alpha and beta receptor effects in blood vessels)
229
Q
  1. What is orthostatic hypotension?
  2. What can it be caused by (3)
A
  1. Low blood pressure what happens when you stand up from sitting or laying down position caused by reduced stroke volume when patient stands
  2. Low blood volume, impaired ventricular filling, or impaired sympathetic activation
230
Q

What are the 5 categories of conditions that can cause orthostatic hypotension?

A
  1. Hypovolemia (low blood volume)
  2. Cardiac disease
  3. Dysautonomia (problems with ANS)
  4. Endocrine disease
  5. Medications
231
Q

Describe what happens in normal compensation when someone gets up from laying down/sitting down?

A

image

232
Q

What is shock?

A
  1. life threatening condition of circulatory failure
  2. State of cellular and tissue hypoxia due to reduced oxygen delivery and/or increased oxygen consumption or inadequate oxygen utilization
233
Q

What are the different types of shock?

A
  1. Distributive shock - caused by low peripheral resistance
  2. Hypovolemic shock - primarily caused by less venous return
  3. Cardiogenic shock - caused by lower contractility
  4. Obstructive shock - reducing filling of either right or left ventricles depending on location of obstruction
234
Q
  1. What does the S1 sound represent?
  2. What about S2?
A
  1. closure of tricuspid and mitral valve
  2. closure of semilunar (aortic and pulmonary valves)
235
Q

What blood pressure can be considered hypertension?

A
  • ≥ 130 mmHg systolic and/or ≥ 80 mmHg diastolic
  • Repeat readings at least 3 times ideally over weeks and months
236
Q

One can diagnose hypertension in one visit if what BP reading is found?

A
  • severely elevated
  • ≥ 160 mmHg systolic and/or ≥ 100 mmHg diastolic
237
Q
  1. When is the DASH diet used and what is its main focus?
A
  1. DASH diet is used as a lifestyle change to work on hypertension
  2. Reducing sodium in diet and focus on eating foods rich in potassium, calcium, and magnesium.
238
Q
  1. What are the different types of diuretics? (4)
  2. Primary uses of each type
A
  1. Thiazide type (primary use is HTN)
  2. Loop ((primary use is diuresis)
  3. Potassium sparing (primary use is HTN)
  4. Aldosterone antagonists (primary use is HTN and heart failure)
239
Q

What agents under thiazide type diuretics should I know? (2)

A
  1. Chlorthalidone
  2. Hydrochlorothiazide
240
Q

What agents under loop diuretics should I know? (1)

A
  1. furosemide
241
Q

What agents under potassium sparing diuretics should I know? (1)

A
  1. Triametrene
242
Q

What agents under aldosterone antagonists diuretics should I know? (1)

A
  1. Spironolactone
243
Q

What are the drug classes for hypertension? (7)

A
  1. Diuretics
  2. Calcium channel blockers
  3. RAAS targets
  4. Beta blockers
  5. Direct vasodilators
  6. Central alpha 2 agonists
  7. Alpha 1 blocker
244
Q

What is the mechanism of action of diuretics for hypertension?

A
  1. diminishes sodium reabsorption in nephron thereby increasing urinary sodium and water losses
245
Q
  1. What are the two categories of calcium channel blockers?
  2. What drugs within each category should I know
A

Non-dihydropyridines (diltiazem)

Dihydropyridines (amlodipine, nifedipine)

246
Q
  1. What is the mechanism of action of dihydropyridine to decrease hypertension?
  2. What about non-dihydropyridine?
A

BOTH DIHYDROPYRIDINE AND NON-DIHYDROPYRIDINE -Blocks L type calcium channels in blood vessels (blocking inward flux of calcium into cell) - Causes relaxation of vascular smooth muscle (reducing arterial blood pressure and dilating coronary arteries)

++NON DIHYDROPYRIDINE- blocks calcium channels to reduce cardiac output by slowing HR and lowering contractility

247
Q

What are the categories of RAAS target drugs?

