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CVR > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What is Pulmonary Circulation?

A

Low Pressure circulation to the lungs

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2
Q

What is Systemic Circulation?

A

High Pressure circulation to send oxygenated blood to tissues

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3
Q

What is Cardiac Output?

A

Volume of blood pumped per minute by each ventricle

Cardiac Output = Heart Rate x Stroke Volume

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4
Q

What is Diastole?

A

Period of Relaxation

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5
Q

What is Systole?

A

Period of Contraction

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6
Q

What is Stroke Volume?

A

Volume of blood ejected by the left ventricle in each cardiac cycle (EDV-ESV)

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7
Q

What is End-Diastolic Volume (EDV)?

A

Volume of blood left in the ventricle at the end of ventricular relaxation

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8
Q

What is End-Systolic Volume (ESV)?

A

Volume of blood left in the ventricle at the end of Ventricular contraction

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9
Q

What is Ejection Fraction?

A

Ratio of SV:EDV

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10
Q

What is the Cardiac Cycle?

A

The time from the start of one heart beat to the start of the next heart beat–> one complete cycle of the heart

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11
Q

What are the 5 Phases of the Cardiac Cycle?

A
  1. Late Diastole
  2. Isovolumetric Contraction
  3. Ventricular Ejection
  4. Isovolumetric Relaxation
  5. Early Diastole
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12
Q

What happens in Late Diastole?

A
  1. Ventricular Filling

2. Atrial Contraction (when the ventricle is 75% full)

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13
Q

What happens to Atrial and Ventricular Pressure during Late Diastole?

A

They both increase in Atrial Contraction

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14
Q

Which Heart valves are open and closed in Late Diastole?

A

AV valves are open, Pulmonary valves are closed

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15
Q

What happens in Isovolumetric Contraction?

A
  1. All Valves are closed
  2. Ventricle starts contracting
  3. Rapid increase in ventricular pressure
  4. Slight increase in atrial pressure due ventricle pushing against AV valves
  5. When Left Ventricular Pressure exceeds Aortic Pressure (80mmHg), aortic valve opens
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16
Q

What happens in Ventricular Ejection?

A
  1. AV Valves are closed, Pulmonary and Aortic Valves are open
  2. Ejection is most rapid during the early part (first 1/3)
  3. Expels Stroke Volume (70mL), leaving 50mL of blood in the heart
  4. Aortic Pressure rises to about 120mmHg
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17
Q

What happens in Isovolumetric Relaxation?

A
  1. All valves are closed
  2. Blood left in the heart is ESV
  3. Ventricle relaxes and Ventricular Pressures falls until the AV valves open and begins filling the ventricle again
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18
Q

What happens in Early Diastole?

A
  1. Ventricular Filling
  2. The Atria is filled and the AV valves open
  3. Atrial Pressure rises due to filling of atrium
  4. Ventricular pressure starts to slowly rise
  5. Aortic pressure slowly decreases to around 80mmHg
  6. Ventricles are about 75% full before Atrial Contraction occurs again
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19
Q

What are the different cells in the heart?

A
  1. Pacemaker cells
  2. Specialised Conducting Fibres
  3. Myocardial Cells
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20
Q

Where is the Action Potential in the heart generated?

A

Sino-atrial (SA Node)

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21
Q

What is the resting membrane potential of the pacemaker cell?

A

-55mV

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22
Q

What is the Threshold Potential of the Pacemaker Cell?

A

-40mV

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23
Q

Describe what happens in an Action Potential of a Pacemaker Cell?

A
  1. Pacemaker cell spontaneously depolarises to threshold due to “funny” channels allowing Na+ into the cell
  2. At threshold, Slow L-type Ca2+ channels open–> Action Potential occurs due to influx of Calcium, not Sodium
  3. After roughly 200msec–> Repolarisation, Ca2+ channels close, K+ channels open
  4. Hyperpolarisation–> K+ channels close, triggers “funny” channels to open again
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24
Q

Describe the Action Potential of A Ventricular Myocardial Cell

A

Phase 0: Rapid Depolarisation–> Opening for fast, voltage-gated Na+ channels due to impulse from nearby cells
Phase 1: Na+ channels close, Slow, L-Type Ca2+ channels open
Phase 2: Plateau Phase of Action Potential–> Weak inward flow of Ca2+, balanced by slow outward flow of K+ driven by concentration gradient (refractory period)
Phase 3: Repolarisation–> Ca2+ channels close and Voltage-gated K+ Channels open
Phase 4: Rest Period–> K+ channels close and excess Na+ is removed by Na+/K+ pump

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25
Q

Why must there be a refractory period in the Action Potential of a Ventricular Myocardial Cell?