A
  1. Angiotensin converting enzyme inhibitors (ACE inhibitors)
  2. Angiotensin receptor blockers (ARBs)
  3. Direct renin inhibitor
  4. Aldosterone antagonists
248
Q

What is the mechanism of action of ACE inhibitors in modulating hypertension?

A
  1. blocks conversion of angiotensin I to angiotensin II (Ang II increases BP) and inhibits degradation of bradykinin (a potent vasodilator)
249
Q

What is the mechanism of action of ARBs in modulating hypertension?

A
  1. competitive antagonists of angiotensin II receptors - activation of receptors mediates vasoconstriction and aldosterone secretion but with antagonists, opposite occurs
250
Q

What is the mechanism of action of renin inhibitors in modulating hypertension?

A
  1. less plasma renin leads to less angiotensin I and II and less aldosterone levels
251
Q
  1. What are the categories of beta blockers?
  2. Which drugs should you know for each category?
A
  1. Cardioselective (Beta 1 receptor) - (metoprolol)
  2. Non-selective (Beta 1 and beta 2) - (propranolol)
  3. Mixed alpha and beta blocker - (Carvedilol and labetalol)
252
Q

What is the mechanism of action of beta blockers to modulate hypertension?

A
  1. Blocks Beta 1 receptors so inhibits increased HR, contractility, and AV conduction
  2. Blocks Beta 2 receptors so inhibits constriction in peripheral vascular muscle and bronchial muscle
253
Q
  1. What direct vasodilators should I know?
  2. What about central alpha 2 agonists?
  3. What about alpha 1 blockers?
A
  1. hydralazine, isosorbide dinitrate
  2. Methyldopa, clonidine
  3. Doxazosin

(these categories of antihypertensive drugs are last resort in treating hypertension)

254
Q

Mechanism of action of direct vasodilators?

A

Relax smooth muscles of arterioles and decrease peripheral vascular resistance

255
Q

Mechanism of action of Central alpha 2 agonists?

A
  1. Stimulates alpha 2 adrenergic receptors in brainstem, thus reduces sympathetic outflow from vasopressor centers in brain stem
256
Q

What is mechanism of action of Alpha 1 blocker (antihypertensive)?

A
  1. blocks alpha 1 adrenergic receptors in arteriolar and venous vascular smooth muscle to reduce arteriolar resistance
257
Q
  1. What antihypertensive should be used in pregnant women?
  2. What is avoided?
A
  1. labetolol is often used, nifedipine (CCB), methyldopa, Hyralazine
  2. ACE inhibitors, ARBs, direct renin inhibitors
258
Q

What is first line of therapy for children and adolescents with hypertension?

A
  1. first is nonpharmacologic treatment - lifestyle changes
  2. ACE inhibitor, ARB, CCB, and thiazide diuretics are acceptable if life style changes alone don’t work
259
Q

What antihypertensive should be used in patients with systolic heart failure?

A
  1. ACE inhibitors, beta blockers, and aldosterone blockers - they have mortality benefit
260
Q
  1. What antihypertensive should be used in patients with diabetes?
  2. What not to use?
A
  1. ACE inhibitors - they are protective of kidneys
  2. Beta blockers, HCTZ (which can increase glucose)
261
Q

What antihypertensive should be avoided in patients with renal failure or hyperkalemia?

A
  1. Avoid diuretics
262
Q

primary (essential) vs secondary hypertension

  1. incidence
  2. etiology
  3. presentation
  4. onset age
A

primary hypertension

  1. more common (90%)
  2. etiology is generally multifactorial (stress, genetic, lifestyle, etc)
  3. have mild to moderate hypertension which gradually progresses over years
  4. 20-50 years

secondary hypertension

  1. less common (10%)
  2. caused by an underlying condition
  3. symptoms of hypertension and underlying disease
  4. young patients <30 years old
263
Q

What is the difference between hypertensive urgency and hypertensive emergency?

A
  1. Hypertensive urgency - elevated BP (>180/120) without symptoms and no progressive organ dysfunction
  2. Hypertensive emergency - >180/120 and shows evidence of organ damage and symptoms

Block 4 (8 decks)

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