A

To allow the ventricle to fully contract and relax before the next action potential–> prevents \summation and tetanus in the heart

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26
Q

Describe the Conduction Pathway in the heart

A

SA node–> Internodal Pathways–> AV node–> Bundle of His–> Purkinje Fibres

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27
Q

What is the function of the AV node?

A
  1. It is the only means by which excitation can reach the ventricles
  2. Delays the impulse by about 100msec–> allows the atria to contract before the ventricles
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28
Q

How do we control cardiac output?

A

We control Heart Rate and Stroke Volume

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29
Q

What neurotransmitter does the Sympathetic Nervous System release and where do they act in the heart?

A

Noradrenaline–> Act on ß1 Adrenoreceptors

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30
Q

What is the action of Noradrenaline on the SA Node?

A

Stimulates Adenylate Cyclase–> Increase cAMP–> cAMP binds to “funny” channels, making them more permeable–> Pacemaker cells will be quicker to depolarise to threshold–> more action potentials–> Increase Heart Rate

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31
Q

What is the action of Noradrenaline on the Atria and Ventricles?

A

Stimulates Adenylate Cyclase–> Increase cAMP–> cAMP increases permeability of calcium–> Greater amounts of calcium in the myocardial cell–> Greater force of contraction–> Increased Stroke Volume

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32
Q

What neurotransmitter does the Parasympathetic Nervous System release and where do they act on the heart?

A

Acetylcholine–> M2 Muscarinic Receptors

33
Q

What is the action of acetylcholine on the SA Node?

A

Inhibits Adenylate Cyclase–> Decrease cAMP–> Pacemaker cells take longer to depolarise to threshold–? less action potentials–> Decrease Heart Rate

34
Q

What is the action of acetylcholine on the Atria?

A

Decrease the force of contraction of the atria

35
Q

What is the action of acetylcholine on the ventricles?

A

Does not inhibit the contraction of the ventricles directly–> the stroke volume is decreased because less blood is pumped into the ventricles from the atria

36
Q

What is Ventricular Escape?

A

It’s when the Ventricle beats at its own slow rate to prevent the heart from completely stopping (when the Atria stops contracting)

37
Q

What is Blood Pressure?

A

Cardiac Output x Total Peripheral Resistance

38
Q

What is the Baroreflex?

A

Reflex stimulated by Baroreceptors in response to changes in blood pressure

39
Q

What are Baroreceptors?

A

They are stretch receptors–> They respond to stretch in the blood vessel wall

40
Q

Where are the Baroreceptors located?

A
  1. Aortic Arch (signals via the vagus nerve)

2. Carotid Sinus (signals via Hering’s Nerve and the Glossopharyngeal Nerve)

41
Q

What is the Baroreflex in response to an increase in blood pressure?

A

Increase in Blood Pressure –> Increase Arterial Wall stretch–> Increase Baroreceptor firing–> Vasodilation, decrease heart rate and stroke volume–> Lowers Blood Pressure to normal

42
Q

What is the Baroreflex in response to a decrease in Blood Pressure?

A

Decrease in Blood Pressure–> Decrease in Arterial Wall Stretch–> Decrease Baroreceptor Firing–> Vasoconstriction, increase Heart Rate and Stroke Volume–> Increase Blood Pressure to normal

43
Q

What is the effect of increased blood tissue demands on cardiac output?

A

If tissue demands increase–> blood vessels vasodilate to increase blood flow–> TPR decrease and Cardiac Output Increase

44
Q

What is the effect of decreased blood tissue demands on cardiac output?

A

If tissue demands decrease–> blood vessels vasoconstrict to decrease blood flow–> TPR increase and Cardiac Output decrease

45
Q

What causes pathologically high cardiac output?

A

Peripheral Vasodilation (decreased TPR)

46
Q

What causes pathologically low cardiac output?

A

Cardiac damage or low venous return

47
Q

What are the effects of exercise on the cardiovascular system of a fit young adult?

A
  1. Heart Rate increase to 300% resting (200bpm)
  2. Stroke Volume Increase to 175% resting (125mL)
  3. Cardiac Output increases to 500% resting (25L)
48
Q

What are the effects of exercise on the cardiovascular system of a top athlete?

A
  1. Heart Rate increase to maximum of 200bpm
  2. Stroke Volume increases beyond 125mL to 175mL
  3. Cardiac Output increases to a maximum of 35L or more
49
Q

In the Frank-Starling Mechanism of the Heart, What is Preload?

A

The End-Diastolic Volume

50
Q

In the Frank-Starling Mechanism of the Heart, What is after load?

A

The arterial/total peripheral resistance the ventricle must pump against to eject blood

51
Q

What is the effect on increased Preload on the heart?

A

An increased preload will lead to increased force of contraction and increased stroke volume because the Cardiac Output must equal Venous Return

52
Q

What is the effect of Afterload in the heart?

A

Increased Afterload–> Decreased Stroke Volume–> Increased ESV–> Increased EDV–> Increase Force of Contraction–> SV increase back to normal

53
Q

What are the Atrial Reflexes to maintain cardiac output?

A
  1. Baroreflex
  2. Sympathetic drive to kidney–> amount of filtration affects blood volume
  3. Sympathetic drive to kidney–> RAAS conservation of water affects blood volume
  4. Vasopressin Secretion–> Conservation of water is affected
  5. Atrial Natriuetic Peptide–> Increases the loss of sodium and water
54
Q

What is the P Wave of the ECG?

A

Atrial Depolarisation

55
Q

What is the PR-Interval of the ECG

A

Atrial depolarisation and contraction

56
Q

What is the QRS Complex of the ECG?

A

Ventricular Depolarisation and Atrial Repolarisation

57
Q

What is the QT interval of the ECG?

A

Single cycle of Ventricular Depolarisation and Repolarisation

58
Q

What is the ST Interval of the ECG?

A

Ventricular Contraction

59
Q

What is the T Wave of the ECG

A

Ventricular Repolarisation

60
Q

What is the TP interval of the ECG

A

Ventricular Relaxation and Filling

61
Q

How’s the ECG Recorded?

A

From the skin–> The current flows from depolarised to non-depolarised

62
Q

What happens to the ECG when a patient has SA Block?

A

No P Wave

63
Q

What happens to the ECG when a patient has 1st degree AV Block?

A

Prolonged PR Interval (0.2s)

64
Q

What happens to the ECG when a patient has 2nd Degree AV Block?

A

Prolonged PR Interval, missed beats and P:QRS rhythm of 2:1 or 3:2

65
Q

What happens to the ECG when a patient has 3rd Degree AV Block?

A

Complete block, P and QRS waves are dissociated and have own rhythms

66
Q

What is Stokes-Adam Syndrome?

A

When a patient has Intermittent complete AV block followed by ventricular escape

67
Q

What causes an Increased Voltage in the QRS complex?

A

Increased Muscle Mass

68
Q

What causes a decreased voltage in the QRS Complex?

A

Decreased Muscle mass or damaged muscle (e.g. Myocardial Infarction)

69
Q

What causes Prolonged QRS Complex?

A

Slow conduction in the ventricles

70
Q

What causes an elevated ST segment?

A

Acute Myocardial Infarction

71
Q

What is Sinus Rhythm?

A

Normal SA node rate (HR) of 60-100bpm

72
Q

What is Sinus Tachycardia?

A

Increased Heart Rate due to Sympathetic Nervous System, Increased Temperature, Cardiac Toxicity

73
Q

What is Sinus Bradycardia?

A

Decreased Heart Rate at rest sue to overactive Vagus

74
Q

What is Sinus Arrhythmias?

A

In deep breathing, Increased heart Rate with Inspiration and Decreased Heart Rate with Expiration

75
Q

What are Ectopic Beats?

A

Premature contractions due to abnormal impulses from abnormal pacemaker sites within the heart outside the SA Node

76
Q

What Starling Forces affect Capillary Filtration?

A

Outwards: Capillary Blood Pressure, Plasma Protein Colloid Osmotic Pressure
Inwards: Interstitial Fluid Pressure, Interstitial Fluid Colloid Osmotic Pressure

77
Q

What Factors determine Venous return?

A
  1. Pressure gradient to Heart
  2. Skeletal Muscle Pump
  3. Negative Interthoracic Pressure During Inspiration
    4 Venoconstriction
78
Q

What causes Inverted T Wave in the ECG?

A

Slow conduction through fibres–> Fibres that depolarise first also depolarise first

79
Q

What are causes Premature Ventricular Contractions?

A
  1. Prolonged QRS
  2. Increased QRS Voltage
  3. Inverted T Wave
  4. Anomalous Pathways between Atria and Ventricles

CVR (5 decks)

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